91. Occlusal Trauma Part I                                     

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 Rapid Search Terms
occlusal trauma defined, signs and symptoms splinting teeth
theories of occlusion and its relationship to the periodontium mobility and wound healing
the effect of non-working contacts altered pathway of inflammation
Primary occlusal trauma Secondary occlusal trauma

 

 

 

 

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?

  1. Miller, S.C. Textbook of Periodontia, Blakiston Co., 1950, p. 125.
  2. Laster L. An evaluation of clinical tooth mobility measurements. J Periodontol 46:603-607, 1975.
  3. Rosenberg D, Quirynen M, et al. A method for assessing the damping characteristics of periodontal tissues: Goals and limitations. Quintessence Int 26:191-197,1995.
  4. Neiderud AM, Ericsson I, Lindhe J. Probing pocket depth at mobile/nonmobile teeth. J Clin Periodontol 1992; 19:754-759.
  5. Perrier M, Polson A. The effect of progressive and increasing tooth hypermobility on reduced but healthy periodontal supporting tissues. J. Periodontol. 53:152-157, 1982.
  6. Kerry GJ, et al. Effect of periodontal treatment on tooth mobility. J. Periodontol. 53:635-638, 1982.
  7. Fleszar TJ, Knowles JW, et al. Tooth mobility and periodontal therapy. J Clin Periodontol. 7:495-505, 1980.
  8. Galler C, 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.
  9. Lemmerman, K. Rationale for stabilization: J Periodontol 1976;47:405-11
  10. Lindhe J, Ericsson I. Influence of trauma from occlusion on reduced but healthy periodontal tissues in dogs. J. Clin. Periodontol. 3:110-122, 1976.
  11. Glickman I, et al. The effect of occlusal forces on healing following mucogingival surgery. J. Periodontol. 37:319-325, 1966.
  12. Polson AM, et al. Osseous repair in the presence of active tooth hypermobility. J Clin Periodontol. 10:370-379, 1983.
  13. 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.
  14. 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?
  1. 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.
  2. Yuodelis RA, Mann WV. The prevalence and possible role of non-working contacts in periodontal disease. Periodontics. 3:219-223, 1965.
  3. Shefter, G, McFall, W, Occlusal relationsh and periodontal status in human adults. J Periodontol 1984:55:368-374
  4. Pihlstrom B, Anderson K, Aeppli D, Schaffer E. Association between signs of trauma from occlusion and periodontitis. J. Periodontol. 57:1-6, 1986.
  5. Nunn M, 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.
  6. Harrel S, 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?
  1. 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.
  2. Glickman I, Smulow J. The combined effects of inflammation and trauma from occlusion in periodontitis. Int Dent J 1969;19(3):393-407
  3. Waerhaug J. Pathogenesis of pocket formation in traumatic occlusion. J Periodontol 26:107-118, 1955.
  4. Comar MD, et al. Local irritation and occlusal trauma as co-factors in the periodontal disease process. J. Periodontol. 40:193-200, 1969.
  5. Lindhe J, Svanberg G. Influence of trauma from occlusion on progressive experimental periodontitis in the beagle dog. J. Clin. Periodontol. 1:3-14, 1974.
  6. Ericsson I, Lindhe J. Lack of effect of trauma from occlusion on the recurrence of periodontitis. J. Clin. Periodontol. 4:115-127, 1977.
  7. 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.
  8. Ericsson I, Lindhe J. Effect of longstanding jiggling on experimental marginal periodontitis in the beagle dog. J. Clin. Periodontol. 1982; 9: 497-503
  9. Ericsson I, Lindhe J. Lack of significance of increased tooth mobility in experimental periodontitis. J. Periodontol. 55:447-452, 1984.
  10. 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.
  11. 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.
  12. Polson AM. Interelationship of inflammation and tooth mobility (trauma) in pathogenesis of periodontal disease. J. Clin. Periodontol. 7:351-360, 1980.
  13. Pihlstrom B, Ramfjord SP. Periodontal effect of non-function in monkeys. J. Periodontol. 42:748-756, 1971.

Reviews
  1. 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)
  2. Gher ME. Non-surgical pocket therapy: Dental occlusion. Ann Periodontol 1:567-580, 1996. (Occlusion portion only) (review)
  3. Serio FG, Hawley CE. Periodontal trauma and mobility - Diagnosis and treatment planning. Dent Clin NA 43:37-44,1999. (review)
  4. Hallmon WW. Occlusal Trauma. Texas Dental J. 118:956-960,2001. (review)

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 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 Results 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: To determine 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 1st 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:
 

 
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 attachment were 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. 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. Mobility increased 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. Hyperfunction was created using a cast gold overcontoured splint cemented on the mandibular anterior teeth to increase the vertical dimension and create excessive apico-labial forces. Hypofunction was 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.
The altered 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 healing of 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 2nd and 3rd premolars 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.


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, 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). 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 contacts on 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:
  1. Retrospective study of charts, models and non standardized radiographs
  2. Mean increase of PD around teeth with facets was 0.4 mm
  3. 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 2nd molars


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 1st molars: 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 1st molars 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 support than teeth without these findings.
2. Teeth with occlusal contacts in CR, working, nonworking or protrusive positions did not exhibit 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 support than teeth without these findings.
4. Given equal clinical attachment levels, teeth with evidence of functional mobility and a widened PDL space had less osseous 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 Results 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.  Excessive pressure more 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: injury to the periodontium, repair of the injured morphology of the periodontium to adapt to 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 1st molars (combination of horizontal & vertical overload). The bite was raised about 7 mm. Crowns were left in place in 3 dogs for the entire experiment (Short Term Animals, STA); In 4 dogs, (Long Term Animals, LTA) crowns were left in place until the antagonists intruded so that normal occlusion was re-established on the other teeth. Crowns were then removed and the teeth were allowed to extrude to normal contact. The crowns were placed on again, removed, and the animals were sacrificed. Direction of forces: mandible- apical/buccal, maxilla- apical/lingual. Left side teeth served as the controls.
R: Teeth became mobile with crowns in position.
Short term
Necrosis of PDL in marginal 3rd of PDL on pressure (buccal) side and PDL wide on tension (lingual) side and narrow on buccal
Reversed in apical area- wide PDL on buccal and narrow on lingual
Lingual side the alveolar crest reached the CEJ. On the buccal side the crest is 0.2 mm below CEJ.
Long term
Distance from CEJ to the alveolar crest is same as on control teeth.
Resorption of cementum on the pressure side is somewhere on the marginal 3rd in all teeth. The distance from the alveolar crest to the epithelial cuff had NSSD in experimental and control groups.
BL: Deepening of pocket below CEJ can be produced by occlusal stress (under extremely unfavorable conditions). Downgrowth of JE will not take place as long as PDL is necrotic with intact fibers coronally. Damage to cementum, PDL and alveolar bone will be repaired when tooth readjusts itself. Sterile necrosis of PDL causes little to no inflammation of the gingival margin. Supporting structures seem to be well suited to prevent permanent damage


Comar, 1969             ARTICLE
Purpose: To investigate the combination effects of local irritant and occlusal trauma on a compromised periodontium in monkeys.
M&M: 4 monkeys had high gold crowns w/overhangs & open contacts placed in monkeys that already had active gingivitis. The crowns were placed so that they would produce jiggling forces on the mand 2nd PMs and encourage food impaction. X-rays & photos taken at 1,2,6,7,11,12,13 weeks, clinical evaluation done weekly and animals sacrificed at 5, 14, 21, & 98 days for histology.
R: Mobility increased up to 21 days & remained stable. Destruction & repair evident at all time periods. Histology shows compression of PDL fibers & osseous resorption, as well as widened PDL on tension side evident early as 5 days. Inflammation on pressure side along the blood vessels. By 21 days, mobility equal in all directions and 2mm pseudopocket surrounding tooth. Evidence of both osteoblastic and osteoclastic activity histologically. By 98 days, gingival proliferation under overhanging margins, no change in mobility. Histo: fibers rearranged but still intact. Opposing tooth has repaired PDL state and increased mobility and was significantly depressed by the excessive occlusal trauma. Furcation area had previous destruction that had showed repair with little or no inflammation. The teeth depressed until functional plane of occlusion was reestablished. The effect of the high crown on the opposing tooth was as great or greater than that of the crowned tooth.
BL: No altered path of inflammation appears to follow blood vessels. No apical migration of epithelium attachment. No infrabony defects. Transeptal fibers are most stable, whereas interdental fibers seem to have a protective function. Pressure on the PDL results in alveolar bone resorption. The most destruction occurred w/in the 1st 14 days. Repair by 98 days, with opposing dentition showing increased mobility, but histo analysis shows a repaired, not traumatic state.


Lindhe 1974             ARTICLE
Purpose: To assess the effect trauma from occlusion and permanent tooth hypermobility would have on the progress rate of experimental periodontitis in beagle dogs.
Materials and methods: Six dogs were fed with diet favoring plaque accumulation on the premolars and molars and showed clinical signs of gingivitis on these teeth. Infrabony defects were created with a diamond bur and a reference notch was made on the root surface and periodontitis was induced with the used of a copper band for three weeks.
Two of the dogs were sacrificed four weeks later and histologic examination was performed.
In four of the dogs trauma from occlusion was produced by installation of cap splints that were producing excessive horizontal forces during chewing (jiggling forces), for 49 days. Contralateral teeth served as controls and dogs were sacrificed 6 months later.
Tooth mobility, gingival inflammation, plaque and radiographic bone loss were evaluate clinically at baseline, 30, 60, 90 and 180 days. Histologic and statistical analysis was performed.
Results: Tooth mobility: Mobility for test and control teeth was comparable at the beginning of the experiment and started to increase gradually at the test teeth while control teeth’s mobility was practically unchanged. Test teeth also showed pronounced axial mobility.
Gingival inflammation: No statistically significant difference of gingival exudate between two groups throughout the study.
Plaque index was also comparable between the two groups and at 60, 90 and 180 days mineralized deposits were present on both test and control teeth.
Radiographic bone loss: Control teeth showed horizontal bone loss of 2.1mm from the reference notch. Test teeth showed pronounced horizontal bone loss, cone shaped widening of the PDL on the pressure side, and markedly widened PDL in the periapical area. Mean distance between the notch and the bone level was 4.9mm.
Histologic findings: The two dogs sacrificed 7 weeks after induction of experimental periodontitis showed epithelialized pockets extended to the level of or slightly apical to the reference notch and inflammatory cells comprised most of the connective tissue.
Control teeth at 180 days showed consistently apical downgrowth of epithelium from the notch in the root surface. Connective tissue was infiltrated with leucocytes and vessels were dilated.
Test teeth showed a more extensive proliferation of the pocket epithelium and leucocyte infiltration area seemed to extend further apically than in corresponding sections of the regions of control teeth. PDL was not infiltrated with inflammatory cells and a few osteoclasts were seen on the alveolar bone surface. On the pressure side PDL was 3.3. times that of the control. PDL on the periapical area was also characterized by presence of large number of small vessels and absence of inflammatory cells. Distance between the notch and the most apical side of the test teeth was 2.2mm comparing to 0.8mm of the control side.
Conclusion: Trauma from occlusion in dogs may accelerate progression of experimental periodontitis.


Ericsson 1977             ARTICLE
Purpose: To assess the effect of jiggling produced by occlusal forces on markedly reduced but non-inflammatory periodontal tissues
Materials and Methods
Results Discussion

Nyman, Lindhe 1978- Dogs             ARTICLE
Purpose: To evaluate if traumatic forces causing progressive tooth mobility influences the rate of destructive periodontitis.
M&M: Healthy periodontium was achieved in five mongrel dogs during a period of 4 weeks preceding the experiment. During the entire study (which lasted 363 days) all oral hygiene measures were abandoned. Periodontitis was induced by diet that causes plaque accumulation and by placement of plaque retention ligatures around mandibular premolars. After 330 days, when approximately 50% of supporting bone had been lost, flaps were raised and notches were prepared in the buccal root surfaces at crest of bone. Flaps were then re-sutured with new ligatures. One week later (Day 0), test teeth were subjected to jiggling forces in buccal/lingual direction using elevators for 30 seconds, and this was repeated on days 4,8,12, 16. Animals were sacrificed on day 26, and light microscopic examination was performed.




Result: Compared to the controls 1) Test teeth showed a significant increase in mobility, bone and attachment loss 2) Periodontal ligament width was increased and more osteoclasts were seen in test group.
BL: Repetitive mechanical injury via Jiggling forces causes progressive increase of tooth mobility and in the presence of a plaque induced inflammation, mediated an enhanced rate of destruction of the supporting apparatus in dogs with an ongoing process of periodontal tissue breakdown.


Ericsson, Lindhe, 1982 – DOGS             ARTICLE
P: To study the effect of a prolonged period of jiggling force application on the rate of progression of ligature-induced, plaque associated periodontitis in dogs.
M&M: 8 beagle dogs were used. Gingiva in the lower premolar region of all dogs were slightly inflamed, bone levels at normal height. Dogs were fed a diet that allowed gross plaque accumulation. Day 0, cotton floss ligatures were placed in mandibular premolars and were replaced once a month. On Day 60, a cap splint was cemented to the canine and the premolars in the left side of the maxilla. The cap splint was designed with an oblique plane which made ‘primary’ contact with the left lower premolar. Premolars became subjected to an excessive force and tilted in a mesio-buccal direction. A bar with a spring was attached to the canine and the 1st M and in the crown of P4. Every time the animal disocluded the spring pulled P4 to its original position. The animals were sacrificed at 360 days. Histological analysis was performed.
R: On day 60 as well as on day 360 the gingiva around the test and control teeth were red and bled on gentle probing. Towards the end of the experiment the lower premolars of all 8 dogs were mobile in mesio-distal, bucco-lingual and apico-coronal direction. Control teeth showed no signs of increased mobility. Radiographs taken on day 360, revealed angular bony defects on 6/8 test teeth. No such defects were found in the control teeth. CAL loss was 45.1% for the controls and 62.6% for the experimental group.
BL: Even though the forces applied were much greater than the forces from occlusal trauma in humans, it seems that jiggling forces act as a co-destructive factor and may enhance the rate of periodontal breakdown in plaque induced periodontitis.


Ericsson, Lindhe, 1984             ARTICLE
P: To study the rate of progression of experimentally produced periodontal breakdown in teeth with normal or permanently increased mobility.
M+M: 6 beagle dogs were used. A preparatory period of 6 weeks: scaling, polishing once weekly and tooth brushing twice daily. Day 0: trauma from occlusion of the jiggling type was induced on test teeth (via cementation of a cap splint). Between Day 0 and Day 120, plaque control measures were performed twice daily. Between Day 120 and Day 300 the dogs were allowed to accumulate plaque and calculus. On Day 120: experimental periodontal breakdown was induced around both control and test teeth by placing cotton floss ligatures around necks of teeth. Mobility measurements and radiographic exams were performed on day 0-300 (once a month). 1 dog sacrificed at 120 days, 5 dogs sacrificed on day 300. Histological analysis done.
R: During an initial 60 day to 90 day period, the test teeth were exposed to forces that gradually increased the horizontal mobility of the tooth. This mobility increase (progressive mobility) was the result of a gradual widening of PDL space without an accompanying reduction of the height of the supporting alveolar bone. Between Day 90 and Day 120, the mobility of the test teeth did not further increase but remained 2-3 times higher than that of the controls. Following the installation of ligatures (Day 120) and the termination of plaque control program, both groups of teeth showed a gradual increase in the horizontal tooth mobility. This mobility increase was similar in test and control group and appeared to be progressive throughout the entire phase of experimental periodontitis. Histologic analysis from biopsies revealed that around 25% of the height of the attachment apparatus in both test and control teeth had been destroyed. Therefore, even if mobility of the test teeth at the end of the experiment was significantly higher than that of the controls, the degree of periodontal tissue destruction observed in the two groups was the same.
BL: The degree of periodontal breakdown, initiated and maintained by ligature placement and plaque accumulation was similar in teeth with a widened PDL space and in teeth with normal width of periodontium. Progression of plaque-associated lesion in the attachment apparatus appeared to be unrelated to the width of periodontal ligament space (to the degree of horizontal tooth mobility).


Polson 1976 - Part III             ARTICLE
P: To characterize the changes that occur to the interproximal alveolar bone between adjacent teeth which were being moved alternately mesially and distally.
M+M: 10 adult squirrel monkeys with little or no gingival inflammation. The interproximal periodontium between the 2nd and 3rd mandibular premolars was subjected to repeated trauma (jiggling forces) by placing wedges alternatively mesial (between 2nd and 1st premolars) and distal (between 3rd premolar and 1st molar), every 48 hours. Contact area between the 1st and 2nd premolars remained closed preventing food impaction. Two animals were sacrificed after 2 weeks, the remaining eight after 10 weeks. The periodontium was examined histologically.
R: Inflammation was minimal clinically prior to start of study and remained unchanged at end of experimental period. Mobility increased in mesio-distal direction seven days after jiggling had begun and at 5 wks had considerable mobility; never in vertical direction.
Histological: After 2 weeks, active resorption, hyalinization- alveolar bone presented large marrow spaces. At 10 weeks, 35% loss of bone volume, osteoclasts were rare, and alveolar bone appeared adapted to the repeated trauma. The trauma caused a loss in crestal bone height and a loss of density in the coronal alveolar bone (with widening of the marrow spaces), but no loss of CT attachment. The distance from the CEJ to the alveolar crest was greater, but no increase in the soft tissue pocket depth. No apical migration of junctional epithelium.

BL: Trauma and subsequent reactions are confined to the crestal and subcrestal periodontal tissues without effect on the marginal supracrestal tissues. Supracrestal gingival fibers prevented apical migration of junctional epithelium. Since there was no loss in CT attachment, traumatic lesions and their sequelae in PDL do not produce periodontal pocketing.

Polson 1976             ARTICLE
Purpose: To investigate whether the bone loss due to trauma alone and the increased bone loss due to repeated trauma superimposed upon marginal periodontitis, are reversible when trauma is discontinued.
Materials and methods: Mandibular 2nd and 3rd bicuspids of 8 squirrel monkeys were jiggled mesio-distally. At the same time marginal periodontitis was induced on one side of the mandible. After ten weeks 4 animals were killed and at this time the jiggling was stopped in the 4 remaining animals which were killed 10 weeks later. Mobility was assessed before the prior to the start of the study and at 10-week intervals thereafter. The coronal interproximal area was examined histologically.
Results: Teeth subjected to 10 weeks of trauma alone were mobile in mesio-distal and bucco-lingual directions. After jiggling had stopped for 10 weeks mobility was not detectable. Gingival inflammation did not change.
10 weeks of jiggling forces combined with marginal periodontitis resulted in extremely mobile teeth in mesio-distal, buccal-lingual and vertical directions. Marginal tissues were very inflamed and tended to blood spontaneously. Mobility was just as pronounced ten weeks after jiggling had stopped, teeth were splayed in different directions, contacts were open and marginal tissues continued to show severe inflammation.
Histologically occlusal trauma did not produce any loss of connective tissue attachment and there was loss in height of the alveolar bone. Ten weeks after jiggling has been discontinued marked regeneration of alveolar bone had been taken place and the interproximal are resembled the normal. PDL had regained normal orientation and cellularity.
10 weeks of jiggling and marginal periodontitis resulted in junctional epithelium apical to the CEJ and connective tissue infiltrated with inflammatory cells. The interproximal areas obtained 10 weeks after discontinuing trauma in the presence of existing marginal periodontitis appeared essentially the same as those obtained at the moment the trauma was stopped.
Conclusion: In the specimens in which trauma was discontinued in the presence of periodontitis, the coronal alveolar bone did not regenerate.


Polson 1980             ARTICLE
Purpose: review of literature to summarize the relationship between occlusal trauma and inflammation in the pathogenesis of periodontal disease.
Discussion: BL: Resolution of marginal inflammation is of prime importance in the management of periodontal dz. After resolution of inflammation, bone regeneration may occur around mobile teeth


Pihlstrom and Ramfjord, 1971 - MONKEYS             ARTICLE
P: To study histologically and clinically the effects of nonfunction on the periodontium.
M&M: Five fully dentate rhesus monkeys had all mandibular teeth on the left extracted, leaving maxillary left teeth w/o functional antagonists. All teeth were scaled and polished 2-3 weeks prior to experiement. All teeth on the right side were left in normal function to serve as controls. The animals were sacrificed at 23,89,189,561 days following extraction. Histometric measurements and inflammatory cell counts were performed on experimental and control teeth.
R: More plaque & calculus was accumulated on the non-functional teeth. The mean gingival index was higher for nonfunctional teeth. The distance from CEJ to alveolar crest was significantly greater for non-functional teeth. The PDL was narrower & the cementum was thicker for non-functional teeth. Clinically, there appeared to be more plaque, calculus and g-vitis associated w/nonfunctional teeth.
BL: 1) Nonfunctional teeth had more inflammation; 2) Non-function leads to increased loss of bony support compared to functional teeth; 3) The distances from the CEJ to the apical end of the epithelial attachment and from the CEJ to the alveolar crest are highly correlated; 4) Non-function leads to narrowing of PDL; 5) Cementum increases in thickness in non-functional teet
Reviews

Ramjford, 1981             ARTICLE
P: To review the literature to investigate the relation between occlusion and periodontal disease.
Disc: Injury to the periodontal tissues as a result of occlusal forces has been defined as the lesion from trauma from occlusion (TFO). Occlusal trauma does not initiate or aggravate marginal gingivitis or initiate pocket formation or accelerate the conversion of gingivitis to periodontitis. In most well controlled studies, pocket formation has not developed with TFO because supracrestal fibers act as barrier to the downgrowth of junctional epithelium. Bone changes in the periodontium as a result from trauma from occlusion without existing inflammation are reversible once the forces are discontinued.
Monkey model: No acceleration of attachment loss on the presence on the presence of TFO. However, the found that TFO caused bone loss.
Beagle dog model: Deepening of periodontal pockets and acceleration of bone resorption by traumatic occlusion.
Increased tooth mobility is often used as the only clinical indicator from TFO. However, hypermobility may be due to bone loss and not TFO. The diagnosis of TFO is difficult and requires that ongoing progressive injury be demonstrated. Diagnosis in made on the basis of progressive mobility, persistent discomfort or tenderness, bone loss and root resorption. Radiographically widened PDL space does not necessarily indicate hypermobility due to occlusal trauma: could be a process of physiologic adaptation or past history of occlusal trauma. Splinting indicated only when mobility interferes with health and comfort of the patient and/or is progressively increasing. TFO has been listed as a possible cause of gingival recession. Gingival recession appears to be more related to plaque than to tooth hypermobility or malocclusion. Both primary and secondary TFO may be caused by bruxism. Habits such as biting on pencils or foreign objects can result in localized destruction of supporting structures.
The role of crowding,rotation, tilting and other specific features of malocclusion in the pathogenesis of periodontal disease has not been studied extensively. Although data from longitudinal human studies are not available , current evidence indicates 1) no significant direct relationship between malocclusion (on the basis of Angle’s classification) and the severity of periodontal disease but malocclusion may indirectly affect periodontal health when it is severe enough to interfere with plaque removal. 2) malocclusion (impinging overbite) can cause trauma to the gingiva and 3)severely malposed teeth may affect periodontal health.
A general principle for the initial treatment of periodontitis in which the etiologic factors are both bacterial plaque and occlusal factors is to eliminate and control first plaque and then the occlusal factors except where delay may unfavorably influence later treatment, or cause discomfort to the patient. Establish a stable occlusion with the least interference to plaque control and perio maintenance. Adjustment should be based on a definite diagnosis of the present of a traumatic lesion rather than the location of some occlusal interferences that may be of no significance. Author recommends splinting when mobility is progressive and interferes with the health and comfort of the patient.

Gher, 1996             ARTICLE
P: A review of articles that evaluated the effects of occlusion on periodontitis (discussed according to the method of research—randomized controlled, cohort or longitudinal, non-controlled, indirect evidence (animal and lab studies). Author wanted to do a meta-analysis, but was unable to do due limited number of studies.
DISC: There have been few well-designed studies that determine whether occlusal trauma contributes to attachment loss in periodontal disease. Most of these studies show that occlusal forces are transmitted to the periodontium and can cause changes in the bone and connective tissue, which can affect mobility and PDs. Occlusal trauma does not initiate periodontal disease, but its role in progressive attachment loss is inconclusive. Studies show that periodontitis can be treated successfully without occlusal adjustment, however, greater gains in attachment levels have been documented when occlusal adjustment was included in the treatment (SS but may not be clinically significant).
BL: Occlusal adjustment as a component of periodontal treatment should be utilized as it relates to patient comfort and function and not only based on the assumption that adjustment is necessary to stop the progression of periodontitis.


Serio 1999             No ARTICLE
Narrative review on the diagnosis and treatment planning of periodontal trauma and mobility
P: To outline some of the basic research relating occlusal trauma and tooth mobility to the health of the periodontium and formulate some meaningful conclusions.
D: Teeth and their surrounding supporting structures are subject to severe occlusal forces during mastication. These intermittent heavy forces can be properly accommodated without tissue destruction.
Ortho or pathologic forces: With light forces there is osteoclastic frontal resorption at the pressure site, which allows the alveolar bone to remodel. Heavy forces lead to pain, necrosis of the cells within the periodontal ligament and undermining resorption which decreases the density of the interproximal bone, at some distance from the tooth. On the tension side bone is apposed on the socket lining to maintain the width of the periodontal ligament.
Jiggling pathologic forces: Forces that applied on teeth during function or parafunction may exceed their adaptive capacity. These forces are applied in every direction, in the x, y, and z-axis. As a result, the periodontal ligament behaves as it is subject to pressure only. Forces exceeding the adaptive capacity of the teeth lead to the lesion of trauma from occlusion.
Occlusion, Perio, and Histology: Glickman suggested that occlusal trauma has three stages, injury, repair and adaptive remodeling. Stage I: (Injury) from excessive occlusal force. If the force is diminished, the injury can be repaired. If the force remains the following changes occur: Increase width of periodontal ligament and increased mobility. Increase in the number of blood vessels with decreased diameter. Decrease in local cellularity and hyalinization. In excessive pressure there is undermining resorption.
Stage II: (Repair) The body tries to recover. Damaged tissues are removed and new connective tissue, cementum and bone are formed. Once the reparative capacity overcomes the destructive process, the occlusion is no longer considered traumatologic.
Stage III: (Adaptive Remodeling) widened PDL, increased but not increasing mobility. Glickman also suggested the model of the zone of irritation (marginal plaque induced gingival inflammation) and the zone of co-destruction (the bone morphology and the occlusal forces on the tooth influence the pathway of inflammation). However, it is an unproven hypothesis!!!!
Animal Studies:
Polson’s monkeys: Morphologic alterations in the PDL due to occlusal forces do not initiate CAL loss. No increase in CAL loss was noted when trauma was superimposed to inflammation. Osseous regeneration was observed when both inflammation and occlusal trauma were controlled, and to some extend when inflammation was eliminated in the presence of persistent occlusal trauma.
Lindhe’s beagles: Depending on the magnitude of the force, frontal or undermining resorption occurred. With lesser magnitude the PDL healed after the removal of the force. With greater magnitude changes became progressively irreversible. Occlusal trauma cannot cause CAL loss when applied to healthy periodontium. It can result in bone loss and increased mobility, which may be transient or permanent. In the presence of inflammation, trauma from occlusion may enhance the rate of perio disease progression.
Clinical impression: Tenderness to percussion, pain, sensitivity to thermal stimuli and fremitus. Teeth may present with significant wear and pathologic migration. Increasing mobility is a sign of pathology!
Radiographic findings: Thickened lamina dura, widened PDL, funneling of the PDL space at the alveolar crest, radiolucence or condensation of the alveolar bone, and possibly root resorption.
BL: Appropriate criteria for diagnosis are widened PDL and progressively increasing mobility. Therefore, proper diagnosis has to be assessed on two occasions (increasing mobility). Hyper-mobility does not initiate CAL loss in healthy periodontium or in gingivitis, but it may accelerate CAL loss in progressive periodontitis. Occlusal forces may interfere with optimal healing in the treatment of periodontitis

 Hallmon 2001             No ARTICLE
Purpose: Review of definitions, clinical and radiographic indicators and treatment of occlusal trauma.
Discussion: Occlusal trauma: Injury resulting in tissue changes with tha attachment apparatus as a result of occlusal forces.
Primary occlusal trauma: Changes resulting from excessive occlusal forces applied to a tooth or teeth with normal support.
Secondary occlusal trauma: Changes resulting from normal or excessive occlusal forces to a tooth or teeth with reduced support.
The applied forces result in pressure zone (PDL compression, bone remodeling, vascular dilation/permeability, hyalinization/necrosis, increased cellularity, thrombosis and root resorption) and in tension zone (widening of PDL, bone repair, vascular permeability, cemental tears and thrombosis), and these are mechanisms through which the periodontium tries to adapt to the excess occlusal forces. If this potential is exceeded it leads to the lesion of occlusal trauma.
Glickman hypothesized but was unable to prove that there were two zones of disease within the periodontium, the zone of irritation and zone of co-destruction which is responsible for angular bony defects.
Wearhaug reported that it was dental plaque that accounted for the presence of angular bony defects and not occlusal trauma.
Studies of jiggling forces in the squirrel monkey model showed that trauma did not result on increased bone loss when superimposed on inflammation. In beagle dogs accelerated progression of pocket formation was observed with trauma in the presence of ongoing destructive periodontitis. No effect was found on healthy periodontium.
Reports in the literature have shown that molars with furc involvement and exhibit mobility have greater pocket depths when compared to non-motile controls with furc involvement. Patients receiving occlusal adjustment as part of their periodontal therapy demonstrate greater attachment gain compared to those who don’t. Clinical studies in general show that occlusal discrepancies contribute to periodontal problems and should be evaluated, diagnosed and managed.
The basic approaches to occlusal treatment bite appliances and occlusal adjustment.
Conclusion: Effective plaque control and compliance with periodontal maintenance recommendations are essential factors necessary to assure successful treatment and control of periodontal disease. Evidence support occlusal trauma as risk factor for periodontal destruction but no evidence indicates it can initiate it.



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