Protected: 55. Bone – Osseous Surgery – IV Augmentation B- Allografts

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131. Non-surgery vs. Surgery

b. Statistical methods

Rapid Search Topics

What treatments does Non-Surgical Therapy include? What is scaling? What is root planing? What are the endpoints to successful root planing therapy? What studies show the effectiveness of SRP? What are some factors that can limit the effectiveness of SRP? Is SRP equally effective in molars and non-molars? Are more experienced practitioners more effective at SRP?

CobbC. Non surgical pocket therapy: Mechanical. Ann Periodontol 1996;1;443-490
BuchananA., Robertson P. Calculus removal by scaling/root planing with and without surgical access. J Periodontol 1987;58:159-163
LoosB et al. Clinical effects of root debridement in molar and non-molar teeth. A 2 year follow up. J Clin Periodontol 1989;16:498-504
Brayer,W et al. Scaling and root planing effectiveness: The effect of root surface access and operator experience. J Periodontol 1989;60:67-72
BaderstenA, et al. Effect of nonsurgical periodontal therapy. I. Moderately advanced periodontitis. J. Clin. Periodontol. 8:57-72, 1981.
BaderstenA, Nilveus R, Egelberg J: Effect of nonsurgical periodontal therapy. II. Severely advanced periodontitis. J. Clin. Periodontol. 11:63-76, 1984.
BaderstenA, Nilveus R, Egelberg J: Effect of non-surgical periodontal therapy. III. Single versus repeated instrumentation.J.Clin.Periodontol.11:114-124, 1984.
BaderstenA, et al: Effects of nonsurgical periodontal therapy. IV. Operator variability. J. Clin. Periodontol. 12:190 -200, 1985.
BaderstenA, et al: Effect of nonsurgical periodontal therapy. VIII. Probing attachment changesrelated to clinical characteristics. J. Clin. Periodontol. 14:425-432, 1987
GreenwellH, Bissada NF, Dodge JR. Disease masking: A hazard of nonsurgical periodontal therapy. Perio Insights December 1998:14-19.
MatthewsD. Conclusive support for mechanical nonsurgical pocket therapy in the treatment of periodontal disease. How effective is mechanical nonsurgical pocket therapy? Evid Based Dent. 6(3):68-9. 2005
RamfjordS, et al. Results of periodontal therapy related to tooth type. J. Periodontol. 51:270-273, 1980.
PihlstromBL, Oliphant TH, McHugh RB: Molar and nonmolar teeth compared over 6.5 years following two methods of periodontal therapy. J. Periodontol. 55:499-504, 1984
ClaffeyN, Shanley D: Relationship of gingival thickness and bleeding to loss of probing attachment in shallow sites following nonsurgical periodontal therapy. J Clin Perio 13:654, 1986.
LoescheW, Soehren S, et al. Nonsurgical treatment of patients with periodontal disease. Oral Surg, Oral Med, Oral Pathol 1996; 81: 533-543.
LoescheWJ, Giordano JR, Soehren S, Kaciroti N. The nonsurgical treatment of patients with periodontal disease: results after 6.4 years. Gen Dent. Jul-Aug;53(4):298-306; 2005
DriskoCH. Nonsurgical periodontal therapy. Perio 2000 25:77-88,2001. (Review)

Is Surgical Treatment more effective than non surgical treatment?

Lindheet al. Long term effect of surgical/non surgical treatment of periodontal disease. J Clin Periodontol 1984;11:448-458
Caffesse,R et al. Scaling and root planing with and without periodontal flap surgery. J Clin Periodontol 1986;13:205-210
PhilstromB, et al: Comparison of surgical and nonsurgical treatment of periodontal disease. A review of current studies and additional results after six years. J Clin Perio 10:524-541, 1983.
Serino,G et al. Initial outcome and long term effect of surgical and non surgical treatment of advanced periodontal disease. J Clin Periodontol 2001;28:910-916

What is the critical probing depth?

LindheJ, Socransky SS, et al. “Critical probing depths” in periodontal therapy. J Clin Periodontol 9:323-336, 1982.

Statistical Methods

What is sensitivity and specificity? What is positive predictive value and accuracy? What is Prevalence? What is negative predictive value? What is equivalence and superiority? What is regression towards the mean?

D. Brunette: Critical Thinking: Understanding and Evaluating Dental Research 2nd Edition Quintessence Publishing Co, Inc ISBN 978-0-86715-426-9; 2007; pp 163-184, pp192-193
HujoelPP, Moulton LH, Loesche WJ : Estimation of sensitivity and specificity of site-specific diagnostic tests. J. Periodontal Res. 25:193-196, 1990.
GunsolleyJC, Elswick RK, Devenport JM. Equivalence and superiority testing in regeneration clinical trials. J Periodontol 69:521-527, 1998.
GunsolleyJ. Equivalence, superiority, and negative clinical trials. J Periodontol 69:608,1998
DukeSP, Garrett S. Equivalence in periodontal trials: A description for the clinician. J Periodontol 69:650-654, 1998.
Gunsolley, J et al: Is loss of attachment due to root planing and scaling in sites with minimal probing depths a statistical or real occurrence? J Periodontol 2001;72:349-353

What is the difference between statistical significance and clinical significance?

RethmanMP, Nunn ME. Clinical versus statistical significance. J Periodontol 70:700-702,1999.
GreensteinG, Lamster I. Efficacy of periodontal therapy: Statistical versus clinical significance. J Periodontol 71:657-662, 2000.
HujoelPP, Armitage GC, Garcia RI. A perspective on clinical significance. J Periodontol 71:1515-1518, 2000.

How can we evaluate the quality of a RCT? What is a meta-analysis and how accurate are their results? What are the major pitfalls in clinical trials design?

JeffcoatMK. Principles and pitfalls of clinical trials design. J Periodontol 1992;63:1045-1051
CohenME, Ralls SA : False positive rates in the determination of changes in probing depth related to periodontal measurements. J. Periodontal Res. 23:161-165,1988.
HujoelPP, Moulton LH : Evaluation of test statistics in split-mouth clinical trials. J. Periodontal Res. 23:378-380, 1988.
LesaffreE, Garcia Zattera MJ, Redmond C, Huber H, Needleman I; ISCB Subcommittee on Dentistry. Reported methodological quality of split-mouth studies. J Clin Periodontol. Sep;34(9):756-61; 2007. Review.
NeedlemanI, Worthington H, Moher D, Schulz K, Altman DG. Improving the completeness and transparency of reports of randomized trials in oral health: the CONSORT statement. Am J Dent. Feb;21(1):7-12; 2008
MontenegroR, Needleman I, Moles D, Tonetti M. Quality of RCTs in periodontology–a systematic review. J Dent Res. Dec;81(12):866-70; 2002. Review.
EspositoM, Coulthard P, Worthington HV, Jokstad A. Quality assessment of randomized controlled trials of oral implants. Int J Oral Maxillofac Implants. Nov-Dec;16(6):783-92; 2001. Review.

Root Caries

What factors may influence the incidence of root caries? Does periodontal treatment increase root caries?

Ravald N, Birkhed D, Hamp SE. Root caries susceptibility in periodontally treated patients. Results after 12 years. J Clin Periodontol. Feb;20(2):124-9; 1993
Paraskevas S, Danser MM, Timmerman MF, van der Velden U, van der Weijden GA. Amine fluoride/stannous fluoride and incidence of root caries in periodontal maintenance patients. A 2 year evaluation. J Clin Periodontol. Nov;31(11):965-71; 2004
De Soete M, Dekeyser C, Pauwels M, Teughels W, van Steenberghe D, Quirynen M. Increase in cariogenic bacteria after initial periodontal therapy. J Dent Res. Jan;84(1):48-53; 2005

Cobb 1996 ARTICLE

P:A literature review regarding: 1) progression of untreated periodontal disease which offers a basis for comparing the effects of mechanical non-surgical treatment 2) the effect of scaling and root planing on specific clinical parameters and selected biologic factors (sub-g microbial flora, cementum and root surface roughness), 3) root preparation using power driven instruments.

Disc:

3- to 4- fold increase in mean annual tooth loss in untreated population
Molar teeth most frequently lost
Annual progression rate of untreated perio dz ranges from 0.1mm to 0.2mm
Positive association between increasing age and increasing loss of perio support
Critical for periodontal therapy: thoroughness of root surface debridement and pt’s OH
Multi-rooted teeth (anatomic factors, furcation) require more skill and time to effectively treat and generally respond less favorable to sc/rp than single rooted teeth.
Clinical predictors for future CAL loss:

Tooth type
Initial CAL loss or bone height at baseline
Moderate and severe gingival inflammation
Sub-g calculus
Smoking

CAL loss after sc/rp of shallow PDs
Greater CAL gain with deeper PDs

1-3mm PD- 0.34mm CAL loss
4-6mm PD- 0.55mm CAL gain
>7mm PD- 1.29mm CAL gain

Amount of reduction directly related to initial PD
Single rooted teeth respond better to sc/rp. Molars with furcation involvement respond less favorably than molars without furcation involvement or single rooted teeth.
Weak correlation between BOP and dz progression. Absence of BOP correlated with periodontal stability
Mechanical non-sx tx- mean reduction in BOP-57%
SC/RP

Reduction in % of motile microbes and spirochetes

Increase in cocci and non-motile microbes

Presence of supra-g microbial plaque facilitates repopulation of sub-g pockets within 4-8 weeks (spirochetes and motile rods)
% of surfaces with residual calculus without flap 17-69%, with flap 14-24%

deeper sites-more residual calculus
no SSD between anterior and posterior teeth
no SDD between closed vs open approach in furcations
no SDD between US and manual instrumentation (faster with US)

Recent studies support that there is no need for extensive cementum removal. Endotoxins bound superficially to root surface.
Root surface roughness after scaling may be associated with increased initial adhesion and retention of microbes. More true for supra-g root surfaces, less dramatic for sub-g root surfaces.
Healing with long junctional epithelium. Re-establishment of the attachment epithelium occurs within one or two weeks. There is reduction in inflammation that appears correlated to reduction of inflammatory cells and GCF flow and repair of connective tissue matrix.

Progression of untreated periodontal disease

Distribution of periodontal disease and factors affecting progression

Annual tooth loss rates in patients with and without periodontal therapy

Mechanical non-surgical therapy

The 1989 Proceedings of the World Workshop in Clinical Periodontics defined scaling as “Instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus and stains from these surfaces. Root planing was defined as “A definitive treatment procedure designed to remove cementum or surface dentit that is rough, impregnated with calculus or contaminated with toxins or microorganisms.

Shallow PDs 1-3mm lost attachment 0.34mm.
PDs 4-6mm had a mean gain of 0.55mm, PDs 7mm exhibited the greatest CAL gain- 1.29mm.
Lindhe- critical probing depth: 2.9mm for sc/rp and 4.2mm for surgical treatment.
Ramfjord and Kiester were the first to report on CAL loss subsequent to scaling on initial shallow PDs.

Effectiveness of scaling and root planing

Effectiveness of calculus removal with or without flap

Amount of cementum removal during scaling and root planing

Comparison of manual instrumentation to sonic/ultrasonic instrumentation

Buchanan 1987 (efficacy) ARTICLE

P:To evaluate the presence and extent of calculus on subgingival root surfaces of teeth that received SRP alone, SRP with modified Widman flap, or no treatment.

M+M:10 pts (28-62 years old) that had at least 3 teeth that needed extractions due to severe periodontitis. Teeth in each pt randomly assigned to one of three groups: SRP alone (29 teeth), SRP w/ MWF (35 teeth), or not tx before extraction (22 teeth). SRP completed with ultrasonic scalers and hand instruments. Teeth were extracted and stained with methylene blue to disclose and looked under 10x stereomicroscope. Each surface was examined to determine the pocket depth, area of root surface exposed to the pocket , and amount of pocket area showing retained calculus. Calculus-positive teeth (CPT) and surfaces (CPS), and percentage of pocket area occupied by calculus (C/A) were derived for each group.

R:The mean treatment time per tooth for SRP alone was 12.9 ± 2.1 minutes, for the SRP w/flap it was 11.5 ± 2.0 minutes per tooth plus an additional 6.6 ±1.9 minutes per tooth for incision, reflection, and removal of granulation tissue, to a total treatment time per tooth of 18.1 ±2.0 minutes.

Pocket depth and area: were similar for all three groups averaged 5.9 mm and 26.0 mm²respectively.

Calculus:

In the no-treatment group was present on most surfaces of all 22 teeth and occupied an average of about 1/3 of the mean pocket area.
Bothtreatment groups showed SS lower values than the no-treatment group for calculus-positive teeth and surfaces and percentage of pocket area with retained calculus.
13/ 35 teeth (37%) had residual calculus after SRP w/flap, whereas 18/29 teeth (62%) had residual calculus after SRP aloneSSD
Increased efficiency in calculus removal by SRP w/ flap as compared with SRP alone was limited primarily to anterior and premolar teeth, and NSSD in calculus positive molar teeth or surfaces were found between the two groups.
All measures of calculus retention were SS greater in the no treatment group than in either treatment group.
The percentage of calculus positive surfaces was lower after SRP w/ flap than after SRP alone for all surfaces, and the difference was SS on facial and lingual surfaces.
Theeffects of SRP w/ and w/o flap access were NSSD in pocket depth ranges of 0 to 6.0 mm. For pocket depths greater than 6 mm, calculus positive surfaces after SRP w/flap remained constant at approximately 17% , but after SRP alone they continued to increase and averaged 45% for-pocket depths greater than 8.0 mmSSD

BL: SRP w/ flap proved to be more effective than SRP alone in reducing the percentage of calculus positive teeth and surfaces. The advantage of SRP w/flap was most dramatic on anterior and premolar teeth, and on facial and lingual surfaces. In pocket depths >6 mm, calculus positive surfaces after SRP alone increased linearly and SS and in pockets deeper than 8 mm, calculus-positive surfaces averaged about 45% after SRP alone whereas after SRP w/ flap they remained constant at about 17%.

Loos 1989 ARTICLE

P:To report on the longitudinal observations over 2 years of the clinical effects of root debridement in molar furcation sites, molar flat-surface sites and non-molar sites.

M&M:12 pts with generalized perio included. Sites grouped as either molar furcation, molar flat-surface or non-molar as well as being shallow (<3.5mm), moderate (4.0-6.5) or severe (>7mm). Pts received OHI 3wks prior to the initial therapy, which consisted of only 2 sessions of SRP (1 each jaw). Every 3 months, pts received supra-g prophy and OHI and had their clinical parameters recorded with an electronic, pressure-sensitive probe set at 0.5N for a 2-year period.

R:Initially moderately deep and deep molar furcation sites responded less favorably to therapy compared to non-molar sites and molar flat-surface sites of similar PD. Initial improvements in PDs for moderately deep and deep molar furcation sites were limited and also tended to revert during the observation interval. For moderately deep surfaces at molar flat-surfaces and non-molar sites, the 3-month gain in PAL from 0.2-0.4mm, followed by a return to baseline. There was no change in PAL in furcation sites at 3 months, followed by a gradual mean loss amounting to 0.8mm at 24 months. 25% of molar furcation sites had PALoss, versus 7% of non-molar sites and 10% for molar flat-surface sites. Reduction in BOP was primarily noted in shallow sites. BOP in moderately deep and deep sites remained high.

BL:Furcations require additional treatment after SRP.

Cr: Only 12 pts. 2 years without addressing sub-g sites is not a realistic clinical situation (hopefully). Initial therapy only consisted of SRP (no elimination of overhangs, occlusal adjustment, etc). No sx pocket elimination performed. Therefore, this study cannot be compared to many traditional perio lit maintenance studys.

Brayer 1982 ARTICLE

Purpose:To investigate 1) if access to the root surface affects an operator’s ability to effectively scale and root plane teeth and 2) if operator skills as measured by experience level affect the ability to effectively perform SRP.

Materials and methods: 29 patients with 114 hopeless teeth were included in the study. Total of four operators performed SRP. Two fully trained Board certified periodontists (EL-1) and two 2^ndyear perio residents (EL-2). SRP was performed either as a closed procedure or after flap access. Unscaled teeth were retained as controls. PDs and calculus index were recorded. No time limits were placed but time was also recorded. Teeth were then extracted and root surfaces were then microscopically evaluated for residual calculus by a periodontists that did not participate in the operating procedures.

Results:Time to elevate the flap: 6.5 min/tooth (EL-1) vs 7.8 min/tooth (EL-2)

Open SRP time: 5.3 min/tooth (EL-1) vs 6.7 min/tooth (EL-2)

Closed SRP time: 8.1 min/tooth (EL-1) vs 9.5 min/tooth (EL-2)

Calculus free areas in open SRP: 96.4% EL-1 vs 91.2% EL-2

Calculus free areas in closed SRP: 86.2% EL-1 vs 65.7% EL-2

In shallow periodontal pockets no significant difference between groups in % of residual calculus, in pockets 4-6mm open SRP resulted in 92% of calculus free areas comparing to 71% with closed SRP.

The more experienced operators produced significantly greater number of calculus-free root surfaces (89% vs 74%) in 4-6mm pockets and >6mm pockets (91% v 69%). No difference in 1-3mm pockets.

Conclusion:In single rooted teeth with PDs more than 4mm SRP with flap access was more effective and the more experienced operators produced fewer root surfaces containing residual calculus.

Badersten 1981(I) ARTICLE

Purpose:To compare the effect of hand versus US instrumentation in patients with moderately advanced periodontitis.

Materials and methods:

15 patients had initial prep only using US or hand instruments in a split mouth design (no molars studied).
A total of 528 sites were treated with average PD of 4.2 mm (most pockets ranged from 2-7 mm, highest PD was 12.5 mm).
Evaluated plaque scores, BOP, PD &CAL up to 13 months.

Results:

All parameters improved during the first 4-5 months after start of treatment, but little change occurred during the rest of the 13 months observation period.
Mean total reduction in PD was 1.3-1.7 mm.
Only 13/106 (12%) of the initial sites exhibited PD of >6 mm after 6 months.
Deeper pockets reduced about 1.1-1.5 mm with a decrease in bleeding
No difference between HI & US.
Shallower sites had some loss of attachment (2-3 months) while deeper sites showed some improvement.

BL:Non-surgical treatment of non-molar teeth with moderate PD is effective, with no difference between HI and US.

Badersten 1984(II) ARTICLE

P:To study the healing events in patients with pockets up to 12 mm deep, to compare hand to ultrasonic instruments

M&M:16 patients, with severe periodontitis, 4-10 teeth in each patient (incisors, canines, premolars), probing depths > 5 mm with calculus & bleeding on probing on > 2 aspects each tooth. OHI over 2-3 visits, extra instructions were given as needed. 3 months after OHI, measurements were taken, then preparation with either ultrasonic or hand instruments in a split mouth design was performed, measuring plaque index, bleeding on probing, attachment level and recession were recorded and repeated every 3 months up to 24 months, instrumentation was performed again at 6 & 9 months. (3 sessions overall)

R:Total of 852 surfaces were treated

– Plaque index: NSD between 2 instruments, higher with reduction with one of the two investigators

– Bleeding On Probing: No change between initial exam & 3 month after OHI. It did, however, decrease after instrumentation (84-90% decreased to 14-18%). Similar decrease in bleeding on probing for both investigators and instruments.

– PD: Initial : 5.5-5.8 mm. 3 months: 5.1-5.3 mm. 12 months: 3.6-3.9 mm. 24 months: residual probing depths decreased irrespective of operator or instrument for all probing depths; 43 surfaces had PD > 7 mm (86% reduction)

– Recession: limited gingival recession during the 3 months but at 12 months 1.6-1.8 mm recession

– PAL:

Residual PD: Loss of attach of ≥1.5 mm in surfaces with residual PD ≤2.5 mm and ≥6 mm. Gain of attachment of ≥1.5 mm for 24-31% of surfaces with residual probing depths of 3-4.5 mm.

Initial PD: Gain/Loss of PAL 1.5 mm or more/less. Found Majority of initial PD < 4-4.5 mm loss of PAL, while PD >6-6.5 mm gain of PAL.

– NSSD between ultrasonic & hand instruments, but 1 operator used less time with ultrasonic.

BL:Deeper sites had more: recession, residual probing depths, gain in attachment. Sites < 3.5 mm lost attachment, sites >8 mm gained attachment. Authors mentioned that decision to proceed with Surgery Treatment should be postponed until 6-9 months after initial instrumentation.

Badersten 1984 (III) ARTICLE

P: To compare the effect of a single session of subgingival instrumentation using ultrasonic scaler with 3 sessions separated by 3 months.

M&M:13 patients (30-55yrs) with PD up to 5-11mm were included in the study. Incisors, canines, premolars only, 6-10 teeth in each patient were used in split mouth design. OHI, US debridement with one side received 1 session and the other received 3 sessions at 0, 3, 6 months. PI, BOP, PD, CAL, and recession were recorded at baseline and every 3 months for 24 months (blinded examiner).

R: Avg PD prior to txt 5.8 mm for surfaces to be instrumented once and 5.9 mm for surfaces to be treated 3 times.

PIwas sig reduced with both forms of txt.

Initial BOP 78%-80% reduced to 15-20% for both treatments, maintained throughout observation.

PD, similar decrease for both groups: initial PD score 5.5-5.9mm. PD reduced to 4.1-4.2 mm after 3 months, and a further reduction to 3.5-3.7 mm was seen at 9-month exam.

Recession:occurred during 1^st 9 months of study and stabilized at an average of 1.8mm.

CAL gain: A mean of 0.4mm if seen after 3 months and remained constant throughout the study.

Sites with <3mm PD showed 0.4-1mm of CAL loss, sites >8mm gained 0.9-2.8mm. Only 25% of PD between 3-4.5 mm gained; >1.5mm of attachment.

Initial healing was the same for both groups. Full effect of healing was not obtained until 6-9 months after instrumentation.

BL:Similar results were recorded with 1 or 3 sessions of SCRP. Repeated instrumentation is of limited value. Clinical parameters remained unchanged during 24 months and did not show recurrence of disease. Full effect of healing not obtained for 6-9 months after instrumentation.

Limitation:molar were excluded from the study

Badersten 1985 (IV) ARTICLE

P: To compare the results achieved by other operators in treating severe periodontitis with a single instrumentation.

M&M:20 patients (28-64 years old) with severe periodontal disease were included. Incisors, cuspids, and premolars in maxilla or mandible were used (each patient had between 6-10 of these teeth). Pockets of at least 5mm with calculus and BOP on at least 2 aspects of each tooth. OHI 2 or 3 times were given during the first month. Additional OHI provided as needed. Periodontal pockets were debrided immediately following the initial examination. Split mouth design was used, one half was assigned to a periodontist, and the other half to a hygienist (5 different hygienist participated); both using US and/or HI for instrumentation. Time of instrumentation was recorded. Pl, BOP, PD, PAL were recorded every 3 months for 24 months.

R: 1056 sites were treated. Significant positive trend was seen in all patients after treatment (improvement at 3 months and essentially the same or slightly better thereafter). Reduction in PI, PD, BOPS with no difference b/w the 2 operator types. The periodontist sites showed slightly greater gains in PAL and less recession than hygienist sites. The average time spent in instrumentation per tooth was 9-12 minutes.

CL: The results of non-sx periodontal therapy b/w different operators were minimal. Overall, it was observed that incisors, cuspids and premolars might be maintained by plaque control and single instrumentation.

Badersten 1987 ARTICLE

P:To observe the effect of non-sx perio tx on probing attachment changes related to clinical characteristics.

M&M:1688 proximal sites in non-molar teeth from 49 pts were monitored for 24 mo. following OHI and root debridement. Gain and loss of CAL was recorded, for incisors, canines, and PM, max or mandibular, presence/absence of endo, and for surfaces w/ and w/o the presence of root concavity/furcation involvement. Changes were compared to: initial PD, radiographic bone score, depth of osseous defect (radiographically), and widened PDL.

R:12% had probing attachment gain, 4% had probing attachment loss (PAL).

Sites w/ clinical attachment gain were more frequent in mand cuspids and premolars
Intially deeper sites had higher occurrence of clinical attachment gain.
More clinical attachment gain occurred in sites w/ more initial bone loss and deeper osseous defects.
Sites w/ a widened PDL at baseline, showed more clinical attachment gain than non-widened
Presence of IP root concavity or furcation involvement was assoc’d w/ lower frequency of attachment gain

CL:outcome of debridement and maintenance in proximal surfaces of non-molar teeth is not compromised by the severity of the initial soft tissue or bony lesion.

More attachment gain is assoc w/ mand cuspids and premolars, deeper initial PD, deeper osseous defects, widened PDL, and w/ no-root concavities/furcas.

Greenwell 1998 ARTICLE

P:To describe situations in which non-surgical therapy can obscure the disease.

D:Periodontal disease masking results when marginal tissue at 3-4 mm within the gingival margin appears healthy, while apical tissue is unhealthy. This can lead to attachment and bone loss, hidden by the relatively non-inflamed appearance of the gingiva. This is most common after SRP where calculus in the apical part of pocket is missed. Primary goal of post-S/RP is to evaluate for inadequate calculus removal, manifested by residual inflammation, BOP or suppuration. The additional SRP should be directed at calculus removal. Prescribing antibiotics or antimicrobials after SRP would further mask unresolved disease. The most appropriate time for antibiotic therapy is after removal of all calculus & plaque-retentive factors, which is post-surgical, not post-SRP. Reports of abscesses post-prophy demonstrate disease masking. The concept of “soft tissue management” is questionable, since it’s the root, not the soft tissue that needs treatment. Proper non-surgical therapy should include meticulous SRP.

Recognizing disease masking: Absence of BOP & improvement/return of radiographic crestal lamina dura may be the best clinical signs of improved health. Although absence of lamina dura does not mean disease activity present, its reestablishment indicates that disease progression has been halted. Be suspicious of an absent lamina dura. Delayed BOP could be a sign of disease masking and its importance should not be minimized.

Case Report: A 43 year-old healthy patient who underwent surgical therapy for posterior quadrants and was put on 9 SPT/year x 3 years. Despite clinical healthy-looking gingival tissue on anterior areas, BOP was erratic & present about 50 % of time on the area; also, no return in crestal lamina dura & no increase in radiographic density. 2 mm increase in PD was found after 3 years & 1 mm AL around teeth 7 & 8. Sx recommended & burnished calculus found. At 3 years after surgery, increase in bone density was seen, no BOP & Attachment level was stable.

BL:Inadequate SRP or inappropriate antibiotic therapy can potentially mask an area with perio disease. Comparing subsequent exams for BOP & CAL is essential to detect unresolved or recurrent disease.

Matthews 2005 ARTICLE

P:Systematic review to answer the question, “How effective is mechanical nonsurgical pocket therapy?”

M+M: The authors used the Cochrane Oral health Group List of Systematic Reviews in Dentistry, Database of Abstracts of Reviews of Effectiveness, Medline, Embase, and Scisearch. No date or language restriction was imposed. Reference lists of located reviews were checked for additional references. 12 reviews were selected for inclusion, and a narrative appraisal of the reviews was conducted.

R: Implications for clinical practice were identified.

Initial Therapy:

Mechanical nonsurgical pocket therapy reduces inflammation and pocket depth and increases clinical attachment level in patients with periodontitis
The amount of PD reduction correlates with greater pocket depth before treatment
Nonsurgical mechanical debridement may cause loss of attachment in shallow pockets (<3mm)
There is no evidence of any difference in efficacy between machine-driven (ultrasonic and sonic) and hand instruments in single-rooted teeth. Machine driven instruments may be faster than hand instruments
Adjunctive therapies have been developed and investigated but, to date, no therapy exists as a stand alone replacement for mechanical nonsurgical pocket therapy.

Maintenance Therapy:

In periodontal maintenance patients, mechanical debridement reduces inflammation and disturbs the bacterial biofilm, which is though critical to disease control including prevention of progression.
Theeffect of mechanical nonsurgical pocket therapy on PD reductionand clinical attachment gain in maintenance patients is unclear; maintenance or stability of pocket PD and clinical attachment level, however , has been demonstrated and meets the goal of maintenance therapy.
There is not clear evidence to form recommendations over time taken, thoroughness and frequency of mechanical debridement for periodontal maintenance care

BL: Existing evidence in the form of systematic reviews provides conclusive support for the beneficial effect and efficacy of mechanical nonsurgical pocket therapy in the treatment of periodontal diseases.

Ramfjord 1980 ARTICLE

P:To determine the influence of tooth type on the results of periodontal treatment over 8 years of a longitudinal study.

M&M: Data from a previous periodontal therapy involving 78 patients over 8 years (Knowles et al., 1979) was analyzed with regard to effect of tooth type on treatment results. Initial probing depths (1-3mm, 4-6mm, and 7-12mm) were used as an expression of the severity of the disease. The dentition was divided into six tooth types: Maxillary molars, mandibular molars, maxillary premolars, mandibular premolars, maxillary anteriors, and mandibular anteriors. Probing depths and attachment levels were measured annually.

R:Tooth type has little influence on the response on the periodontal treatment outcome. Reduction in probing depths and potential for attachment level gain were slightly better in anteriors than molars teeth. Poorest results were seen in maxillary premolars and molars, and one of the reasons could be possibly due to furcation complications. The trend was for probing depths to return more rapidly in deep molar pockets than deep anterior pockets. Anterior teeth sustained gain in attachment better than the rest of the teeth in the arch.

BL:Prognosis for treatment of periodontal pockets is good for all tooth types, and this applies to moderate as well as to deep pockets.

Previous Critique: Measurements taken did not really account for furcation involvement, since the straight buccal probing depths were taken from root prominences rather than furcation areas.

Pihlstrom 1984 ARTICLE

Purpose:To investigate the periodontal response of molar and nonmolar teeth to either SRP alone or SRP followed by modified Widman flap (MWF).

Materials and methods: 17 subjects 22-59 years old. After initial scoring of the clinical measurements thorough SRP and OHI were performed by a periodontist in training. Overhangs and defective restorations were corrected and occlusal adjustment was performed when needed. Two quads (one maxillary and one mandibular) per patient were selected to receive MWF. Periodontal prophylaxis was then performed 3-4 times/year. Hopeless teeth were not extracted in the initial treatment, but during the maintenance phase if needed. Clinical measurements were obtained prior to any therapy, 6 months after completion of the therapy and then annually for 4 years. PDs and AL were recorded at 6 sites/tooth.

Results:Of the 17 initial subjects 10 remained as participants after 6,5 years.

PDs 4-6mm: There was 0.4mm less pocket depth at baseline for nonmolar teeth treated with SRP and 0.27mm for nonmolar teeth treated with MWF comparing to molars treated with these procedures. This difference increased throughout the study and 6,5 years nonmolar teeth had an average of 1mm less PD irrespective of typed of procedure performed.

Attachment loss was greater at pretreatment baseline was greater for molar teeth (0.74mm more) and tended to remain the same over the 6,5 year period.

PDs of 7mm or more: For teeth treated with SRP there was a difference of 1.86mm and 2.32mm in PD only at 2 and 3 years post-treatment respectively (deeper in molars). No SSD between the teeth group in other time intervals but there was a tendency for more shallow PDs in nonmolar teeth. Teeth treated with MWF nonmolar teeth had 0.41mm less PD at baseline and the magnitude of this difference increased dramatically over the 6,5 years (2.36mm at 6,5 years with 1.22mm standard error). Differences in AL were only SSD at 2 years after flap procedure with nonmolar teeth having 0.93mm less attachment loss than molars.

Tooth loss: Total tooth loss was 4%. 8/19 teeth before therapy was completed. 11/19 after therapy was completed (2.5% of teeth receiving therapy). 7/11 max molars, 2/11 mand molars, 1/11 deciduous cuspid and 1/11 mand lateral incisor. 5/11 were lost after SRP and 6/11 after SRP + MWF.

Conclusion:1) Both procedures were effective in treating periodontitis in terms of maintenance of CAL on molar and nonpolar teeth

2) For initial PDs of 4-6mm, there was greater PD and a more apical CAL on molar than nonmolar teeth treated by either method

3) For pockets initially 7mm or more, the flap resulted in less PD on nonmolars than molars but there was no difference in CAL between tooth types for either method of therapy.

Claffey, Shanley, 1986 ARTICLE

Purpose:To examine the relationship of gingival thickness, bleeding, and the tendency for attachment loss in shallow buccal sites (< 3.5mm PD) following non-surgical periodontal therapy.

Materials & Methods:

15 pts with moderate-severe perio dz were selected for the study.
Pt’s were given 2 sessions of OHI, and on the 2nd session received SRP (Incisors, Canines, PM).
Pts received an additional session of OHI 1 week post-SRP. No further OHI or therapy was performed for 3 months.
Clinical measurements (CAL, PD, BOP, PI, & gingival thickness) were performed at baseline and at 3 months following debridement for 6 surfaces of experimental teeth.

Results:

Slight attachment loss ( 0.1 ± 1.0 mm) was observed for sites initially < 3.5 mm PD.
A slight gain (0.5 ± 1.2 mm) noted for pockets initially 4.0 6.5 mm, and a > gain (1.4 ±1.5 mm) for those initially 7.0 mm.
Thin gingiva (<1.5 mm thickness), initially non bleeding sites displayed a mean loss of probing attachment of 0.3mm.
Thick gingiva (2.0 mm), non-bleeding sites displayed a less noticeable mean loss of probing attachment, whereas bleedingsites of both categories of gingival thickness showed a tendency towards gains in probing attachment levels.
A mean loss of probing attachment was seen with thin, nonbleeding sites.

BL:Sites with bleeding prior to instrumentation did not seem to lose attachment. Thin, non-bleeding sites seem to be ones primarily associated with this probing attachment loss.

Loesche 1996 (sx prevention) ARTICLE

P:To determine whether the short-term use of systemic antimicrobials (metronidazole or doxycycline) and locally delivered antimicrobials (metronidazole, chlorhexidine) in patients with advanced forms of periodontal disease could prevent access surgery.

M+M: Inclusion criteria: presence of an anaerobic infection, spirochetes greater than 20% of the microscopic count and the hydrolysis of benzoyl- DL-arginine napththylamide (BANA-positive reactions) in at least 3 of 4 subgingival plaque samples taken from the site in each quadrant that had the greatest PD. Subjects examined for number of teeth in need of surgery, those that had >4 teeth needing to be extracted were kept in the study. Study was conducted in a double-blind fashion in which patients were randomly assigned to antimicrobial treatment groups. No patient would receive more than two rounds of systemic antimicrobial treatments or more than three rounds of local antimicrobial treatments about individual teeth. A placebo treatment would be used only in the first round of systemic treatment or in the first round of local treatment. Any patient or tooth still in need of treatment after the first round of the systemic or local treatment would be retreated with the opposite medication from what they had received in the first round. All patients progressed through the first round of treatment. After SRP the patients were randomly assigned to receive either placebo, metronidazole, or doxycycline, for 2 weeks unsupervised at home. If anyone had > 6 teeth in need of surgery or extraction after first round of systemic medication, they were retreated with systemic medication. If they had 6 or less teeth, they were treated with ethyl cellulose (EC) films containing either no addition (placebo), 20% metronidazole, or 20% chlorhexidine. If they had no teeth in need of surgery, SPT every 3 months. 90 of 125 patients initially recruited completed all phases of the study and entered into the recall maintenance program.

Loesche 2005 NO ARTICLE

B:In a previous study involving patients at the dental clinic of a hospital in Detroit, 87% of teeth that initially had been recommended for surgery or extraction were spared either treatment through a combination of debridement and short-term usage of antimicrobial agents.

P:The purpose of the current study was to determine the changes that occurred to these teeth after a median of 6.4 years in the maintenance phase of treatment.

M&M:90 Patients were scheduled for maintenance therapy at 3-month intervals over a period of 6.4 years. Subjects were diagnosed as having an anaerobic periodontal infection if 3 or more of their plaque samples contained spirochetes exceeding 20% of the microscopic count and were capable of hydrolyzing the synthetic peptide benzoyl-DL-arginine naphthylamide (BANA*-positive).

Treatment phase: Pts with 4 or more teeth requiring sx were entered in the protocol.

After debridement, the patients were randomly assigned in a double-blind design to receive metronidazole (500 mg twice daily), doxycycline (100 mg daily), or placebo tablets/capsules for two weeks. Re-eval after 4-6 weeks. Pts that required surgery on 1-6 teeth were treated with locally delivered antimicrobial agents and > 6 teeth requiring surgery were retreated with systemic agents. No patient received more than two systemic treatments and 3 local treatments. Pts were scheduled for debridement every 3 months.

Maintenance phase: q3 months. OHI given, PD and AL, BOP, root topography and nature of bony defect via x-rays, mobility were assessed. Double-blind design prophylactic antimicrobial with metronidazole 500 BID x1wk or placebo was given.

R: 10-15% of the 90pt who entered the maintenance phase were lost.

The results during the maintenance phase were as follows:

55% – no new surgical needs or reduced surgical needs

24% – new surgery or extraction recommended for either 1 or 2 teeth

15% – new surgery or extraction recommended for 3 or 4 teeth

6% – Extraction recommended of at least 8 teeth

Initial antimicrobial treatments reduced the surgical needs to an average of 0.5-1.7 in these outcome groups
Most of the relapse occurred in multi-rooted teeth, esp. among pts with aggressive periodontitis.
The initial antimicrobial treatments reduced the surgical needs of both groups by approximately 85%. There was no difference between the 2 groups during the maintenance phase until the 6.4 year examination, an average of 0.5-1.7 in these outcome groups.
Current smoking remained a predicator of surgical needs.
An increase maintenance visits were a powerful predictor of increased surgical needs, while prophylactic metronidazole was strongly associated with reduced surgical needs.

C: These findings indicate that an antimicrobial regimen reduced the initial surgical needs of patients by approximately 85%, and this result can be sustained in the maintenance phase by home care, periodic sessions of SRP and annual prescriptions of 1 week of metronidazole.

BANA test*= examines dental plaque, measuring the presence of an arginine hydrolase possessed by 3 anaerobic species associated with periodontal infections (P. Gingivalis, T. denticola, T. forsuthensis).

Drisko 2001(Review) ARTICLE

P:To review literature that addresses the non-surgical approach to treat periodontal disease.

Discussion:

Anti-infective therapy: Successful periodontal therapy depends of the elimination of pathogens. Since perio disease primary etiology is plaque, and most of the pt are not skilled in removing plaque, periodically professional cleaning is indicated. Includes Mechanical and chemotherapeutic approaches. Debridement is performed to produce a root that is biologically acceptable for a healthy attachment.

Risk Factor: Non-compliance or no regular maintenance care. Insufficient debridemen

132. Effects of Therapy:

a. Results of Non-Treatment

b. Evaluation of Therapy

HOME PERIO TOPICS

1. What are the consequences of non-treatment of periodontal disease? How fast does untreated periodontal disease progress?

BeckerW, Berg L, Becker BE: Untreated periodontal disease: a longitudinal study. J. Periodontol.50:234 -244, 1979.

BeckerW, Becker BE: Bone loss in untreated periodontal disease: a longitudinal study. Int J Perio Restor Dent1:25-33, 1981.

GoodsonJM, et al: Patterns of progression and regression of advanced destructive periodontal disease. J. Clin. Periodontol.9:472-481, 1982.

LindheJ, Haffajee AD, Socransky SS. Progression of periodontal disease in adult subjects in the absence of periodontal therapy. J. Clin. Periodontol. 10: 433-442, 1983.

LindheJ, Okamoto H, Yoneyama T, Haffajee A, Socransky SS: Longitudinal changes in periodontal disease in untreated subjects. J. Clin. Periodontol. 16:662-670, 1989.

JeffcoatMK, Reddy MS: Progression of probing attachment loss in adult periodontitis. J. Periodontol. 62:185-189, 1991.

MachteiEE, Norderyd J, Koch G, Dunford R, Grossi S, Genco RJ. The rate of periodontal attachment loss in subjects with established periodontitis. J Periodontol1993; 64:713-718.

PapapanouPN, Wennstrom JL. A 10-year retrospective study of periodontal disease progression. Clinical characteristics of subjects with pronounced and minimal disease development. J. Clin. Periodontol. 17:74-84, 1990.

2. Are patients doomed to lose all their teeth if they do not receive periodontal treatment? What is the rate of tooth loss with and without periodontal treatment?

HirschfeldL, Wasserman B. A long-term survey of tooth loss in 600 treated periodontal patients. J. Periodontol. 49:225, 1978.

McFallWT: Tooth loss in 100 treated patients with periodontal disease. A long term study. J. Periodontol. 53:539-549, 1982.
GoldmanMJ,Ross IF,Goteiner D. Effect of periodontal therapy on patients maintained for 15 years or longer. A retrospective study. J Periodontol.1986 Jun;57(6):347-53.

McLeodD, Lainson P, Spivey J. The effectiveness of periodontal treatment as measured by tooth loss. JADA 1997; 128: 316-324.

HujoelPP, Leroux BG, Selipsky H, White BA. Non-surgical periodontal therapy and tooth loss. A cohort study. J Periodontol 71:736-742, 2000.

3. Do patients benefit from periodontal therapy? How effective are different treatment modalities in the short/long term? What are the most significant factors in the success of periodontal treatment?

LindheJ, Nyman S: The effect of plaque control and surgical pocket elimination on the establishment and maintenance of periodontal health. A longitudinal study of periodontal therapy in cases of advanced disease. J. Clin. Periodontol. 2:67-79, 1975.

BaderstenA, Nilveus R, Egelberg J : 4-year observations of basic periodontal therapy. J. Clin. Periodontol.14:438-444, 1987.

RenvertS, et al: 5-year follow-up of periodontal intraosseous defects treated by root planing or flap surgery. J Clin Periodontol 17: 356 – 363, 1990.

RamfjordSP, et al. 4 modalities of periodontal treatment compared over 5 years. J. Clin. Periodontol.14:445-452, 1987.

BeckerW, Becker BE, Caffesse R, Kerry G, Ochsenbein C, Morrison E, Prichard J. A longitudinal study comparing scaling, osseous surgery, and modified Widman procedures: results after 5 years. J Periodontol. Dec;72(12):1675-84. 2001

KaldahlWB, Kalkwarf KL, Patil KD, Dyer JK, Bates RE: Evaluation of four modalities of periodontal therapy. J Periodontol. 59: 783 -793, 1988

HarrelSK, Nunn ME. Longitudinal comparison of the periodontal status of patients with moderate to severe periodontal disease receiving no treatment, non-surgical treatment, and surgical treatment utilizing individual sites for analysis. J Periodontol. 2001 Nov;72(11):1509-19.

Kaldahl WB, Kalkwarf KL, Patil KD. A review of longitudinal studies that compared periodontal therapies. J. Periodontol. 1993; 64: 243-253. (Review) – No need to abstract, Keep for Reference

WassermanB, Hirschfeld L. The relationship of initial clinical parameters to the long-term response in 112 cases of periodontal disease. J Clin Periodontol 15:38-42,1988.

HaffajeeAD, Dibart S, Kent Jr. RL, Socransky SS. Factors associated with different responses to periodontal therapy. J Clin Periodontol 22:628-636, 1995.

Van der Velden U, Abbas F, Armand S, Loos BG, Timmerman MF, Van der Weijden GA, Van Winkelhoff AJ, Winkel EG. Java project on periodontal diseases. The natural development of periodontitis: risk factors, risk predictors and risk determinants. J Clin Periodontol. 2006 Aug;33(8):540-8.

FisherS, Kells L, Picard JP, Gelskey SC, Singer DL, Lix L, Scott DA. Progression of periodontal disease in a maintenance population of smokers and non-smokers: a 3-year longitudinal study. J Periodontol. Mar;79(3):461-8. 2008

TelesRP, Patel M, Socransky SS, Haffajee AD. Disease progression in periodontally healthy and maintenance subjects. J Periodontol. May;79(5):784-94. 2008

4. What changes can we expect in the subgingival microbiota over time in untreated and treated periodontitis?

MacFarlaneTW, Jenkins WMM, et al. Longitudinal study of untreated periodontitis. II. Microbiological findings. J. Clin. Periodontol. 15:331-337, 1988.

RosenbergES, Evian CI, Listgarten MA : The composition of the subgingival microbiota after periodontal therapy. J. Periodontol. 52:435, 1981.

MombelliA, Nyman S, et al. Clinical and microbiological changes associated with an altered subgingival environment induced by periodontal pocket reduction. J Clin Periodontol 22:780-787,1995.

5. What changes can we expect in the maxillary sinus after periodontal therapy?

FalkH, Ericson S, Hugoson A: The effects of periodontal treatment on mucous membrane thickening in the maxillary sinus. J. Clin. Periodontol.13:217-222, 1986.

6. Are there differences in patient perception to different tx modalities?

KalkwarfK, Kaldahl W, Patit K. Patient preference regarding 4 types of periodontal therapy following 3 years of maintenance follow-up. J Clin Periodontal 1992; 19:788-793.

Abstracts

What are the consequences of non-treatment of periodontal disease? How fast does untreated periodontal disease progress?

Becker 1979 ARTICLE

P: To determine the rate teeth are lost in untreated periodontal patients.

M&M: 30 patients, 20-71 years old (16M/14F) who were referred to a private periodontal practice and decided not to undergo treatment were given at least two exams over a period of 18- 115 months. Mean time period was 3.72 years. Clinical parameters records: PD, REC, MOB. No reference points were used. Medical history forms were filled and missing teeth were recorded. FMX taken at each appointment, no standardized radiographs.

R: 10.6% of teeth lost between exams. One patient lost 25 teeth and was eliminated from the study. This brought the % of teeth lost down to 7.7. The adjusted mean annual tooth loss per patient was 0.61. Teeth with hopeless prognosis were excluded and this gave 0.36 teeth per pt/per yr. lost. Aside from the 3rds, mandibular 1^st and 2^ndmolars were the most frequently lost teeth and the max molars were slightly less frequently lost. Mandibular central incisors, laterals and canines appeared the most resistant to loss. Teeth which were lost between examinations had initial PDs significantly higher that the PDs of teeth present in the 2^nd examination. The greatest increase in PDs was on disto-lingual and mesio- lingual surfaces closely followed by the lingual surface. The buccal or facial surface had the smallest increase. Maxillary and mandibular molars had the highest mean annual PD increase followed by maxillary bicuspids and canines. A significant correlation existed between patient age and PD increase. No correlation between PD and MOB. Teeth that were lost between examinations had significantly greater mobility than teeth that were present at 2^nd examination. MOB remained the same in 50% of teeth and increased in 38 % of teeth. Mandibular 1^st molars and incisors had the greatest MOB. All patients showed radiographic bone loss, horizontal and vertical, this was greatest in the posterior segments. Diabetes and HTN showed no correlation to increase in PD or AL loss but smoking did.

BL: Untreated periodontal disease results in loss of .61 teeth per pt/per yr. If hopeless teeth are not included then the number decreased to .36 teeth per year. Mandibular anterior teeth were the most resistant to loss and maxillary and mandibular molars were the most commonly lost.

Becker 1981 ARTICLE

P: To evaluate bone score changes in untreated periodontitis.

M+M: 27 untreated patients (25-71 years old, 15 M, 12 F) with minimum of 2 exams, baseline and followup of 18-115 months. 54 sets of FMX, patient evaluated, long cone technique (with an attempt to duplicate angulation of initial exam); bone scores determined (similar to the Bjorn technique: scale constructed, 15 inches long, divided into 20 horizontal and vertical lines, photographed, reduced 8 times, then placed over the films to evaluate them, mesial and distal of all teeth evaluated, except 3^rd molars, bone scores read as % of bone present). The optimal bone score was considered to be 65 +/- 5 % of the total root length.

Mean bone scores on first exam was 49.5% (range 39 to 60%). Mean bone scores for second exam was 43.2% (range 35.4 to 53.4%).
A decrease in mean bone scores was seen for all 27 patients.
The distal surface had lower bone scores than the mesial surfaces.
The molars with the lowest initial bone scores (max molars lowest overall) and showed the greatest decrease between 1^st and 2^ndexams -19.8%, bicuspids- 10.6%, anteriors – 7.9%.
PDs seemed to parallel bone scores, however, the correlation was SS.
Progression varied from patient to patient and tended to be age related. Pts < 44 year had greater decrease in bone score than older group.

BL: Bone scores in pts with untreated periodontal disease decreased from the initial to the final exam. Distal surfaces had lower bone scores than mesial surfaces, and molars had the lowest initial and greatest change in bone scores between exams. Bone scores may be used to evaluate periodontal disease progression.

Goodson 1982 ARTICLE

P: To determine if a more reliable estimate of disease progression could be obtained by regression analysis of a series of measurements and if sites which were “breaking down” could be identified.

M&M: 22 patients (13-63 yo, 8 m, 14 f) with untreated perio disease with at least 20% of their PD >4 mm, were monitored by repeated monthly measurements of PD & AL at 2 sites per tooth, for 9.3-23 months.

R: 82.8% of sites remained unaltered. 5.7% became significantly deeper & 11.5% became significantly shallower (>2 mm). Among those sites in which the PD increased, approximately half exhibited a cyclic deepening followed by spontaneous recovery to their original depth. In 15 pts, sites were found which became significantly deeper while other sites within the same subject became significantly shallower. In 6 pts, 11-36% of their sites became significantly shallower and virtually no sites became significantly deeper. In general, deeper initial sites became deeper/shallower at a more rapid rate. No evidence of synchronization between sites within any individual oral cavity could be seen.

Disc: Diseased sites may undergo cycles of exacerbation & spontaneous remission. This suggests that at least some forms of disease may be characterized by cycles of bacterial attack followed by host response. Existence of pockets alone cannot substantiate the existence of active disease. Disease activity may be a transient phenomenon, which would be altogether missed by an inadequate frequency of monitoring.

BL: Periodontal disease is characterized by periods of exacerbation and remission as well as periods of inactivity. Disease activity may be missed by inadequate frequency of monitoring.

Lindhe 1983 ARTICLE

Purpose: To monitor the attachment level changes in a group of 64 adults over a 6-year period during which they were not subjected to periodontal therapy and to compare disease progression to that which occurred in a second group with initially more advanced destructive periodontal disease.

Materials and methods: 64 Swedish subjects between 16 and 64 years of age at initial examination. Subjects had at least 20 teeth and treated for caries and associated lesions once a year. Subjects were informed and accepted that periodontal disease would not be treated over a 6-year period. They had mild moderate bone and attachment loss.

20 male and 16 females Americans between 13-62 years of age with advanced periodontal disease were selected for comparison. This group did not receive periodontal treatment for a period of 1 year. Swedish group was examined at baseline and at 3 and 6 years. The American subjects were monitored more often but data from baseline and 1 year visits were used. Probing attachment level measurements were recorded.

Results: In the Swedish group in the first 3 years 3.9% of sites showed attachment loss of more than 2mm. No change was found in 35.1%. The overall mean attachment level change was -0.82 +/- 0.87mm. The proportions of sites which changed and the extent of change did not appear to be related to the initial attachment level.

Between 3 and 6 years 57.4% of sites showed no measurable change. The overall mean change was -0.45+/-0.84mm. The average loss was approximately half of loss observed in the first period.

During the 6 years, 11.6% showed additional AL of more than 2mm. 20% of sites showed no measurable attachment loss. The overall AL was -1.29+/-1.12mm.

2/3 of the sites that showed some attachment loss in the first 3 years, showed no AL in the next 3 years.

In the American group, 26% showed no measurable change, and the overall mean attachment change was 0.08+/-1.4mm. There appeared to be a relationship between the extent of attachment level change and initial attachment level (more pronounce decrease in sites with initially advance loss of attachment) but regression analysis did not support that.

Conclusion: Data do not support the hypothesis that periodontal disease in a given individual is a slowly progressive disorder, but rather imply that certain sites in some individuals are affected by progressive disease. Maximum loss in Swedish population was 7mm in 3 years and in American population 7mm in 1 year. Haffajee (1983) indicated that attachment loss of up to 5mm can occur with a 2-month period. The attachment loss in the Swedish population may have occurred within a short span of time during monitoring period.

Lindhe 1989 ARTICLE

Purpose: To report effect on periodontal tissue alterations occurring 1 and 2 yrs following baseline data collection without any type of treatment.

Materials and methods:

319 pts (age 20-79) were divided into 6 groups by age. Clinical measurements (BOP, PD, AL, recession, missing teeth, PI, GI) were taken at baseline, 12 mo. and 24 mo, with no OHI or tx rendered.
Mean values for subjects in each age group were computed. 57 pts dropped out of the study.
Those who returned for both 1 and 2 yr exams were identified as respondents vs. those who came only to one re-exam (either 1 or 2 yrs) were identified as non-respondents.

Results:

Mean values describing gingivitis and periodontitis tended to increase with age. 82 teeth were lost in 53 subjects. 26/82 (32%) teeth extracted were due to periodontal dx and 62% were in the oldest age group.
PI and GI decreased in all groups over the 2 yr even though no OH was discussed with patient; however, within each age group was a subgroup that had failing OH.
PD increased slightly in all groups over the two years, with most pronounced deepening in the oldest age group (60-79). Mean PAL had no sig variation.

Conclusion: Pts with untxted perio dx fail to show a marked deterioration with 2 yrs of monitoring. Rather, the majority undergo little change and a small subset show marked disease progression.

Jeffcoat 1991Florida Probe ARTICLE

P: To describe the results of a 6-month study of probing attachment loss in adult periodontitis using an automated probe (w/ a resolution of 0.1mm).

M&M: 30 patients age 20-73. Inclusion criteria: presence of 3-8mm PDs, at least 4mm of AL, and bone loss evident on vertical bite-wing radiographs. Effort was made to include patients who had sites demonstrating progressive perio by comparison of their vertical bite-wings taken from the start of the waiting list (1 year prior). All patients had suprag prophy to remove calculus. Automated probing attachment levels were taken at 0,2,4 and 6 months in 5 posterior tooth sites. Instrument repeatability was confirmed by taking 5 measurements for each indv tooth site and calculated by averging the st. dev. from all sites.

R: This study confirmed the repeatability of the automated probe. Overall repeatability was 0.17mm + 0.2mm. There was no SD in the repeatability of the measurement in shallow (<4mm AL) or deep sites (>4.5mm AL). This data verified that the repeatability of measurement was better than 0.2mm. The prevalence of activedisease in the 6-month period was 29% when a cut off of 0.4mm was used. 77% of the pts exhibited one or more active sites during the study period. Mean probing at baseline was 4.4 +/- 0.8mm. Increasing the cutoff to 2.4mm resulted in 2% of active sites. 76% of sites with attachment loss followed a linear pattern. 12% showed a burst pattern, with the burst tapering off at 2 months and 12% showed exacerbations and remissions.

D: Ability to detect disease is dependent on the sensitivity and specificity of the system used to measure. Changes in probing attachment level can be due to true changes in CAL or change in tissue tone or both. With a high-resolution probe, it is possible to increase the sensitivity at the expense of specificity. This probe has been designed to limit this by applying a constant force (35gm) and has a 0.5mm ball at the tip, decreasing the probability of penetration into the CT (previous studies in beagles show this probe is accurate to within 0.9mm in detecting the attachment level). The prevalence of active sites was dependent on the threshold or cut-off for disease activity selected.

BL: High precision probing attachment measurements improves the detection of active disease and patterns of CAL over time.

Machtei 1993 ARTICLE

P: To assess the nature of progression of periodontal disease among subjects with established periodontitis using a stepwise approach to determineactive sites and attachment level changes.

M+M: 51 patients (21F, 30M; 28-62 years old) out of 1427 examined selected for longitudinal study. Inclusion criteria: established perio disease (CAL greater or equal than 6mm in 2 or more teeth); presence of 14 or more teeth; bw 25-65 years old; written consent. Patients had not received periodontal treatment in 12 months prior to study. PD using a constant-force electronic probe (20 g), CAL, relative attachment level (RAL) were taken at baseline, which was 3 months after the screening exam, and every 3 months for another 9 months (total 12 months after initial exam). Sites were sorted by PDs (Shallow = 0-3.9 mm; moderate 4-6.9 mm; deep >7 mm); molars vs non-molars and buccal vs lingual sites. Losing sites were determined by plotting individual sites over time. Linear, exponential, and logarithmic regression models were tested for each site. The slope of the regression model was used to generate AL changes and were compared to individual site measurements. Sites with AL exceeding these thresholds were determined to exhibit true AL.

R: 581 sites, 8.3% of all sites measured had AL, 2.5% when corrected type I error. Net losing sites 5.8%. Linear progression occurred in 33.6% of losing sites. Logarithmic progression (early burst with smaller changes thereafter), occurred in 38.5% of losing sites. 20 pts had small percentiles of losing sites (<5%), 16pts had moderate(5-11%), and 13pts massive (>11%). Deeper pockets (>7mm) lost attachment faster. Mean loss for all patients was 0.2 mm but deep sites lost 1.03 mm, moderate lost 0.34 and shallow lost 0.1mm. Lingual sites lost attachment faster than buccal (0.24 vs 0.16). NSS between molars and non-molars.

BL: Deeper pockets (>7mm) lost attachment faster.

Critique: Have to assume over a long period of time, any sites can exhibit different patterns of progression, ie linear, non-linear, or non-progression. Good that true changes were documented only if they exceeded the regression model.

Papapanou 1990 ARTICLE

P: To describe clinical characteristics based on a 10-year retrospective study of periodontal disease progression and to analyze the correlation between radiographic and clinical assessments of proximal loss of periodontal tissue support.

M&M: 2 groups of 14 patients were chosen from a sample of 191 individuals who had FMX exams in 1975 and 1985. The 1^st group experienced pronounced bone loss during a 10-year period (mean 4.13 mm). The 2^ndgroup had suffered no or minimal periodontal disease progression (mean bone level change +0.35mm). Clinical examination included: PI, GI, BOP, PD, CAL. A questionnaire was completed from all subjects regarding OH habits, frequency of treatment, and type of periodontal therapy received over the 10 preceding years.

R: The 1^stgroup had more plaque and gingivitis, deeper PD and greater attachment loss than the 2^nd group. The longitudinal tooth loss was more pronounced in 1^st group. Subjects in 1^stgroup lost on average approximately 7 teeth over the 10 year period, as compared to 4 teeth in 2^nd group. The radiographic assessments of alveolar bone loss were strongly correlated with the assessments of probing attachment loss. In 92% of the sites, the difference between the radiographic and the clinical assessment of periodontal tissue loss was within 2mm. Self- reported data on questionnaires showed that both groups practiced similar OH, all subjects reported brushing their teeth at least once daily, while 50-65% of the subjects regularly used some means of interdental cleaning. Subjects from both groups were subjected to dental treatment equally often. However, subjects in 1^st group claimed to have received a greater amount of periodontal treatment over the 10-year period compared to subjects in 2^nd group.

BL: Both groups had similar oral hygiene habits and frequencies of dental care visits. Patients with more loss of periodontal support had a worse periodontal status and more extensive periodontal treatment done. Radiographic assessments of alveolar bone loss were strongly correlated with the assessments of probing attachment loss. Both groups had similar bone loss at baseline but behaved differently with respect perio disease progression. The subjects in the 1^stgroup were ineffectively treated, with respect perio disease.

Are patients doomed to lose all their teeth if they do not receive periodontal treatment? What is the rate of tooth loss with and without periodontal treatment?

Hirschfeld 1978 ARTICLE

P: To report on the tooth loss over an average of 22 years of maintenance therapy.

M&M: 600 pts. from private practice under 4 to 6 month recall. 2X as many females as males, predominantly Caucasian, middle class, and highly motivated in dental health. Average age at the start of treatment was 42. 76.5% were classified as having advanced periodontal disease, 16.5% intermediate severity, and 7.0% had early disease. Patients were divided into well maintained (WM, lost 0-3 teeth), downhill (D, lost 4-9 teeth), and extreme downhill (ED, lost 10-23 teeth). The prognosis was also evaluated for those that remained in maintenance. Most received sc/rp (few surgeries). Recall visits w/ deep scaling every 4-6 months.

R: Distribution: Over 22yrs 7% of tooth loss was due to periodontal reasons. Half of the total sample lost no teeth during the 22 year period. WM – 83%, D – 13%, ED – 4%. WM had an average tooth loss of .68 th/yr. Of the teeth lost in the WM group, 79.5% were initially marked questionable. The D group lost 22.7% and ED lost 55.4% of teeth (with higher percentages of non-questionable teeth lost). The most likely teeth to be lost were upper molars and many of these had furcation involvement. The least likely to be lost even with a poor initial prognosis were the canines. When surgery was performed, the mandibular teeth would have repeated surgery 4x more often than the maxillary.

B/L: There appears to be a pattern of cyclic and sporadic outbursts of disease. The degree of plaque control does not always parallel disease progression. Tooth retention is more closely related to the case type than the surgery performed. Periodontitis is bilaterally symmetrical and there is a predictable order of likelihood of tooth loss according to position in the arch.

McFall 1982 ARTICLE

P: To follow the format established by Hirschfield and Wasserman to evaluate 100 treated periodontal patients maintained for longer than 15 years.

M&M: 100 patients (59M, 41F), treated & maintained for >15 yrs. All patients were on periodic maintenance (3-, 4- or 6- months intervals). Average duration of maintenance was 19 years. Periodontal parameters were recorded at initial exam and at maintenance (PD, REC, FURC, MOB, mucogingival considerations). 36/100 patients had advanced periodontal disease, 53/100 intermediate severity and 11/100 were in the early stages. The patients were classified as: WM-well maintained, lost 0-3 teeth (77 patients), D-downhill, lost 4-9 teeth (15 patients) and ED-extreme downhill, lost 10-23 teeth (8 patients). Teeth were given a prognosis based on PD, mobility, furcation and gingival issues. The degree of tooth loss in each group was evaluated (did NOT include teeth extracted as part of initial therapy). All patients had SRP, OHI and occlusal adjustment. Patients that were treated surgically in 50s and 60s received mostly gingivectomy and in 80s with OFD or osseous.

R: Over an average of 19 years: 2,627 teeth were initially present and 259 (9.8%) were lost due to periodontal disease and 40 (1.5%) lost to other causes. 45% of patients lost NO teeth. Of the total number of teeth lost due to all causes 30.7% occurred in the WM group, 30.7% in the D group and 38.6% in the ED group. For disease severity, 100% of ED and 87% of D were initially classified as having advanced periodontal disease.

WM: 0.68 teeth/pt were lost (similar to Hirschfeld and Wasserman), 45/77 of the WM group lost no teeth. D: 6.7 teeth/pt were lost, ED: 14.4 teeth/pt were lost.

62% of teeth lost were originally labeled as questionable. Highest loss of max molars and lowest loss of mandibular cuspids. Compared to the Hirschfeld and Wasserman studies, fewer patients were diagnosed with having advanced disease (3.6% vs. 76%). As seen in previous studies, the majority of tooth loss occurs in a small % of patients, often after years of no progression. This study reaffirms bilateral symmetry and cyclical nature of the disease. Teeth with furcation involvement appear no more likely to be lost than other questionable single rooted teeth. Further supports the benefits of treatment and maintenance.

BL: Periodontal disease often presents with bilateral symmetry. There seems to be an irregular cyclical nature of tooth loss. Treatment appears to be effective in most of the patients who are well maintained. A higher percentage of teeth lost were in a patient population that had more advanced disease, less molars at initial exam, and more teeth w/questionable prognosis. A minority of the patients got worse no matter what.

Goldman 1986 ARTICLE

P:Retrospective study to provide additional information on the effects of periodontal treatment and maintenance therapy on a group of patients who were seen in a private practice setting for at least 15 years.

M+M:211 patients (122 F, 89 M, mean age=42 years, predominantly Caucasian). Initial exam included FMX, and FMX would be taken every two years to assess bone level changes, all teeth present were counted.

Initial therapy: OHI and SRP, occlusal adjustment (on all patients) , bite guards fabricated.

Surgical therapy: gingivectomy-gingivoplasty, OFD, at no time was osseous tissue removed, frenectomies, root amputations.

Maintenance: Extra and intraoral exams, occlusion checked for trauma and mobility- where extensive mobility, pt was rescheduled for either occlusal correction or intracoronal splinting. Teeth with extensive bone loss were maintained for many years by periodic recalls. Residual pocket depth was also kept stable in many instances by frequent maintenance.

Response to therapy was classified based on Hirschfield and Wasserman classification of well maintained (WM)- 0 to 3 teeth lost, down hill (D)- 4 to 9 teeth lost, and extreme downhill (ED)- 10 or more teeth lost.

R:On the basis of response to therapy, 131 patients were classified as WM (62%), 59 D (28%) and 21 ED (10%). During maintenance period a total of 771 teeth were lost (13.4%). Molar teeth (max> mand) are the most prone to loss and the mandibular cuspid is the most resistant.

WM group- 59 pts lost no teeth, remaining 72 pts lost 1 tooth/patient

D group- lost an avg of 5.8 teeth/patient (2^ndand 3^rdmolars comprised 45.6% of the teeth lost)

ED group- lost an avg of 14.2 teeth/patient (2^ndand 3^rdmolars comprised 26.% of teeth lost)

BL:The teeth at highest risk of being lost are molar teeth, especially the maxillary first and second

molars. Only one mandibular cuspid was lost. This study emphasizes the importance of maintenance therapy.

McLeod 1997 ARTICLE

P: To evaluate the effectiveness of perio treatment as measured by tooth loss.

M&M: 114 patients (26-79 years old at the start of treatment), seen by periodontist for maintenance for an average of 12.5 years, (99% on 3-month recalls). All had moderate (ALoss 4-7mm)-advanced (ALoss >7mm) perio. Records were reviewed for medical and dental history. Patients were divided into well-maintained (0-3 teeth lost), downhill (4-9 teeth lost), and extreme-downhill (10-23 teeth lost).

R: 2987 teeth present at initial exam; 88 (3%) extracted during periodontal treatment; 220 (7.6%) lost during maintenance. Tooth loss: 5% due to perio, 1.6% because of pros or restorative reasons. More molars lost than non-molars and bilateral pattern of tooth loss was observed. Greatest tooth loss max 2^nd M > 1^stM> 1^st PM> mand 2^ndM. Least tooth loss max C> mand C> 1^st PM> 2^nd PM. More patients were initially included in the well-maintained group after perio treatment, than in the down-hill, than extreme down hill group (96, 15, 3 respectively). Average tooth loss for all patients was 1.9. Tooth loss in well maintained= 0.9 per patient, downhill=6, extreme downhill=12. 17% of the teeth with furcations initially, were lost after active treatment. Only 2 patients had systemic diseases that predisposed them to periodontitis (Juvenile diabetes, and systemic lupus erythematosus).

C: Perio treatment followed by periodontal maintenance was effective in decreasing tooth loss; however, surgical treatment did not significantly improve tooth retention in the high-risk groups.

Hujoel 2000 ARTICLE

Purpose: To assess the relationship between non-surgical periodontal therapy and tooth loss in patients with chronic periodontitis.

Materials and methods: Study was conducted in the Kaiser Permanente Dental Care Program a dental care system that includes 14 offices in the US and provides comprehensive dental services. Subjects were patients with chronic periodontitis with initial exam between 1988 and 1992, age 40-65 at the initial exam and FMX were taken between 1 year prior to and 6 months after the periodontal exam. The non surgical periodontal treatment was divided in 1) continuous prior therapy (one or more non-surgical procedures performed during each of the prior 3 years) 2) no prior therapy performed during each of the prior 3 years and 3) intermittent prior therapy (one or more non-surgical procedures performed during some but not all of the prior 3 years). Number of teeth lost in each year subsequent to the initial exam was determined based on a review of the electronic database records. Results were adjusted for periodontal disease severity (more or less than 5mm PD), age, gender, prior periodontal therapy, caries activity and dental attitude (diagnostic, preventive and non-periodontal interventions).

Results: Mean age of the patients was 50.2 years and 48.7% were males. On average they were followed for 7.1 years and the mean number of teeth at the initial exam was 25.3. Mean number of sites with PD 5mm or more was 35.4 and mean PD of all sites (excl. 3^rd molars) was 3.6mm, and mean clinical PD of site with 5mm or more was 5.6mm. 1021 individuals participated in the study, 319 became ineligible during follow-up and data were used until that point. No association was found between tooth loss during study and dropout.

The mean tooth loss rate during the entire follow up was 7.5/1,000 teeth per year. 57% lost no teeth, 19% lost one tooth, 8% lost 2 teeth, 6% lost 3 teeth and 10% lost 4 or more teeth. Subsequent to the first 3 years after initial exam, tooth loss rate was 6.9/1,000 teeth per year.

Disease severity at baseline (mean PD, number of sites with 5mm or more PD, average depth of these site and having fewer teeth present) was associated with an increased tooth morality rate. For every additional site deeper than 5mm, tooth mortality rate increase by 2%. For every additional 1mm increase in the average PD of sites deeper than 5mm, tooth mortality rate increased by 56%. For every additional tooth present at baseline, tooth mortality rate increased by 16%. Gender and age were not significantly related to tooth loss.

Compared to periodontal therapy cessation for ≥3 years, intermittent or continuous non-surgical periodontal therapy was associated with a reduction in the tooth loss rate by approximately half (58% for continuous non-Sx therapy and 48% for intermittent therapy). For each additional periodontal procedure performed in the prior 3 years, tooth mortality decreased by 6%.

Conclusion: Non-surgical periodontal treatment may reduce tooth loss substantially and at a dose-response relationship exists.

Do patients benefit from periodontal therapy? How effective are different treatment modalities in the short/long term? What are the most significant factors in the success of periodontal treatment?

Lindhe 1975 ARTICLE

Purpose: To test whether periodontitis can be cured in advanced cases if pts are willing to exercise excellent plaque control.

Materials and methods:

75 pts with greater than 50% attachment loss that were capable of maintaining optimal plaque control and were willing to appear regularly at least once every 6 months were enrolled in the study.
Initial therapy with repeated OH instruction/motivation was given to each pt.
Teeth from which endodontic and cariologic view points could not be successfully treated, teeth with perio pockets extending down to the apex, and teeth which on prosthodontics indications should not be maintained were extracted.
The pre-sx observation period was 3-6 months in order to evaluate the degree of cooperation of the pts. Sx pocket elimination was performed for pockets greater than 4mm. Pts came to maintenance visits every 3 to 6 months.

Results:

The 75 pts had a total of 1898 teeth when they enrolled in the study. During the pre-sx tx period, 278 teeth were extracted.
A total of 1620 teeth were maintained for 5 years. The mean PD was 5.7mm before tx, and later was reduced to less than 3mm.
Also, after 5 years PDs exceeding 3mm were only found on 8 teeth. On no occasion did PD exceed 6mm.
However, 422 teeth did show signs of increased mobility at the end of the study. Only 14 new carious lesions were detected at the recall appointments.

Discussion: Microbial plaque is the major, maybe only, factor of importance in the etiology of gingival inflammation and incipient perio dz.

BL: It is possible to treat perio dz successfully, even in advanced stages, in pts willing to carry out optimal plaque control.

Badersten 1987 ARTICLE

P: To report a 48-month follow-up of the previous Badersten studies on non-surgical periodontal therapy (1984, 1984, 1985).

M&M: A total of 2214 sites from non-molar teeth in 46 pts (PD ≥5mm, BOP and calculus on at least 2 aspects of each tooth) were analyzed. 24-month status was used as baseline. SPT was performed every 6 months and OH was continuously reinforced. Data pooled by PD ≤3.5mm, 4-6.5mm and ≥7mm.

– 53 teeth (13%) were discontinued: 20 pt preference, 25 progressive attachment loss, 8 fracture/esthetics, etc.

– Mean plaque score increased slightly from 8-20% to 10-30%.

– BOP and PD improved in the > 7mm group and did not change for the other groups.

– 2-3% of sites lost attachment during 24-48 months

– Few sites that showed PAL during the 0-24-month period showed continued loss during the subsequent 24-48-month period.

– Initially shallow/deep sites that showed loss/gain of attachment had some loss/gain attachment during the 0-24-month period

BL: Plaque control and root debridement may be an effective way to treat chronic periodontal disease over several years in non-molar teeth in a patient population with good compliance. Probing attachment loss over 4 yrs: ≤3.5mm PD = 19-24%, 4-6.5mm PD = 5-7%, and ≥7mm PD =1-4% of the sites. This study failed to demonstrate that sites with deeper PD were more difficult to maintain than shallower sites

Renvert 1990 ARTICLE comparison of various forms of treatment

P: To report 5-year clinical observations following treatment of intraosseous periodontal defects with root planing alone compared to treatment with flap surgery. Results of sub-g microbial samples taken after 42, 48 and 60 months are reported.

M&M: 14 patients, 32-62 years of age were included. 21 defects were treated with root planing alone and 21 defects were treated with flap surgery. Defects surgically treated: FTF, defects were degranulated, root surfaces were planed and treated with citric acid, no osseous recontouring, flaps were replaced and sutured to obtain complete closure of the wounds. Defects treated with root planing: roots were instrumented with curettes, intentional soft tissue curettage was not performed. Oral rinses with 0.2% CHX were prescribed adjunctively to OH procedures for the first 2 weeks post-op. Pts were seen at weekly intervals the first 3 weeks post-op and at 6, 12, 18 and 24 weeks for OHI and polishing of the teeth. Maintenance therapy from 6 to 60 months was limited to reinforcement of OH and tooth polishing every 6 months. No sub-g instrumentation was done at the defects sites at these visits. The following parameters were recorded at 6, 12, 24, 36, 42, 48, 54 and 60 months post-op: plaque scores, BOP, PD, AL, probing bone level. Microbial samples were taken from the buccal aspect of the proximal defect sites at 42, 48 and 60 months.

R: Surgically treated lesions responded with a slight more reduction of PD and more gain of probing bone level than root planed lesions. Mean gains of AL were similar for the 2 treatments. Some relapse of clinical conditions could be observed towards the end of the 60-month observation interval. The majority of defects subjected to either treatment showed 60-month recording of probing attachment and probing bone levels equal or slightly improved compared to baseline. The results of the microbial counts at 42, 48 and 60 months revealed similar counts of the various bacterial groups at all 4 time points and for both treatments.

C: Although the results indicate similar long term results following root planing and surgical treatment, this should not be interpreted as documentation that root planing is an adequate therapy in all situations.

Cr: small number of patients

Ramfjord 1987 ARTICLE

P: To clinically assess, over 5 yrs, tx results following 4 diff modalities of perio tx.

M&M: After initial SRP and OHI, 90 mod-adv perio pts had the 4 quads randomly treated with 1) S/RP, 2) MWF, 3) APF + osseous, or 4) subg-curettage. This was followed by OHI and prophy every 3m. PD sites were grouped: shallow (1-3 mm), mod (4-6 mm), or adv (>7 mm). PD and AL were recorded annually and % sites w/ 2+mm and 3+mm AL gain/loss were compared. Pts w/ overt bleeding or suppuration were re-tx’d. 72 of these pts were followed for 5 yrs.

Shallow sites: all had ALoss, but it was less w/ SRP or curettage and most w/APF.

Mod sites: More PD reduction: sx > SRP > curettage. All 4 types of tx had some ALoss, but APF had the most.

Adv sites: all showed PD reduction and most showed att gain but there were NSD b/w the 4 methods of tx.

At 5y, there were few sites w/ ≥2-3 mm gain or ALoss – shallow sites had the most losses and almost no gains. Mod sites had more losses than gains and adv sites had more gains than losses. Adv sites rarely lost att regardless of tx. 1% of the treated tth were lost (22)-17 for perio reasons (16 furc involvement).

BL: SRP alone is as effective as other modalities of tx as long as access to the root surface can be obtained. For pts ≥7 mm, the results are similar for all 4 types of tx. There is no benefit to curettage vs SRP. Regardless of tx, furc involvement is the greatest hazard in the prognosis. Re-tx is needed more often after SRP than after the other procedures, but with additional scaling, the results are as good as for any other procedure.

Becker 2001 ARTICLE

to present 5-year results from a longitudinal study comparing the effectiveness of SRP, osseous Sx, and MWF procedures as performed by periodontists who are proponents of the specific technique.

133. Effects of Therapy:

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a. Supportive Periodontal Therapy (Maintenance)

b. Re-treatment

c. Refractory Periodontitis

Why is maintenance therapy necessary? What is performed at these visits?

Schallhorn RG, Snider LE. Periodontal maintenance therapy. JADA 101:227-231, 1981.

Ramfjord SP. Maintenance care for treated periodontitis patients. J Clin Periodontol 14:433- 437, 1987.

Echeverria JJ, Manau GC, Guerrero A. Supportive care after active periodontal treatment. A review. J Clin Periodontol 23:898-905, 1996. (Review)

Tonetti MS, Steffen P, et al. Initial extractions and tooth loss during supportive care in a periodontal population seeking comprehensive care. J Clin Periodontol 27:824-831, 2000.

Ramfjord SP, et al. Oral hygiene and maintenance of periodontal support. J Periodontol 53:26-30, 1982.

Becker W, Berg L, Becker B. The long-term evaluation of periodontal treatment and maintenance in 95 patients. Int J Perio Rest Dent 4(2):54-71, 1984.

Lindhe J, Nyman S : Long-term maintenance of patients treated for advanced periodontal disease. J. Clin. Periodontol. 11:504-514, 1984.

Rosling B, Serino G, et al. Longitudinal periodontal tissue alterations during supportive therapy. J Clin Periodontol 2001; 28:241-249.

Teles RP, Patel M, Socransky SS, Haffajee AD. Disease progression in periodontally healthy and maintenance subjects. J Periodontol. 2008 May;79(5):784-94.

Muzzi L, Nieri M, Cattabriga M, Rotundo R, Cairo F, Pini Prato GP. The potential prognostic value of some periodontal factors for tooth loss: a retrospective multilevel analysis on periodontal patients treated and maintained over 10 years. J Periodontol. 2006 Dec;77(12):2084-9.

Listgarten MA, et al: Clinical and microbiological characteristics of treated periodontitis patients on maintenance care. J. Periodontol. 60:452-459, 1989.

Pontoriero R, et al : The angular bony defect in the maintenance of the periodontal patient. J. Clin. Periodontol. 15:200-204, 1988.

Lindhe J, et al: Long-term effect of surgical/non-surgical treatment of periodontal disease. J. Clin. Periodontol. 11:448-458, 1984.

Slots J, Jorgensen MG. Efficient antimicrobial treatment in periodontal maintenance care. JADA 131:1293-1304, 2000.

Matuliene G, Pjetursson BE, Salvi GE, Schmidlin K, Brägger U, Zwahlen M, Lang NP.Influence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance. J Clin Periodontol. 2008 Aug;35(8):685-95

Position Paper: Supportive Periodontal Therapy (SPT). J Periodontol 69:502-506, 1998. (Review)

Discuss the reported level of patient compliance with maintenance recommendations and its implications for periodontal practice? How important is compliance for prognosis of teeth?

Wilson TG, Glover ME, Schoen J, Baus C, Jacobs. Compliance with maintenance therapy in a private periodontal practice. J. Periodontol. 55:468-473, 1984.

Wilson Jr. T, Hale S, Temple R. The results of efforts to improve compliance with supportive periodontal treatment in a private practice. J Periodontol 1993; 64: 311-314.

Novaes A, Novaes A Jr, Moraes N, Campos G, Grisi M. Compliance with supportive periodontal therapy. J Periodontol 1996; 67: 478-485.

Miyamoto T, Kumagai T, Jones JA, Van Dyke TE, Nunn ME. Compliance as a prognostic indicator: retrospective study of 505 patients treated and maintained for 15 years. J Periodontol. Feb;77(2):223-32. 2006.

Miyamoto T, Kumagai T, Lang MS, Nunn ME. Compliance as a prognostic indicator. II. Impact of patient’s compliance to the individual tooth survival.J Periodontol. 2010 Sep;81(9):1280-8

König J, Plagmann HC, Rühling A, Kocher T.Tooth loss and pocket probing depths in compliant periodontally treated patients: a retrospective analysis.J Clin Periodontol. 2002 Dec;29(12):1092-100.

What are the effects of maintenance therapy on wound healing?

Yumet JA, Polson AM. Gingival wound healing in the presence of plaque induced inflammation. J. Periodontol. 56:107-119, 1985.

Westfelt E, Nyman S, Socransky S, Lindhe J. Significance of frequency of professional tooth cleaning for healing following periodontal surgery. J. Clin. Periodontol. 10:148-156, 1983.

What happens if treated patients are not maintained?

Becker W, Becker B, Berg L. Periodontal treatment without maintenance – A retrospective study in 44 patients. J Periodontol 55:505-509, 1984.

Becker BC, Karp CL, Becker W, Berg L. Personality differences and stressful life events. Differences between treated periodontal patients with and without maintenance. J. Clin. Periodontol. 15:49-52, 1988.

Is there a difference in treatment results if maintenance is done in general dentists offices?

Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal disease. J. Clin. Periodontol. 8:281-294, 1981.

Johansson LA, Oster R, Hamp SE. Evaluation of cause-related periodontal therapy and compliance with maintenance care recommendations. J Clin Periodontol 11:689-699, 1984.

Kerr NW. Treatment of chronic periodontitis- 45% failure rate after 5 years. Brit Dent J 150:222-224, 1981.

McFall WT, Bader JD, Rozier RG, et al. Clinical periodontal status of regularly attending patients in general dental practices. J. Periodontol. 60:145-150, 1989.

Fardal Ø. Interviews and assessments of returning non-compliant periodontal maintenance patients. J Clin Periodontol. 2006 Mar;33(3):216-20.

What is the ideal MT frequency after periodontal treatment ?

Mousques T, Listgarten MA, Phillips R. Effect of scaling and root planing on the composition of the human subgingival microbial flora. J Perio Res 15:144-151,1980.

Sbordone L, Ramaglia L, Gulletta E, Iacono V. Recolonization of the subgingival microflora after scaling and root planing in human periodontitis. J Periodontol. 1990 Sep;61(9):579-84.

Listgarten MA, et al: Comparative longitudinal study of two methods of scheduling maintenance visits; 4-year data. J. Clin. Periodontol. 16:105-115, 1989.

Rosen B, Olavi G, et al. Effect of different frequencies of preventive maintenance treatment on periodontal conditions. J Clin Periodontol 26:225-233, 1999.

Shiloah J, Patters MR. Repopulation of periodontal pockets by microbial pathogens in the absence of supportive therapy. J Periodontol 1995; 67: 130-139

What causes failure of treatment? When would you consider retreatment for a patient? How often do we need to retreat patients for periodontitis?

Chace R. Retreatment in periodontal practice. J Periodontol 48:410, 1977. (Review)

Rateitschak KH.Failure of periodontal treatment. Quintessence Int. 1994 Jul;25(7):449-57.

Fardal and Linden. Re-treatment profiles during long-term maintenance therapy in a periodontal practice in Norway.J Clin Perio 2005; 32:744-749

Morrison EC, Ramfjord SP, et al: The significance of gingivitis during the maintenance phase of periodontal therapy. J Periodontol 53:31-34, 1982.

What is “Refractory Periodontitis” and how can it be managed?

Jenkins WM, Said SH, Radvar M, Kinane DF. Effect of subgingival scaling during supportive therapy. J Clin Periodontol 27:590-596, 2000.

Haffajee AD, Uzel NG, Arguello EI, Torresyap G, Guerrero DM, Socransky SS. Clinical and microbiological changes associated with the use of combined antimicrobial therapies to treat “refractory” periodontitis.J Clin Periodontol. 2004 Oct;31(10):869-77.

Why is maintenance therapy necessary? What is performed at these visits?

Schallhorn 1981 NO ARTICLE

P: To discuss the different aspects of prevention programs and to give the time frame of a typical maintenance visit.

D:PREVENTATIVE PERIODONTAL MAINTENANCE prevents inception of periodontal disease in individuals without periodontal disease.

TRIAL PERIODONTAL MAINTENANCE maintains borderline cases.

COMPROMISE PERIODONTAL MAINTENANCE is designed to slow the progression of periodontal disease in individuals who for what ever reason do not undergo surgical or nonsurgical therapy.

POSTTREATMENT PERIODONTAL MAINTENANCE to prevent re occurrence of periodontal disease in patients that have undergone active therapy.

Maintenance intervals should be individualized.

Factors: nature and extent of periodontal problem, type of therapy performed, effectiveness and frequency of plaque control, rate of calculus formation, systemic health, BOP.

The article outlines the components of an average maintenance appointment as performed by the dental hygienist (total under 1 hour). Greeting and health/dental history 8.5 minutes, Dental screening (extraoral and intraoral exam) 1.12 min., Periodontal assessment (BOP, PD, REC, fremitus, color/ architecture of gingiva),3.25 min., Plaque index 3.0 min., Oral hygiene inst. 4.20 min., Polish/Floss 10.9 min., SC/RP 10.9 min., Ultrasonics 6.83 min., Caries assessment 1.0 min., Chemical therapy (irrigation with antimicrobial agents) 1.50 min., Fluoride 1.0 min, Dismissal 1.0 min.

Patients vary with respect to number of teeth present, PDs, amount of calculus and staining and other considerations influencing the time required for therapy. Appointments should be individualized for the patient with either shorter or longer time allocations as appropriate for adequate therapy.

If the patient’s condition is stable with lack of inflammation, minimal calculus deposits and optimal plaque control, the interval can be extended between maintenance visits. If there are adverse findings the interval should be shortened until the optimal recall time for the patient is determined.

Ramfjord 1987 ARTICLE

P:Review of current literature with clinical observations to evaluate maintenance care

Caton 1982 showed that initial gross clinical results of therapeutic procedures are established 4-6 wks after completion of therapy, although changes can be observed 6-9 months after completion of treatment.
Maintenance appointments should include prophylaxis of all teeth, OHI and fluoride. Maintenance should be scheduled every 3-4 months(although post surgical, recommend professional plaque removal once/wk for first month then 3 month maintenance).
Pts with better plaque control will have better surgical results, but once they have healed, maintenance results are similar regardless of OH (Ramfjord 1982) as long as pts have professional tooth cleaning every 3 months.
Pocket depth after treatment may not be the most critical determinant for prognosis.
Retreatment is often necessary to remove residual accretion of calculus and the treatment of new active lesions (bleeding or suppuration). These areas should be re-evaluated after 2-3 weeks to retest and decide if more SRP or surgery is needed.
Maintenance visits should also be used to monitor sensitivity, caries, pulpal status, evaluate old restorations and check occlusion.

BL: Maintenance should be completed every 3 months.

Echeverria1996 ARTICLE

P: This review addresses the most significant questions regarding supportive (maintenance) care after active periodontal treatment: the effectiveness and ideal frequency of maintenance appointments, the adequacy of the supportive therapy according to pt needs, the possible alternatives to currently accepted protocols, and the relative value of personal in the overall context of supportive care.

Disc: Periodontal diseases are infections with a high potential for recurrence, progressive loss and eventually, tooth loss. Current treatmentsfor periodontal diseases are highly predictable in arresting disease activity. Supportive periodontal care has been shown to be very effective in maintaining support when adapted to each particular case. Nevertheless, current maintenance therapies may be unsuccessful in preventing further ALoss in a smallnumber of sites for some patients. Tests aiming at bacterial identification and the subgingival application of antimicrobials may be helpful in the management of such cases, however the practical value in a specific setting is not known. There is growing evidence of the fundamental role of personal in supportive periodontal care. Careful consideration of the pt’s personal risk factors relating to the development of further disease is essential in the long-term management of the periodontal pt after the completion of active tx.

BL: In cases with rapid and severe periodontal destruction and where local and/or systemic risk factors are present, personal becomes a key factor in the long-term preservation of periodontal support.

Tonneti 2000 ARTICLE

Purpose: To describe 1) the prevalence of tooth loss and 2) the dental pathologies associated with extraction during active periodontal therapy and in the subsequent supportive periodontal care (SPC) period in a periodontal population who received comprehensive care at a University clinic and was maintained in an individualized recall program.

Materials and methods:Retrospective longitudinal survey of tooth extraction during active periodontal therapy tooth loss during the following SPC interval at University of Bern. Number of teeth present was determined at three time points: the initial consultation, the first SPC apt following active treatment and the latest clinical session of SPC. Clinical diagnosis according to ADA case type was retrospectively performed. Consecutive patients presenting for SPC between January and April 1995 were invited to participate in the study. 270 patients, 58% females between 16-1 years of age were included. The had completed active periodontal therapy 6 months previously, the did not have a contributory medical history and the clinical records were available. Whenever surgery was performed it did not include osseous recontouring. Each tooth that was extracted was classified as having one of the following pathologies: periodontal disease, caries, endodontic problems, technical failures (e.g. root fractures) or unknown. If teeth were used as abutments or had furc involvement was also recorded. Smoking status and radiographic bone loss were also assessed.

Results: Patients remained in an SPC program for 67+/- 46 months. 39.6% were current smokers and 27.8% previous smokers. 6.2% had gingivitis, 20.5% mild, 48.4% moderate and 24.9% severe periodontitis. Average frequency of the recall visits was 4.4+/- 1.5 apts/year.

Pts presented with 6503 teeth at their initial examination and 5929 at the recall. 574 were extracted totally, 311 (4.8% of total teeth, 1.1 extractions/patient but performed in 46% of patients) during the initial phase of treatment and 263 (4.2% of teeth present after completion of active treatment) during the recall period. 15.7% were 3^rd molars and 1.9% retained primary teeth.

299 were maxillary teeth (106 molars, 47 multi-rooted upper premolars) and 175 mandibular (79 molars).

Pathologies associated with tooth extraction:

In the initial phase extractions that were associated with periodontal disease only were 63% and during recall 50%.

The teeth extracted with periodontal disease as the only pathology had an average radiographic bone loss of 56%. 62% in single rooted teeth and 49% in multi rooted teeth.

Caries, endodontic, and technical problems represented the leading pathology associated with gingivitis and mild periodontitis patients. Severe periodontal disease alone or in combination with other problems was present in 76-94% of initial extractions in moderate and severe periodontitis cases respectively.

During recall the incidence tooth loss/year was 0.17+/-0.31 teeth. During this period 41% of subjects had extractions, number of teeth that was extracted amounted to 2.35+/- 1.9 teeth/patient in this population and 0.4+/-0.37 teeth/year. The % of teeth that were extracted because of technical problems increased from 14% during initial phase to 27% during recall visits. During maintenance visits, 45% of patients presenting with moderate periodontitis at baseline had extractions and 48% of patients that had severe periodontitis had extractions. 86% of extraction in severe periodontitis patients were extracted because of periodontal reasons alone or in combination with other etiologies. In moderate periodontitis teeth extracted for this reason were 60%.

Conclusion: 8.8% of teeth present at baseline were extracted either during active therapy or in the subsequent SPC period. 4.2% of teeth were extracted during SPC and this suggests that initial extractions should be taken into account to compare the overall impact of comprehensive therapy on tooth loss.

Advanced periodontitis was associated with the majority of teeth that were extracted and was the only obvious pathology in 57% of the cases.

Tooth extractions were experienced by specific sub-populations and a minority of cases accounted for the majority of extractions.

Ramjford 1982 ARTICLE

Purpose: To evaluate if PD and AL gained by therapy can be maintained despite variations in levels of OH while on 3 months maintenance.

Materials and methods:

78 patients previously treated and on 3 month recall over 8 years.
PD and AL related to plaque scores above and below the median were assessed. 25% of sample having lowest plaque score was compared with 25% of sample with the highest plaque score over 6-8 years of maintenance.
All pts were given repeated instruction and motivation to improve their OH.

Results:

Plaque score was not critical for maintenance of posttreatment PD and AL in patients with professional prophylaxis every 3 months.
Initially OH had an effect (the better the OH, the better the results for 4-5 years) on PD and AL, but their effect did not hold long term.
Although initial post-tx gain of AL appears highly related to the degree of OH, the long-term results were not dependent on plaque scores.

BL: AL and PD 1 year after therapy can be maintained over 6-8 years with maintenance every 3 months, regardless of unavoidable variations in the effectiveness of the patient’s plaque control.

Becker 1984 ARTICLE

P: A retrospective study to evaluate the clinical results of periodontal therapy and maintenance.

M&M: 95 diagnosed, treated and maintained perio patients (ages 25-74) in a private practice (average length of tx was 6.5 yrs). Each patient had minimum of 2 exams, excluding 3^rd molars. Clinical exam included PD, GM, furcations, and FMX. On the basis of clinical and radiographic findings, teeth were given a questionable prognosis (bone loss 50% of root length, PD 6-8mm, Class II Furcation) or hopeless prognosis (bone loss over 75%, PD 8-10mm or more, Class III furcation). All teeth not questionable or hopeless were given a good prognosis. Bone scores were determined using the Bjorn bone score. Tx included OHI, 1-3 sessions of SRP, occlusal adjustment, and pocket reduction surgery. All pts were placed on 3-4month recall.

6.21% of the total teeth were lost (150/2414) or 0.24 teeth per pt. per year(w/o hopeless teeth corrected to 0.11).
The maxillary second molars lost most often. Canines and mandibular incisors were lost least often.
Mortality based on prognosis, 87 of 102 (85%) given a hopeless prognosis were lost, thus 87/150 (58%) of the lost teeth were hopeless teeth.
Only 1.7% of teeth w/ good prognosis were lost.
22% of molars with no furcations had furcations by the last exam.
55% of the pockets 4-6mm at the first exam were in the 1-3mm range at the second exam
Over 50% had no changes in bone score.
Maintenance interval average was 5.2 mos. They had a 22% drop out rate.

BL:Perio Tx and maintenance are successful in reducing mod to deep pockets with minimal long term bone loss.

Lindhe 1984 ARTICLE

PURPOSE: To evaluate the perio condition of pts who had undergone treatment for advanced periodontitis and were well maintained for 14 years.

M&M: 61 of the 75 original patients treated in 1969 for advanced perio dz. All patients had received treatment consisting of OHI, SRP, Sx (pocket elimination) and then 3-6 month recall interval. Once a year plaque, GI, PD, AL and alveolar bone height were examined. This was evaluated at 1, 3, 5, 8, 10, 12, and 14 years after the completion of active therapy.

RESULTS: Prior to txt, 76% of sites examined had PD>4 mm, with 47% having PD >6 mm. Initial therapy reduced GI and improved plaque control, which was maintained over the life of this study. 92-99% of sites remained <4mm over 14 yrs. <1% developed PD >6 mm over 14 yr period. Individual mean values describing PD, AL and bone heights did not significantly vary over the 14 years; however, a small number of sites in a few pts lost substantial attachment. 0.8% of sites lost >2 mm of attachment over 14 yrs. During the entire treatment course, 30 teeth were lost out of 1330 (2.3%) from all 61 pts. Looking at individual data, 16 teeth were lost from 7 pts.

BL:Tx of advanced forms of periodontal disease can be maintained over a period of 14 years. Recurrent disease in well-maintained pts is a site-specific disorder which evidently develops and progresses in a few unpredictable sites and is not a generalized phenomenon

Rosling 2001 ARTICLE attachment loss

P:To evaluate disease progression in “normal” susceptibility patients (NSG) and “high” susceptibility patients (HSG) to periodontitis during SPT.

M&M: HSG : 109 patients, NSG: 232 patients. All received 4-6 one hr sessions of S/RP, followed by 3-4x/year recalls. If BOP or PD>5mm noted at recall, site was re-treated. Teeth that presented with abscess or unresolved mob were extracted. The following clinical parameters measured at baseline (1 year after S/RP) and 12 years: # of teeth, PPD, PAL, RA bone level (standardized).

R:NSG: most subjects maintained their perio condition unchangedduring the MT period; only a few subjects experienced small amount of bone and ALoss (0.5 mm and 0.3 mm respectively). HSG: patients lost significant amounts of bone and attachment during the 12 years of SPT. Thus, in this group of subjects, the mean overall PAL loss amounted to 0.8 mm (0.06 mm/tooth surface/year). In the NSG, the overall ALoss was significantly smaller: 0.5 mm (0.04 mm/tooth surface/year). The subjects in the NG lost 0.3 teeth during the 12 years interval while the corresponding loss in the HSG was 1.9 (0.8 non-molar and 1.1 molar teeth). 20% of the HSG patients and 3% in the NG were exited of the study after 3-5y of SPT due disease progression.

BL:In patients with a high susceptibility for perio disease it is possible to maintain bone and Attach Levels at a reasonably stable level over a 12-year period after no-sx therapy. SPT in pts with normal susceptibility to perio disease, prevented almost entirely major tooth, bone and attach loss. Some patients and sites could be identified that responded poorly to therapy despite good plaque control and regular recall appointments.

Teles 2008 ARTICLE

P:To determine whether the rate of attachment loss in periodontally healthy subjects in a prevention regimen would differ from the rate of disease progression in periodontitis subjects in a maintenance program.

M&M:55 periodontally healthy patients and 57 periodontitis patients were clinically and microbiologically monitored at baseline and at 1, 2, and 3 years. Parameters measured included BOP, plaque, PD, and AL. Periodontally healthy and maintenance groups received SPT every 6 and 3-6 months respectively. Subgingival plaque samples were taken from the MB aspect of every tooth and were measured by checkerboard DNA/DNA hybridization. No subgingival treatment was carried out within 3 months prior to the annual examinations.

R:Clinical parameters for both groups improved over time. 4% of the sites in the periodontitis patients lost ≥2 mm of attachment. Only 1% of the healthy periodontal patients lost ≥2 mm of attachment. Maintenance group lost 0.12 teeth/subject/year, whereas the prophylaxis group lost 0.02 teeth/subject/year over 3 years of study. At baseline, the maintenance subjects showed SS higher levels of red complex species compared to prophylaxis subjects. By year 2, both groups demonstrated reductions in the mean levels of most species.

BL:Treated periodontitis patients under maintenance displayed more rapid attachment loss than periodontally healthy subjects in a preventive regimen. This may be related to an elevated exposure to periodontal pathogens in the red complex.

Muzzi 2006 ARTICLE

P:To evaluate the value of some clinical, genetic, and radiographic variables in predicting tooth loss in periodontal patients treated and maintained for 10 years.

M&M:retrospective analysis, 60 (29M/31F) healthy, mean age 46.77 years, non-smoking patients, all 40-60 years of age and of white heritage (study from Italy) with moderate to severe periodontitis, treated in private practice with SRP and surgery per need (MWF or Osseous), and all received maintenance for 10 years. Probing depths, number of teeth, prosthetic restorations recorded. CEJ- to root apex, CEJ- to bottom of defect, CEJ- to bone crest, bone crest to bottom of defect, and bottom of defect to root apex (residual supporting bone) all were measured from radiographs. IL-1 genotypes were recorded.

R:two-level variance analysis for both patient level prognostic variables and tooth level prognostic variables.

SS prognostic relationship was found for molar teeth (positive correlation). Molar teeth were found more prone to loss. Bottom of defect to root apex distance was associated with tooth loss. The lower the amount of residual supporting bone, the greater the probability of losing the tooth. Bone crest to bottom of the defect distance was associated with tooth loss (negative correlation). The greater the distance the lower the probability of losing the tooth. Deep infrabony defects tend to respond better to regenerative procedures. Tooth mobility, PDs, presence or restorations and CEJ-bottom of defect were not found predictive for tooth loss.

C:Molar teeth, infrabony component of the defect and residual supporting bone may be considered prognostic factors for tooth loss.

Listgarten 1989 ARTICLE

P:To determine whether the presence of Aa, Pg, Pi in selected periodontal sites can predict future disease recurrence.

M+M:98 adults (>25 years old) with moderate to advanced periodontal disease that had been treated surgically and in maintenance programs for at least 1 year (75% over 5 yrs) were evaluated for PI, GI, PD, AL and microbiological analysis with paper points from sites with greatest PD in each sextant. A site was considered infected and positive for Aa, Pg, or Pi, if the above mentioned microbes were found at levels of > 0.01% for Aa, 0.1% for Pg, and 2.5% for Pi.

PI scores were higher for molars than the rest of the teeth.
GI was uniform throughout the dentition.
PD tended to be greater for the M/D than the B/L surfaces with a bilateral symmetrical pattern, PD increased from midline to posterior.
Sites positive for Aa, Pg, and Pi tended to have greater PD (mean: 4.14mm) than non-infected sites in the same pts (mean: 3.76).

BL:There was a positive correlation between Aa, Pg, Pi, Capnocytophaga and increased AL loss, as well as greater GI and PD.

CR:While it does somewhat correlate to disease activity, it is not enough to rationalize its routine use, especially in maintenance pts.

Pontoriero 1988 ARTICLE

P:To evaluate some long-term alterations of the alveolar bone level at sites with angular & horizontal bone loss.

M&M:48 patients were treated for advanced perio disease and then placed on SPT with recalls q 3-6 months for 5-16 years. 100 teeth with angular defects that could be detected after active treatment phase were included. A comparison was made between post-tx radiographs to current radiographs. Contralateral or neighboring teeth with horizontal bone loss used as controls. The following measurements were taken and measured with the Bjorn technique at 2x:

1.distance between base of defects & apex (B-A)

2.distance between alveolar crest & base of defect (C-B)

3.Distance between crest & apex on control teeth.

R: Current measurements (5-16 years post-active tx):

1.B-A distant remained unchanged.

2.The average C-B distance decrease from 1.41 bone scoring units (BSU) to 1.07 BSU. 12% of the sites showed ~ 0.7 to 2.0 mm apical shift in this distance (possibly downhill patients).

3.Distance from crest to apex remained almost unchanged in controls.

BL:The presence of angular bony defect after active treatment does not make a site more prone to additional bone loss in well-maintained patients. After perio treatment, most sites with angular or horizontal patterns of AB loss underwent none, or very little additional bone loss after 5-16 years of SPT.

Crit:Non-standardized radiographs. Authors do not describe what active perio tx included. Where there attempts to eliminate the defects that were unsuccessful (osseous, GTR)? The distance between bone crest-base of defect initially was 1.4, which is not a very deep bony defect…

This study does not apply to pts that present with deep verticals defects.

Lindhe(2) 1984 ARTICLE plaque control

Purpose: 1) To further analyze the role played by the patients’ self performed plaque control in preventing recurrent periodontal disease and 2) TO assess the periodontal conditions of patients 5 years after completion of active treatment (SRP or SRP + MWF) with special emphasis on sites with initial PD>3mm.

Materials and methods:15 subjects 32-57 years old were selected. After baseline examination patients received SRP or SRP + MWF in a split mouth design and had follow-up for 24 months. After the 24-month examination, the recall appointments were extended to 4-6 months. Maintenance program was restricted to OHI and supra-g tooth cleaning (sub-g instrumentation was avoided) and at 26, 48 and 60 months after Tx the quality of patients’ plaque control was assessed. At 60 months a final examination was performed and included the same parameters as assessed at baseline. Data include 11/15 patients that took part in the entire 5-years study and represent baseline – 60-month changes as well as 24-60 months changes.

Results: Group I: patients that maintained an excellent standard of OH during the 5 -year period at each re-examination. Group II: patients who failed to maintain a proper standard of OH at each re-examination.

24-60 months: AL remained unchanged in 86-88% of the sites. 2% gained 2mm or more of attachment and 10-12% exhibited attachment loss of 2mm or more. Attachment loss was more prevalent in interproximal surfaces. In Group I 2-3% of sites had attachment loss and 95% of istes remained unchanged or gained attachment, in Group II no sites had attachment gain and 20% had attachment loss.

Baseline-60-months in sites with PD>3mm at baseline: 55-65% showed PD reduction. 1-2% showed increase in PD. 85% in of sites with 4mm or more PD in Group I were reduced in depth, in the majority more than 2mm. Such a reduction of the PD was less prevalent in Group II. In Group II 60% of sites remained unaltered.

For sites with PD of 4mm or more, more sites lost attachment in the patients in Group II (20% and 6% vs 7% and 2%). Gain of attachment occurred more frequently in the patients of subgroup I.

24-60 months for PD>3mm at 24 month re-eval: 75-85% of PDs and 85% of AL remained unchanged. Reduction in PD and AL gain occurred mainly in patients in Group I while further increase in PD was found mainly in patients in Group II.

It is likely that attachment level gain is the result of reduction of inflammatory infiltrate after treatment and increase in collagen.

Conclusion: Patients’ standard of OH had a decisive influence on the long – term result of treatment of periodontal disease.

Sites with an initial PD exceeding 3mm responded equally well to the non-surgical as to the surgical mode of treatment.

Slots 2000 ARTICLE

Purpose:To outline the current approaches to follow-up care after initial (“definitive”) perio tx and advance a suitable protocol for perio maintenance care.

Discussion:

Preventive periodontal therapy can be categorized as primary, secondary or tertiary. Primary prevention aims to reduce risk factors before clinical presentation of disease and can be accomplished by intervention strategies aimed at both the general public and special, high-risk populations.
The aim of secondary prevention is to intervene at early disease or precursor
Tertiary prevention seeks to limit the impact of established disease.
Perio exam should include full-mouth probing, with PD, BOP, AL, PI, plaque score. Calculus removal using hand instruments or ultrasonic. Recommend using 10% povidone-iodine diluted 1:9 with water for irrigant in the ultrasonic. After ultrasonic use air-polishing device on each tooth for 5 sec. OHI is given to the pt along with any necessary prescription or rinses like CHX.
Mechanical and chemical antimicrobial intervention is the mainstay of preventive periodontal therapy. Chemotherapeutics alone are unlikely to be effective in the presence of subgingival calculus, subgingival mechanical debridement is very important.
Toothbrushing and rinsing alone do not reach pathogens residing in periodontal pockets of increased depths, oral hygiene procedures should include subgingival treatment with home irrigators or other appropriate self-care remedies.
Recall every 3 months in pts with ongoing perio destruction and microbial sampling may be needed. Pts with stable perio diagnosis can be scheduled for maintenance every 4 months.

Matuliene 2008 ARTICLE

P:To investigate the influence of residual PPD 5mm and BOP after active periodontal therapy (APT) on the progression of periodontitis and tooth loss.

M&M:Retrospective longitudinal study, 172 patients (95F/77M), 14-69 years of age were included in the study. Complete clinical periodontal (PD, REC, CAL, BOP, MOB, FURC) and radiographic examinations were performed (full mouth x-rays) at baseline, at the end of the active therapy and at re-evaluation. At re-eval the full mouth x-rays were replaced by panoramic x-rays. Periodontal therapy consisted of OHI, SRP and periodontal surgery if indicated. Prosthetic therapy using dental implants or fixed prosthesis was performed. Following completion of comprehensive periodontal treatment, patients were enrolled in SPT program. Re-eval was performed after a mean of 11.34.9 years of age. Smoking habits, health status and frequency of recalls during SPT were assessed. A case was defined as being progressive if there were at least 2 teeth with 3mm attachment loss at the end of APT and re-eval.

Number of residual PPD increased during SPT.
Increased PPD was associated with tooth loss. The increase by 1mm PPD increased the odds and therefore the probability of tooth loss in a statistically significant way.
Heavy smoking (, initial diagnosis (severe periodontitis), duration of SPT (>10years) and PD6mm were risk factors for disease progression.
PPD6mm and BOP 30% represented a risk for tooth loss.

C:Residual PPD 6mm after APT represented a risk factor for both progression of periodontitis and tooth loss during SPT.

Position Paper: Supportive Perio Therapy 1998 NO ARTICLE

P:To provide an overview of the role of SPT in the tx of perio dz

D:SPT includes an update of medical and dental hx, extraoral and intraoral soft tissue exam, dental exam, perio evaluation, rx review, removal of plaque and calculus from supra-g and sub-g regions, selective root planing if indicated, polishing of teeth, and a review of the pt’s plaque removal efficacy.

Tooth loss in some pts has been shown to be inversely proportional to the frequency of SPT. Ten years after perio therapy, pts who had received at least periodic SPT had SS decreased PD and tooth loss. Less CALoss has also been linked to frequency of SPT. Some individuals still may suffer CALoss despite maintaining a regular SPT schedule. Additional microbial analysis as well as anti-microbial therapy may be necessary for those individuals.

For pts without a history of periodontitis (simply gingivitis), SPT performed every 6 months is sufficient. Although there are several different opinions on how often perio pts should receive SPT, the data suggests that it should be performed at least every 3 months. Nevertheless, the frequency of SPT should be individualized. SPT may be performed by the dentist and/or periodontist depending on severity of the perio dz.

Discuss the reported level of patient compliance with maintenance recommendations and its implications for periodontal practice? How important is compliance for prognosis of teeth?

Wilson 1984 ARTICLE

P:To determine compliance of maintenance schedules recommended in a private periodontal practice.

M&M:961 patients with chronic periodontitis were divided based on the severity of disease. Procedure performed was either SC/RP, flap with osseous, or flap alone. During active therapy, the importance of recall was stressed to patients. After active therapy, all patients were placed on 3-month recall schedule and later modified as needed. 92% of the patients were on a 3- or 4-month recall interval. Compliance was classified as complete, erratic, or none based on the longest recall interval possible for each classification. Study period was 8 years.

R:Only 16% completely complied with recommended maintenance recall. Erratic compliance was found in 49% of patients, and 34% never reported for any maintenance therapy. Compliance decreased over time after active therapy. Patients who had periodontal surgery were in compliance slightly more often, and patients with mild disease kept their maintenance schedules the best. Patients with a poor prognosis had the worst record of all categories (higher proportion of non-compliant, and least completely compliant). The less often patients were required to return for maintenance, the better they complied.

BL:The vast majority of patients (84%) did not completely comply with maintenance recall. One third didn’t return after active therapy.

Wilson 1993 ARTICLE

Purpose:Comparison of a literature review on compliance improvement techniques and the results shown by implementing these techniques in a practice.

Methods: 604 patients were studied during the 5 yrs from which data were collected. Some patients were alternating maintenance with their general dentist office. Efforts to improve compliance included simplifying compliance, maintaining records of compliance, informing patients of the consequences of noncompliance, and attempting to identify non-compliers before active therapy was initiated. Also patients’ scheduling included accommodating patients’ schedules and post card reminders.

Results: Mean age 46 yrs (range 18-78). 32% were complete compliers. 48% were erratic. 20% were non-compliers. 44% were men. Noncompliance was highest in the 0-2 month group.

Conclusion: Non-compliance can be reduced if the problem is recognized and efforts are made to increase compliance.

Novaes 1996 ARTICLE

P:To present data from private periodontal practice records to analyze compliance according to age, sex, and type of therapy and to discuss about the need for an aggressive office routine to keep patients committed to supportive therapy.

M&M:Data was obtained from 1280 records of patients seen over a 20- year period in a private periodontal practice in Brazil. All patients had completed the proposed treatment including the procedures indicated. Cases were considered surgical if they received basic periodontal therapy followed by surgical intervention in at least 3 areas. Recall visits were scheduled with intervals 2-6 months. Those who fulfilled 2/3 of the appointments were considered regular (R) less than 2/3, irregular (I); and those who did not return for any appointments, noncompliant (N). Patients were classified according to age, sex, and type of therapy. The compliance and noncompliance groups were further subdivided according to age: <20, 21-40, 41-60, & > 60 years. The 854 patients who initially co-operated and then abandoned supportive periodontal therapy were analyzed according to sex and type of surgery.

25.2% were non-compliant and 74.8% returned for at least some appointments
Among those who returned, 40.1% returned regularly, 34.7% returned irregularly
Number of women who returned was greater than the number of men (76.5% vs 72.2%)
Patient ages 21-40 and 41-60 showed the greatest interest in supportive therapy
Proportion of surgical patients who returned for supportive therapy was significantly greater than non-surgical patients, however there was not SSD between surgical therapy and non-surgical therapy for regular compliance (40.5% vs 38.9%)
854 patients begun but did not continue with SPT (66.7%), more females than males (59.5% vs 40.5%), greater among surgical cases than non-surgical

C:The vast majority of patients did not comply w/ the recommended recall periods. The authors recommended an intense program of education and motivation for the 1^st year of therapy.

Miyamoto 2006 ARTICLE

P: To evaluate the impact of compliance (complete vs erratic) on common clinical parameters in a long term observation period (15-23 years).

M+M: A retrospective study of 505 patients over an observation period of 15-23 years. Patients were classified by two methods of classification:

Compliance 1 classification– pts attended at least 70% of all expected maintenance visits were considered complete compliers while those who failed >30% of maintenance visits were considered erratic

Compliance 2 classification– pts who attended most of their scheduled maintenance visits were considered complete compliers while those who failed to attend a maintenance visit for a minimum of 2 years were considered erratic

In both classification schemes, patients who did not respond to recommendations for maintenance therapy or disappeared completely during the active phase of treatment were designated as total non-compliers. Total non-compliers were excluded from this study.

The groups were evaluated for: Plaque index reduction vs. no reduction; bleeding index reduction vs no reduction; reduction in pockets >3 mm vs no reduction; no increase in DMFT vs increase; and no tooth loss vs tooth loss

R: Complete compliers tended to show a reduction in BOP and a reduction in plaque index compared to the other groups.

Complete compliers under compliance 2 were less likely to see a reduction in pockets

Protected: 82. Root Surface – Management: Mechanical

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91. Occlusal Trauma Part I

HOME PERIO TOPICS

What is occlusal trauma? What are the clinical signs and symptoms of occlusal trauma? Describe the types of occlusal trauma. Which system do you use to classify mobility? What is fremitus? Is there a relationship between mobile teeth and success of periodontal treatment? What are the indications and contraindications of splinting mobile teeth?

Miller, S.C. Textbook of Periodontia, Blakiston Co., 1950, p. 125.
Laster L. An evaluation of clinical tooth mobility measurements.J Periodontol 46:603-607, 1975.
RosenbergD, Quirynen M, et al. A method for assessing the damping characteristics of periodontal tissues: Goals and limitations. Quintessence Int 26:191-197,1995.
NeiderudAM, Ericsson I, Lindhe J. Probing pocket depth at mobile/nonmobile teeth.J Clin Periodontol 1992; 19:754-759.
PerrierM, Polson A. The effect of progressive and increasing tooth hypermobility on reduced but healthy periodontal supporting tissues. J. Periodontol. 53:152-157, 1982.
KerryGJ, et al. Effect of periodontal treatment on tooth mobility.J. Periodontol. 53:635-638, 1982.
Fleszar TJ, Knowles JW, et al. Tooth mobility and periodontal therapy. J Clin Periodontol.7:495-505, 1980.
GallerC, Selipsky H, Phillips C, Ammons WF Jr. The effect of splinting on tooth mobility. (2) After osseous surgery. J Clin Periodontol. 1979 Oct;6(5):317-33.
Lemmerman, K. Rationale for stabilization: J Periodontol 1976;47:405-11
Lindhe J, Ericsson I. Influence of trauma from occlusion on reduced but healthy periodontal tissues in dogs. J. Clin. Periodontol. 3:110-122, 1976.
Glickman I, et al. The effect of occlusal forces on healing following mucogingival surgery. J. Periodontol. 37:319-325, 1966.
Polson AM, et al. Osseous repair in the presence of active tooth hypermobility.J Clin Periodontol. 10:370-379, 1983.
Schulz A, Hilgers RD, Neidermeier W. The effect of splinting of teeth in combination with reconstructive periodontal surgery in humans. Clin Oral Invest 4:98-105,2000.
Harrel SK. Occlusal forces as a risk factor for periodontal disease. Periodontol 2000 2003;32:111-7.

Describe the different theories of occlusion and its relationship to the periodontium. Do teeth with occlusal contacts in excursive positions exhibit any greater severity of periodontitis? Do occlusal discrepancies affect gingival recession?

Waerhaug J. The angular bone defect and its relationship to trauma from occlusion and downgrowth of subgingival plaque. J. Clin. Periodontol. 6:61-82, 1979.
Yuodelis RA, Mann WV. The prevalence and possible role of non-working contacts in periodontal disease. Periodontics. 3:219-223, 1965.
Shefter, G, McFall, W, Occlusal relationsh and periodontal status in human adults. J Periodontol 1984:55:368-374
Pihlstrom B, Anderson K, Aeppli D, Schaffer E. Association between signs of trauma from occlusion and periodontitis. J. Periodontol. 57:1-6, 1986.
NunnM, Harrel SK. The effect of occlusal discrepancies on treated and untreated periodontitis, part I: relationship of initial occlusal discrepancies to initial clinical parameters. J Periodontol 2001;72(4):485-94.
HarrelS, Nunn M. The effect of occlusal discrepancies on periodontitis, part II: relationship of occlusal treatment to the progression of periodontal disease. J Periodontol 2001;72(4):495-505.

What are the histological findings from trauma from occlusion?

Glickman I, Smulow JB. Alterations in the pathway of gingival inflammation into the underlying tissues induced by excessive occlusal forces. J Periodontol 33:7-13, 1962.
Glickman I, Smulow J. The combined effects of inflammation and trauma from occlusion in periodontitis. Int Dent J 1969;19(3):393-407
Waerhaug J. Pathogenesis of pocket formation in traumatic occlusion. J Periodontol 26:107-118, 1955.
Comar MD, et al. Local irritation and occlusal trauma as co-factors in the periodontal disease process. J. Periodontol. 40:193-200, 1969.
Lindhe J, Svanberg G. Influence of trauma from occlusion on progressive experimental periodontitis in the beagle dog. J. Clin. Periodontol. 1:3-14, 1974.
Ericsson I, Lindhe J. Lack of effect of trauma from occlusion on the recurrence of periodontitis. J. Clin. Periodontol. 4:115-127, 1977.
Nyman S, Lindhe J, Ericsson I. The effect of progressive tooth mobility on destructive periodontitis in the dog. J. Clin. Periodontol. 5:213-225, 1978.
Ericsson I, Lindhe J. Effect of longstanding jiggling on experimental marginal periodontitis in the beagle dog. J. Clin. Periodontol. 1982; 9: 497-503
Ericsson I, Lindhe J. Lack of significance of increased tooth mobility in experimental periodontitis. J. Periodontol. 55:447-452, 1984.
Polson AM, et al. Trauma and progression of marginal periodontitis in squirrel monkeys. III. Adaptation of interproximal alveolar bone to repetitive injury. J Periodontal Res 11:279-289, 1976.
Polson AM, et al. Trauma and progression of marginal periodontitis in squirrel monkeys. IV. Reversibility of bone loss due to trauma alone and trauma superimposed on periodontitis. J. Periodontal Res. 11:290-298, 1976.
Polson AM. Interelationship of inflammation and tooth mobility (trauma) in pathogenesis of periodontal disease. J. Clin. Periodontol. 7:351-360, 1980.
Pihlstrom B, Ramfjord SP. Periodontal effect of non-function in monkeys. J. Periodontol. 42:748-756, 1971.

Reviews

Ramfjord SP, Ash MM Jr. Significance of occlusion in the etiology and treatment of early, moderate and advanced periodontitis. J Periodontol. 52: 511-517, 1981. (review)
Gher ME. Non-surgical pocket therapy: Dental occlusion. Ann Periodontol 1:567-580, 1996. (Occlusion portion only) (review)
SerioFG, Hawley CE. Periodontal trauma and mobility – Diagnosis and treatment planning. Dent Clin NA 43:37-44,1999. (review)
HallmonWW. Occlusal Trauma. Texas Dental J. 118:956-960,2001. (review)

Miller 1950 NO ARTICLE
Classification of mobility
Miller #1 – the first distinguishable sign of movement.
Miller #2 – movement of a tooth up to 1mm from normal position.
Miller #3 – movement of a tooth >1mm in any direction or rotated in socket.
It is important to measure mobility with 2 rigid instruments to obtain a more accurate measurement

Laster, 1975 ARTICLE
P: To evaluate the reliability and reproducibility of the modified Miller Index of teeth mobility.
M+M: Two diagonal quadrants (max right/mand left or max left/mandib right) were selected to measure horizontal tooth mobility on random basis using two methods:Periodontometer(O’Leary and Rudd, modified by Friedman and Cohen) and Miller Index(activate tooth with 2 instruments and moving side to side, 1-first sign of movement more than normal, 2-mobility as much as 1mm in B/L direction, 3- crown move more than 1 m in B/L or depressed into socket) modification that half scores were used. 5 subjects (22-65 yrs old), a total of 50 teeth measured- with each patient having horizontal mobility of 10 teeth measured five times.
R:There was a high positive correlation between the periodontists’ assessment of clinical tooth mobility and the measurements of the periodontometer. 3 periodontists were highly accurate in their ability to rank teeth in order of their mobility as determined by the periodontomenter. They were not as consistent when comparing teeth with the Miller Index across different subjects. The periodontists did not accurately utilize the Miller Index as it was originally described. They consistently scored a 2 mobility on a tooth that moved approximately 0.5mm, not 1.0mm as described by Miller.
BL: The modified Miller Index provides an efficacious system to clinically evaluate horizontal tooth mobility for large population. For individual teeth, it may not off the required degree of sensitivity.

Rosenberg, 1995 ARTICLE
BG:
Damping: to decrease the magnitude of an electrical or mechanical wave
Periotest: an objective, noninvasive clinical diagnostic method. It is a dynamic procedure that measures the resistance of the periodontium to a defined impact load. It was developed to produce a reproducible percussive force to apply defined and reproducible impacts. According to Schulte and Lukas, the Periotest value depends to some extent on tooth mobility, but mainly on the damping characteristics of the periodontium. The real meaning of the measurements and the limitations of the Periotest measuring principle seem to be poorly understood.
P:To determine the relationship between damping characteristics of periodontal tissues and tooth mobility.
M&M:58 maxillary anterior teeth from 11 periodontally healthy patients and 54 maxillary anterior teeth from patients seeking perio tx with some degree of mobility were used.10 teeth exhibited degree I mobility, 27 teeth degree II mobility and 17 teeth with degree III mobility. To assess mobility, a Muhlemann Periodontometer was used to measure the amount of mobility in a labial-palatal direction against forces of .5N, 1.0N, 2.0N, and 5.0N. Damping characteristics were assessed by a Periotest device. Two examiners performed the Periodontometer and Periotest measurements twice on each tooth.
R:The best correlations between tooth deflection and periotest values were found for teeth showing a degree of clinical mobility. Correlation was lower with healthy subjects. The better correlation found for forces > 1.0N indicates damping characteristics found with Periotest are related to secondary tooth movement (distortion of the alveolar plate).
BL:The Periotest method has proved to be objective and highly reproducible for measurement of damping characteristics of healthy teeth. However, it has certain limitations that can give different interpretation of the values.

Neiderud 1992 ARTICLE
Purpose:To induce increased tooth mobility and to study the resistance offered by the periodontal tissue to probing.
Materials and methods: 6 beagle dogs, 9 months old. Throughout the period of observation animals were fed a soft pellet diet. One month prior to the initiation of the experiment the teeth of the animals were scaled polished once a week and exposed to careful toothbrushing 3 times a week. On Day 0 the mandibular molars and premolars were free from plaque accumulation and exhibited minimal gingival inflammation. Mobility was determined using the Periotest.
Grooves were prepared 2mm from the gingival margin and pins were anchored in them in buccal and lingual side of the teeth. An orthodontic elastic was activated and positioned on the buccal side of the test teeth and in 3 days it was removed and placed on the lingual side. The position of the elastic was changed twice a week during a 3-month period.

The dogs were 3 times a week exposed to meticulous toothbrushing. Tooth mobility measurements were performed on Day 0 and Day 90.
At that day, clinical examination assessing plaque and gingivitis was performed and standardized wooden probe (0.50N, groove was prepared) was inserted in the sulcus and block biopsies were taken.
Height and width of free gingival margin, volume fractions occupied by oral epithelium (OE), junctional epithelium (JE) and connective tissue (CT), fibroblasts, collagen, vascular structures and residual tissues were assessed.
Distances from gingival margin to the apical portion of the probe, CEJ to alveolar crest, probe to bone crest and gingival margin to apical end of connective tissue were also assessed.
Results:At Day 90 all teeth surfaces were plaque free and no or minimal signs of inflammation were present. Perio test values were similar on Day 0 for test and control teeth and on Day 90 significantly higher for test teeth (30 vs 5.6). Average height and width of free gingival margin were also comparable.
CEJ-BC distance was significantly larger at test teeth.
Histological PD at test sites was almost twice as great as observed at the controls.
Apical extension of CT was comparable between the two groups, but the height of supracrestal CT located between BC and the probe was significantly greater at the test teeth.
Morphometric measurements showed the free gingival unit had similar composition in both groups (about 40% epithelium and 60% connective tissue).
The supracrestal CT at the test teeth had less collagen and more vascular structures compared to controls.
Conclusion:Tissue alterations (marginal bone loss, less collagen, more vascular elements) which occur at mobile teeth with clinically healthy gingivae and normal height of connective tissue attachment, may reduce the resistance offered by the tissues to clinical probing leading to increased probing depths.

Perrier, 1982 ARTICLE
Purpose:to assess the effect of progressive and increasing tooth hypermobility upon a periodontium reduced by marginal periodontitis, but in which the inflammatory lesion had been resolved.
Materials and methods

4 monkeys, marginal periodontitis was induced with silk ligature. Ten weeks after ligatures were removed and OH instituted
After 10 weeks of OH the interproximal periodontium was subjected to repeated trauma by jiggling the teeth mesio distally
Animals sacrificed at 10 weeks after initiation of jiggling forces.
Control side induction of periodontitis, then 10 weeks of OH
Mobility and inflammation were assessed, histology was performed

Results

The mobility of the teeth increased progressively throughout the period of jiggling and at the conclusion of the study there was mobility in mesio distal, buccal and vertical directions.
The clinical appearance of the gingival tissues had not changed during the period of tooth jiggling.
The coronal PDL in the compressed areas was narrow, there’s vascular obstruction and acellular .In the area under tensional force, and the PDL was widened, highly cellular and had dilated blood vessels.
Alveolar bone of experimental group had islands of osseous tissue surrounded by CT of the marrow spaces & PDL.
A significant reduction in the % of alveolar bone had occurred subsequent to the mesio-distal jiggling forces, but the height was not significantly reduced

BL:Teeth w/ reduced but stable periodontal tissues continually accommodate increasing multidirectional forces by alterations independent of alterations in the connective tissue attachment.

Kerry, 1982 ARTICLE
P:Todetermine the effect of periodontal treatment on tooth mobility.
M&M:Retrospective eval: 93 pts (2421 teeth) w/ moderate to severe p-itis. Mobility was determined at baseline, 1 month after SRP+ occlusal adjustment, 1 month after perio tx, l year after perio tx and 2 years after completion of tx. Perio treatment was either: 1) pocket elimination 2) subgingival curettage 3) MWF 4) SRP. Patients were in 3 month recall.
R– NSSD was found b/w any of the treatment groups at 1 month post-op. At 1 month there was significant increase in proportion of teeth w/ zero mobility. At 2 years a SS decrease in moderate mobility proportions with MWF and SC. Other treatments showed NSSD at 2 yrs.
BL:Mobility decreased after phase 1 therapy (SRP/OHI/ occlusal adjustment). Mobility was NOT significantly altered by phase II treatment (scaling, subg curretage or MWF). Mobility increased 1 month after pocket elimination surgery, but returned to pre-surgical level 1 year later.Teeth with higher initial mobility tended to improve more than teeth with lower initial mobility

Fleszar, 1980 mobility and wound healing
P: To determine whether any relationship exists between tooth mobility and clinically measurable responses to conventional periodontal treatment.
M&M: 82 pts completed at least the 1^st year recall and scoring (total of 1974 teeth), 72 patients 5 years, and 43 pt 8 years. PD, AL, Mobility were measured. SRP, OHI, occlusal adjustment was provided and then one of three treatments: 1) Subg curettage, 2) MWF, 3) pocket elimination Sx. 3 month recalls and divided into groups to mild (1-3mm), moderate (4-6mm) and severe (7-12mm) periodontitis based on initial pocket depth. Mobility was measured as M0 = firm tooth, Ml = slight increase in mobility, M2=definite increase in mobility but no impairment of function, M3= extreme mobility, uncomfortable in function.
R:

Groups with PD 1-3 mm showed CAL with treatment and this is increased with increased mobility. M2-3 ~1mm CAL by the 2^nd year.
Groups with PD 4-6mm showed sites with limited mobility M0-M1 reveals gain in attachment, M2 do not appear to gain attachment, and might show loss, and M3 lose attachment within 2 years.
Groups with PD 7-12mm had more CAL gain, with the most gain in M0 group and ~0.5 mm less in each group and grade of mobility increases. Stability of attachment occurred after the second year in all disease levels.

BL: Increased tooth mobility can detrimentally affect healing. Pockets of clinically mobile teeth do not respond as well to periodontal treatment as firm teeth showing same initial dz severity. The effect stabilizes after 2 years and clinically mobile teeth can be treated and maintained.

Galler 1979, ARTICLE
P:Determine if splinting the teeth after osseous surgery has positive effects regarding tooth mobility, bone level, attachment level over unsplinted teeth.
MM:Following phase I therapy, osseous surgery was performed to 10 healthy patients, with bilateral bone loss and at least 2 maxillary teeth with mobility. One segment was splinted and the other unsplinted. Tooth mobility was measured one week before and then at 3,6,12 and 24 weeks after surgery by the periodontomer with a 500g force. Sulcus bleeding and gingival attachmentwere measured with a pressure-sensitive modified Michigan “0” probe calibrated to 5g force before surgery and at 24 weeks. Bleeding was measured 5 seconds after insertion of the probe. Bone index were recorded with the Michigan “0” probe with the flap open pre and post osseous and bone sounding at 24 weeks. Before measurement splints were removed. Prophylaxis and OHI were given every 3 weeks. Occlusion was adjusted as needed.
R:Splinting didn’t show positive effects over unsplinted teeth in any of the above parameters. Tooth mobility increased 3 weeks after surgery and then gradually decreased (as showed in other studies). An average of 0.6mm of bone was removed post-osseous, NSD was found of this with tooth mobility post surgery.
BL: Fixed splinting the teeth after osseous surgery have no positive effect on tooth mobility, bone level, attachment level, nor bleeding. Its use for this purpose is unjustified. Increase mobility is expected after surgery with a gradual decrease to pre- surgical values after 24 weeks.

Lemmerman, 1976 ARTICLE
P:To review rationales for stabilization and to discuss its use in periodontics with supporting evidence.
Rationales for Stabilization: Reasons for splinting in normal periodontium are to prevent mobility from acute trauma or occlusal therapy for the treatment of bruxism. Another reason to splint in normal Periodontium is to prevent drifting of the dentition. Reasons for splinting in a diseased periodontium would be to promote patient function and allow for tissue repair during periodontal treatment. Splinting would also be used for the prevention of drifting dentition as seen in the normal periodontium.
Discussion:A review of the literature on stabilization reveals that much of the confusion that comes from whether to splint or not in periodontal treatment arises from differences in semantics. Authors generally use the same terminology but their meanings vary. There are many reasons that contribute to tooth mobility but there is no agreement in the literature over what is “physiologic mobility.” As a result it is difficult to determine which teeth should be stabilized. Not all visible tooth mobility should be considered abnormal and there for not all mobile teeth require splinting. Mobility must be evaluated after taking into consideration health of the periodontium, occlusion, functional considerations, as well as other clinical factors.
Another area of confusion is correlating occlusion, trauma from occlusion, and periodontitis. The literature generally agrees that trauma from occlusion does not cause periodontitis but literature on the effect of trauma of occlusion on existing periodontitis is still unclear. If trauma from occlusion and periodontitis are believed to be related then splinting would be important. If these two factors are determined to be unrelated then splinting becomes less important in the treatment of periodontitis. Lindhe published an animal study where he found that after 6 months, teeth with periodontitis that were subjected to trauma from occlusion had more apical epithelial proliferation and angular bone loss than the control. This would suggest that trauma from occlusion and periodontitis have a correlation.
Lemmerman suggests that because mobility, in the absence of local factors, does not lead to periodontitis, the terms “pathologic mobility” and secondary trauma from occlusion should not be used interchangeably. Lemmerman prefers the terms reversible and irreversible mobility, the latter being an indication for splinting.
Splinting should be considered especially to promote “functional stability” rather than preventing progression of periodontitis. Lemmerman points out that just because a tooth is splinted does not mean that it is free from trauma from occlusion. Furthermore a study by Glickman, Stein, and Smulow showed excessive forces on a splinted tooth caused comparable damage to the all teeth that are splinted.
There are several objections to splinting. Chayes believed that ridged splinting would result in reduced circulation to the periapical areas of splinted teeth but this was refuted by Amsterdam. Others believe that splinting results in a higher potential for gingival inflammation and poor oral hygiene. A third objection is that splinting practices are abused and should be avoided whenever possible. Lastly, there is a lack of research on the clinical efficacy of splinting.
Conclusion:Diseased Periodontium and normal Periodontium should be treated equally in regards to splinting except for in the case of secondary trauma from occlusion. Valid reasons for splinting are to prevent mobility, prevent drifting, and to treat secondary trauma from occlusion. Temporary splinting in periodontal treatment should be avoided because mobility in itself does not impair healing, except in cases of secondary trauma from occlusion. More research should be done to determine the relationship between trauma and periodontitis and the efficacy of splinting.

Lindhe, Ericsson, 1976 ARTICLE
P:To study influence of occlusal trauma (OT) on periodontal breakdown once inflammation has been removed.
M&M:Experimental periodontitis was induced on 5 beagle dogs. During a pre-experimental period the teeth were scaled and polished. At Day 0 none of the dogs presented gingivitis. Throughout the study the dogs were fed a diet which allows gross plaque formation. On days 0, 180, 280 and 370, gingival inflammation, plaque (Loe and Silness), tooth mobility and bone levels using standardized radiographs were assessed.

Day 0: Inflammation was induced, narrow infrabony pockets, 1mm deep were prepared on mesial and distal aspects of lower premolars. A copper band was cemented in order to prevent reattachment of periodontal tissues. The copper bands were removed 21 days later and cotton ligatures were placed.
Day 180: Trauma from occlusion (TFO) was produced with cap splints on both sides of maxilla and bar devices.
Day 280: MWF was performed and traumatic occlusion eliminated on one side(control teeth). A notch was made to the bottom of the clinical infrabony pocket. Good OH was maintained until sacrifice at day 370. Histological examination was then done.

R: At the start of the study the gingiva around test and control teeth were normal and no plaque could be detected. At days 180 and 280 the gingiva exhibited signs of severe chronic inflammation. Following scaling, pocket elimination and daily tooth cleanings the clinical signs of gingivitis almost disappeared.Mobilityincreased during the experimental periodontitis period and had a more pronounced increase after induction of occlusal trauma (OT). Removal of OT at day 280 resulted in a decrease in mobility in the control teeth.In the test teeth, however, there was a further increase in mobility towards the end of the study. Bone:Apical movement of alveolar bone during induced periodontitis with widening of the PDL as result of jiggling forces. Reestablishment of narrow PDL and marginal bone in the control side occurred after removal of OT and inflammation. Radiographs from test teeth at the end of the study showed an even and rather distinct outline of marginal bone, PDL still appeared markedly widened. Histology: PDL on pressure side of test teeth showed a greater number of vascular units when OT was present. In the control side, the crest was located at the level of the apical border of the notch, while on the test side the crest was apical to the notch. No signs of inflammatory cells in the supraalveolar CT or in the PDL of both, experimental and control.
BL:Jiggling type OT and hypermobility alone were not factors that affected periodontal healing. Provided plaque and inflamed periodontal tissues were removed and a proper OH regimen was established, healing also occurred in cases where jiggling forced were acting on hypemobile teeth. Microbial plaque is the main causative factor in the progressive lesion where TFO may act as co-destructive component.

Glickman, 1966 ARTICLE
P:To determine if post-surgical healing is affected by altered occlusal forces.
M+M:9 dogs were divided into 3 groups. Group I: unaltered occlusion (2 animals), Group II: hyperfunction (3 animals), Group III: hypofunction (3 animals). One animal served as unoperated control. Hyperfunctionwas created using a cast gold overcontoured splint cemented on the mandibular anterior teeth to increase the vertical dimension and create excessive apico-labial forces. Hypofunctionwas created by extraction of the mandibular incisors. Mucogingival surgery was performed in the maxillary anterior region at the time the occlusion was altered. The maxillary anterior region was divided into two areas. On the right side resected gingival flap was performed (periosteum intact) and on left side on labial surface, a mucoperiosteal flap was reflected and then replaced and sutured at the level of the bone. The palatal marginal gingiva was removed with gingivectomy on both sides. Dogs were sacrificed at 3 months and histological analysis was done.
R: Group I: The gingiva was healed with the sulcus restored at the level of CEJ. There was a slight reduction in the height of labial bone and the periodontal ligament was intact with dense fiber bundles perpendicular to the bone and to the tooth.
Group II: The healing was the same except widened PDL, longer gingival attachment, thinned coronal labial plate and thickened in the apical half.
Group III: The fibers of PDL were reduced in number and in some areas were disoriented and parallel to the tooth.The gingival portion of the labial plate was thinned and tapered while the apical half was thickened.
Thealtered occlusion did not cause reduction in bone height beyond that produced by surgical procedures. In all operated animals the reduction in labial bone height was greater with the repositioned flap.
BL:Extreme and abrupt alterations in occlusion can affect healingof surgical wounds.

Polson, 1983 ARTICLE
P:To evaluate the periodontal response after resolution of inflammation in continued presence of active, continued tooth hypermobility.
M+M:Periodontitis induced unilaterally around mandibular 2^ndand 3^rdpremolars by tying silk ligatures at ginigival margins in 4 squirrel monkeys. Mesial-distal jiggling forces between premolars begun at 5 weeks and continued for 20 weeks. Ligatures removed 10 weeks after initiating jiggling, and regular OH regimen begun (3x/wk). Jiggling forces continued during OH.
Animals sacrificed 10 wks after OH begun.
Controls- on contralateral side of each mandible. Periodontitis and trauma produced but timed so that the 10 weeks of jiggling forces/ligatures would correspond to 10 weeks of good hygiene on experimental side.
Marginal inflammation and tooth mobility assessed. Mandibles evaluated histologically.
R:Clinical: Prior to experiment there was no gingival inflammation and no clinical mobility. 5 weeks after periodontitis induced, premolars had gingival inflammation and increased mobility. During first 10 weeks of jiggling, inflamed gingival tissues did not change, but mobility increased. After ligatures removed,OH of 10 weeks led to resolution of gingival inflammation and decrease of tooth mobility although the teeth were still subjected to active jiggling forces. At conclusion of study, mobility still present slightly, but was much improved from mobility associated with induced periodontitis.
Histological: In the presence of jiggling forces but 10wks after OH was initiated (experimental group), accumulation of inflammatory cells adjacent to epithelium was 19.2% of supracrestal CT fibers. In control group, jiggling forces with periodontitis, 57.6% accumulation inflammatory cells of supracrestal fibers. No difference in levels of connective tissue attachment or alveolar bone between both sides. Significant bone repair occurred in experimental group once periodontitis resolved even though jiggling force remained.
D:If residual tooth hypermobility, which remains after resolution of marginal inflammation associated with periodontitis, is without effect upon CT attachment levels it indicates that there is no scientific basis for considering that this mobility should be reduced in order to preserve periodontal health. Since there was no coronal gain in bone or CT levels after resolution of inflammation, the decrease in mobility was most likely due to the increase in bone density.
BL:Osseous repair can occur in the presence of active, continued hypermobility if resolution of inflammation is achieved. Continued tooth hypermobility after resolving inflammation did not lead to further loss of CT attachment. Mobility will decrease if inflammation is resolved, regardless of continued forces. Some mobility will remain, compared to no mobility prior to experiment.

Schulz 2000 ARTICLE
Purpose:To evaluate the effect of splinting on the result of periodontal reconstructive surgery using a specific bone replacement graft (BRG) material (natural coralline calcium carbonate).
Materials and methods:45 patients underwent periodontal surgery that included surgical debridement of osseous defects and if required placement of an alloplastic BRG. They were randomly assigned to one of 4 treatments: BRG and presplint teeth (18 teeth), BRG with postsplint (16 teeth, one week post-op), BRG with nonsplint (17 teeth) and debridement alone with non-splint (19 teeth). Clindamycin was administered for 6 days post-op. Splints were not removed until 8 months after surgery, and periodontal condition (PD, AL, mobility) of all teeth was recorded during a period of 0-48 weeks. Measurements were standardized and mobility was evaluated by desmodontometry and the use of periotest. Statistical analysis was performed.
Results:Significant decrease between the 4 Tx groups after 48 weeks comparing to baseline was observed for PD, AL and mobility.
PD: reduction was significantly greater in splinted teeth comparing to non-splint. Debridement alone lead to a decrease similar to presplint and postsplint.

AL: The maximum increase was seen in presplint (5.1mm) and postsplint (3.5mm) teeth. In nonsplint teeth it was significantly smaller (1.7mm), as well as in the debridement alone group (0.6mm).
Mobility: Decrease in periotest values of presplint teeth was significantly greated to all other groups. Quasistatic mobility showed significant decrease in postsplint and presplint groups comparing to the other two.
Conclusion:1. Presurgical splinting appears to have the greatest positive impact on the results of reconstructive periodontal surgery.
2. BRG + splinting resulted in greater clinical improvement comparing to nonsplinting and debridement alone in teeth with deep infrabony pockets.
3. In nonsplinted teeth the use of BRG showed nearly the same results as surgical debridement alone.

Harrel 2003 ARTICLE
Purpose: Review on occlusal forces as a risk factor for periodontal disease
Discussion
Historical Perspective: Several authors indicated that occlusal forces played a significant role in the initiation and progression of periodontal destruction. At the end of the 1930’s it was still felt that excessive occlusal forces were a major cause of periodontal disease and occlusal adjustment should be a part of periodontal treatment. In the 50’s and 60s studies in animals could not support the concept that excessive occlusal forces were a primary causative agent of periodontal destruction. During this period Glickman and Coworkers performed a series of studies in human autopsy material.Glickman’s theory of Co-Destruction continued to hold to the thesis that occlusion was, in concert with bacterial plaque, a causative factor in periodontal attachment loss and bony destruction. Glickman’s concept believes that occlusion directly changed the disease process and was thereby, in the presence of bacterial plaque, a causative agent for periodontal destruction.
Animal studies: Mainly on squirrel monkeys (Polsol) and beagle dogs (Lindhe), in these animal models, occlusion had an effect on the periodontium in the form of bone rarefaction (loss of density), which resulted in the clinical manifestation of mobility. However, these studies also found that bacterial plaque must be present to cause a loss of attachment. The author warns that it is unlikely that these animal studies give us significant information about the pathophysiology that may occur when excessive occlusal forces are present in humans who may be genetically prone to periodontal destruction and who may also have additional risk factors for periodontal disease beyond occlusal forces and bacterial plaque.
Human studies:While there are many apparently contradictory findings from human studies, there appears to be a trend toward evidence that excessive occlusal forces may play a role in periodontal destruction and the response of the periodontium to periodontal treatment. However, the 1999 International Workshop for Classification of Diseases and Conditions indicated that there was no clear evidence that occlusal forces were a factor in plaque-induced gingival disease or connective tissue loss. Since the 1999 Workshop, studies have shown that occlusal interferences have a negative effect on the periodontium and tend to cause more rapid pocket formation and poorer prognosis when compared to teeth that do not have occlusal interference. There is also recent evidence that treatment of the occlusion to minimize interferences in addition to other forms of periodontal treatment, may positively affect periodontal destruction.

Waerhaug, 1979 ARTICLE
P:To re-evaluate the scientific basis for the hypothesis that angular bone defects and infrabony pockets are the result of occlusal trauma (OT) in combination with gingival inflammation.
M & M: Histologic study of 64 sets of teeth from victims of violent death in 1944-5. Bite analysis was carried out before the jaws were fixed. Impressions & X-rays were taken.
R:Before any attachment loss, the level of the interproximal septum is determined by the location of CEJ of neighboring teeth (confirms Ritchey & Orban 1953). It is also determined by the level of subgingival plaque (The height of bone is established no closer than 1 mm to the CEJ).

The distance from the apical border of the plaque to the nearest PDL fibers ranged from 0.2-1.8 mm (average 0.96 mm). Distance from Alveolar Crest to subgingival plaque (zone of destruction) ranged from 0.5-2.7 mm (average 1.63 mm).
Angular bony defects occurred equally often adjacent to non-traumatized as adjacent to traumatized teeth. No correlation between angular defects and OT. Inflammation (and infrabony pockets) are associated with downgrowth of plaque.

BL: Bacterial plaque in conjunction with variation in local anatomy is the primary cause of intrabony defect formation and not trauma from occlusion. No evidence that traumatic forces are co-factors in causing angular defects.

Yuodelis, Mann, 1965 No ARTICLE
P:To determine the prevalence of nonworking contacts in patients with periodontal disease and the possible effects of non-working contactson the periodontium.
M&M:Retrospective study. Information regarding mobility, PD, septal bone loss, and the presence or absence of non-working contacts were taken from the charts of 54 patients under treatment for periodontal disease at the University of Washington. 413 molar teeth were studied. Bone loss was measured with ruler on non-standardized radiographs. Nonworking contacts determined in lateral excursions, study models used for evidence of faceting
R:53% of molars had nonworking contacts noted by either wear facets on study models or notes in charting. SSD in mobility, bone loss, and PD in groups with nonworking interferences. NSSD between mesial and septal bone loss for maxillary and mandibular groups. Mobility, bone loss, and PD were significantly higher in teeth with nonworking contacts. Nonworking contacts showed no significant effect on patterns of bone loss around molar teeth.
BL: Bone loss, mobility, & PDs all significantly increased in the group with nonworking contacts.
Critique:

Retrospective study of charts, models and non standardized radiographs
Mean increase of PD around teeth with facets was 0.4 mm
All patients had periodontal disease, no healthy controls

Shefter, McFall 1984 ARTICLE
P: To obtain data on both occlusion and periodontal status in a group of human adults in order to evaluate the relationship.
M+M: 66 subjects (33 M, 33F, 15-62 yrs old) in good health. Pts had to have 28 teeth and no hx of occlusal adjustment by selective grinding. Presence or absence of periodontal disease not a criterion. Recorded plaque score, mobility, PDs (grouped into 3 Ramfjord categories) and examined occlusion (classification of malocclusion, analysis of centric displacement, excursive movements, tooth contacts, and wear facets). Radiographs taken.
R: Angle’s classification:Class I> Class II> Class III= end to end

Functional analysis:Group function>Canine function

Nonfunctional contacts:Mostly in max and mand 2^ndmolars

PDs and Type of contacts: NSSD b/w PDs and nonworking contacts

Mobility, wear and radiographic features: NSSD in mobility found b/w teeth with wear facets and nonfaceted teeth. Teeth w/ wear facets did not show radiographic signs of occlusal trauma.

BL: NSSD b/w PDs and nonworking contacts. Mobility was not significantly influenced by nonfunctional contacts. NSSD in mobility found b/w teeth with wear facets and nonfaceted teeth. Only 4% of teeth with wear facets and nonfaceted teeth demonstrated radiographic signs of occlusal trauma. Suggest a minimal role for occlusal factors in the progression of periodontal disease.
CR: Why group the PDs into the 3 Ramfjord categories of 1-3mm, 4-6mm, and >7mm? A 4 mm PD and a 6 mm PD are significantly different.

Pihlstrom, 1986 ARTICLE
P:To evaluate the association of possible signs of trauma from occlusion (TFO), with both severity of periodontitis & radiographic record of bone support.
M&M:Maxillary first molars of 300 individuals (2040 years old) independently evaluated for PD, CAL, rec, mobility (both bidigital and functional), plaque, calculus, wear facets, uneven marginal ridges, pattern of occlusal contacts (centric, working, nonworking, protrusive) by 2 examiners. Radiographic findings recorded by third examiner without knowledge of clinical exam: widened PDL, root resorption, hypercementosis, root fracture, thickened lamina dura, presence of calculus on mesial surface. Bone loss was evaluated using bjorn technique on mesial aspect only.
Teeth categorized as not having signs of trauma from occlusion required agreement by both clinical examiners and judgement by the radiographic examiner that a normal PDL space was present. All three independent examiners (2 clinical and 1 rx) also had to be in agreement to classify the teeth as displaying signs of trauma from occlusion. These restrictions limited the number of teeth of the total sample to only 14 having signs of occlusal trauma. A total of 319 teeth were classified as not having signs of occlusal trauma.
R:Max 1^stmolars: 22% had thickened lamina dura, 19% widened PDL and 19% had radiographically visible calculus. Teeth with wear facets or a thickened lamina dura had less CALoss and more osseous support that teeth without these findings.
BL: from information concerning max 1^stmolars in pts 20-40 yrs old:
1. Teeth with bi-digital mobility, functional mobility, a widened PDL space or the presence of radiographically visible calculus had deeper PD, more CALoss and less % radiographic osseous supportthan teeth without these findings.
2. Teeth with occlusal contacts in CR, working, nonworking or protrusivepositions did notexhibit any greater severity of periodontitis than teeth without these contacts.
3. Teeth with both functional mobility and radiographic widened PDL space had deeper PD, more clinical ALoss and less radiographic evidence of osseous supportthan teeth without these findings.
4. Given equal clinical attachment levels, teeth with evidence of functional mobility and a widened PDL space had lessosseous support than teeth without these findings.
Cr:319 healthy tth vs 14 tth with occlusal trauma

Nunn 2001 ARTICLE
Purpose:To investigate the relationship of occlusal trauma to the severity of periodontal disease as reflected in clinical parameters and possible effects of occlusal treatment on the progression of periodontal disease.
Materials and methods: Retrospective epidemiological study, data were obtained from the clinical records from 24 years of practice. A complete perio exam was performed initially and patients had another complete exam at least 12 months after the initial. Examinations and data collection were performed by the same examiner. Occlusal analysis included notation of initial contact, discrepancies between initial contact and centric relation, centric occlusion and working and balancing contacts in lateral and protrusive movements.
Two groups were created, an untreated group that had none of recommended periodontal treatment performed between the 2 examinations and a partially treated group that had completed the non-surgical portions of the surgery but not the surgical. Control group included 41 patients that had completed all the recommended periodontal treatment at least 12 months prior to final examination. All data were recorded and a database was created and designed so that the data could be evaluated for the effect of presenting factors, non-treatment, partial treatment and complete treatment on the progression and/or resolution of periodontal disease.
Results:Data from 89 patients were collected. 41 pts completed all treatment recommended (control group), 18 pts in the partially treated group and 30 refused any treatment. 17/41 pts in the control group and 9/18 in the partially treated group received occlusal adjustment. 30 patients had occlusal discrepancies but were not treated for these (5 in partially treated and 25 in the untreated group).
It was found the patients with occlusal discrepancies were statistically significantly younger than patients without occlusal discrepancies.
Teeth with occlusal discrepancies were found to have significantly deeper initial PDs, worse initial prognoses and greater mobility than teeth without initial occlusal discrepancies. No significant differences in initial bifurcation involvement.
On average teeth with an initial occlusal discrepancy will have approximately 1mm greater PD when compared to teeth without an initial occlusal discrepancy even when adjusted for significant confounders, such as smoking, gender, and oral hygiene status.
Initial occlusal discrepancies were found to be the only significant predictor of initial PD.
Parafunctional habits were not found to be associated with initial PD, mobility, furc involvement or prognosis.

Harrel, 2001 ARTICLE
Purpose:to evaluate the effect of occlusal adjustment on the progression of treated and untreated periodontal disease.
Materials and Methods

Data from private practice, patients had complete periodontal examination, occlusal analysis. All patients had non surgical and surgical periodontal treatment, and a second examination 12 months after.
3 groups, 89 patients total. Control (41pts, all treatments done), Untreated (30 pts, No treatment between exams) and Partially treated (18 pts, Non surgical only)

Results

Of the 59 treated fully or partially, 26 received some for of occlusal adjustment.
Teeth w/ no occlusal discrepancies or those with treated discrepancies were 60% less likely to have a downgrade in prognosis as those w/ no occlusal treatment.
Teeth with no occlusal treatment were shown to have a significantly greater increase in PD per year than either teeth w/o initial discrepancies or teeth w/ treatment.
Teeth without initial discrepancies and treated had no significant increase in probing depth per year
Teeth with no initial discrepancies were significantly less likely to worsen in mobility compared to treated or untreated occlusal discrepancies.
NSSD when worsening of furcations among any of the occlusal treatment group.

BL: this study provides evidence of an association between untreated occlusal discrepancies and the progression of periodontal disease. Occlusal treatment significantly reduces the progression of periodontal disease over time.

What are the histological findings from trauma from occlusion?

Glickman 1962 NO ARTICLE altered pathway of inflammation
P:To determine the effects of excessive functional forces upon the pathway of inflammation from the gingiva into the underlying periodontal fibers
M+M:6 monkeys with excessive occlusal forces that were created by placing gold crowns in abnormal functional relationships over a 10-132 days experimental period. The jaws were sectioned. Teeth not involved in experimental procedure were used as controls.
R:Controls: Interproximal inflammation followed blood vessels directly to the interdental alveolar septum. Labially and lingually gingival inflammation extended over the crest of bone and along the lateral surface adjacent to the periosteum.
Experimental teeth with occlusal forces:
On the pressure side had the most prominent changes, periodontal fibers parallel to root and bone, osteoclastic resorption, and widening of PDL space, inflammation directly into the PDL rather than interdental septum.
In areas of severe pressure:bone necrosis at crest, resorption, and inflammation on normal course to the septum.
In long term (3-4 months)- changes underwent repair and periodontum was restored unless long term excessive pressure resulting in angular resorption of crest of alveolar bone and widening of PDL space.
On the tension side- less significant changes than pressure side, elongation of periodontal fibers, and apposition of alveolar bone.
BL:Excessive occlusal forces alter pathway of gingival inflammation into underlying periodontal tissues and cause bone loss. Excessivepressuremore significant than excessive tension, producing a widened PDL and angular resorption of the bony crest on the pressure side. The PDL fibers were most changed crestally and on the pressure side were organized parallel to root surface permitting spread of inflammation. Injury by artificial alterations in occlusion is reversible, but injury induced by attrition tends to persist.

Glickman 1969 ARTICLE
Summary:This article discusses trauma from occlusion as a co-destructive factor in periodontitis.
The pathway of inflammation from the gingiva to supporting periodontal structures is a critical factor in periodontal disease because it affects the pattern of bone destruction. Ordinarily, when inflammation spreads from the gingival to the supporting periodontal structures, the fluid and cellular exudate passively follow the least resistant pathway. Findings in animal experiments indicated that excessive occlusal pressure altered the alignment of the transseptal and alveolar crest fibers as well as the deeper fibers of the periodontal ligament. The excessive occlusal forces also changed the pathway of spreading inflammation so that it extended directly into the PDL leading to angular bony resorption of the alveolar bone and infrabony pocket formation. Furcation areas were the most susceptible to trauma from occlusion.

Trauma from occlusion occurs in 3 stages: injuryto the periodontium,repairof the injured morphology of the periodontium to adaptto the occlusal forces (widening of PDL which is most pronounced in coronal half accompanied by angular resorption of the bone).

Zone of irritation: consists of marginal gingiva and papillae and is bounded by gingival fibers. Local irritants stimulate inflammation in this zone. Its most severe effects include degeneration and necrosis of gingival CT, epithelial ulceration and suppuration. Trauma from occlusion does not affect the gingival margin or interdental papillae. Therefore, inflammation confined to this zone (gingivitis) is unaffected by occlusal forces.
Zone of co-destruction: consists of PDL, alveolar bone and cementum. The zone begins with transseptal fibers interproximally and with the alveolar crest fibers, labially and lingually. Occlusal forces constantly regulate the condition and morphology of the PDL and bone. Here inflammation and trauma form occlusion become co-destructive factors in perio dz. When

inflammation reaches this zone, its further spread and resultant destruction come under the influence of occlusal forces.

-Infrabony pockets and angular osseous defects are not necessarily pathognomonic of trauma from occlusion. There may be trauma from occlusion and no angular bony defects. However, we must always consider trauma from occlusion when angular bony defects are present.
-Trauma from occlusion does not affect the inflammation only so long as it remains confined to the gingiva (gingivitis).
-Trauma form occlusion per se does not cause any type of periodontal pocket. Local irritation is required to initiate the inflammatory changes leading to pocket formation.
-Trauma from occlusion may also produce angular bone defects without perio pockets in the absence of local irritants severe enough to cause pockets.
-Trauma from occlusion is a co-destructive factor in periodontitis rather than a separate disease entity. When combined with inflammation it may create angular or crater-like defects.
-Trauma from occlusion and inflammation are different pathological processes that cause tissue destruction in periodontal disease, they are not different diseases

Waerhaug, 1955 No ARTICLE
P:To assess to what extent longstanding repeated occlusal overload would lead to a deepening of a pocket.
M+M:Occlusal trauma (OT) was induced in 7 dogs with high crowns on the LR 1^stmolars (c

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