Etiology and Treatment (Root coverage):
-
FreeGingival Graft
-
Rootcoverage and increasing keratinized tissue
-
CoronallyPositioned Flaps
-
Laterallypositioned Flaps
DiscussionTopics
Whatis(are) the known or suspected cause(s) of recession? Do you considerrecession a pathologic or physiologic process? How do we classifyrecession? Is recession progressive? What is it’s relationshipto the underlying bone?
-
LoeH, Anerud A, Boysen H. The natural history of periodontal diseasein man: prevalence, severity, and extent of gingival recession. J.Periodontol 63:489-495, 1992
-
JoshipuraK, Kent R, Depaola P. Gingival recession: Intra-oral distributionand associated factors. JPeriodontol1994;65:864-870
-
SerinoG, Wennström JL, et al. The prevalence and distribution ofgingival recession in subjects with a high standard of oral hygiene.J Clin Periodontol. 1994 Jan;21(1):57-63.
-
HujoelPP, Cunha-Cruz J, Selipsky H, Saver BG. Abnormal pocket depth andgingival recession as distinct phenotypes. Periodontol 2000.39:22-9;2005
-
RajapakseP et al: Does tooth brushing influence the deveopment andprogression of non-inflammatory gingival recession? A systematicreview. J Clin Periodontol 2007; Dec; 34(12)1046-61
-
KapfererI, BeneschT, GregoricN, UlmC, HienzSA. Lip piercing: prevalence of associated gingival recessionand contributing factors. A cross-sectional study. JPeriodontal Res. 2007 Apr;42(2):177-83.
-
PiresIL, Cota LO, Oliveira AC, Costa JE, Costa FO. Associationbetween periodontal condition and use of tongue piercing: acase-control study. J Clin Periodontol. 2010 Aug 1;37(8):712-8.Epub 2010 Jun 17.
-
Endo,Rees, Hallmon, Kono, Kato: Self –inflicted gingival injuriescaused by excessive oral hygiene practices. TexDentJ 2006 Dec;123(12):1098-104
-
MillerPD. A classification of marginal tissue recession. Int J Perio Restor Dent 5:9- , 1985
-
LostC. Depth of alveolar bone dehiscences in relation to gingivalrecession. J Clin Periodontol 11:583-589,1984.
-
Zimmer,Seifi-Shirvandeh: Changes in gingival recession related toorthodontic treatment of traumatic deep bites in adults: J OrafacOrthop; 2007 May; 68(3): 232-44
-
ClossL et al: Gingival margin alterations and the pre-orthodontictreatment amount of keratinized gingvia: Braz oral Res 2007 Jan –Mar: 21(1)58-63
Whatis the relationship of keratinized tissue and recession? Are patientswho are lacking keratinized tissue more likely to develop recession?Are recessions on teeth with limited KG more likely to progress?
-
MaynardJG Jr, Wilson RD. Physiologic dimensions of the periodontiumsignificant to the restorative dentist. J Periodontol. 1979Apr;50(4):170-4.
-
WennströmJ, Lindhe J. Role of attached gingiva for maintenance of periodontalhealth. Healing following excisional and grafting procedures indogs. J Clin Periodontol. 1983 Mar;10(2):206-21.
-
MiyasatoM, Crigger M, Egelberg J. Gingival condition in areas of minimal andappreciable width of keratinized gingiva. J Clin Periodontol. 1977Aug;4(3):200-9.
Whatis the theory behind a free gingival graft? How does it heal? Inwhich situations is a free gingival graft appropriate? Describe thetechnique you prefer for a Free Gingival Graft. Is there anydifference if attempting to increase keratinized tissue vs coveringrecession? What are the drawbacks or complications of a free gingivalgraft?
-
SullivanHC et al. Free autogenous gingival grafts. I. Principles ofsuccessful grafting. Periodontics. (1968)
-
MillerPD: Root coverage using the free soft tissue autograft followingcitric acid application. III. A successful and predictableprocedure in areas of deep-wide recession. Int J Perio Restor Dent. 5(2):15-37, 1985.
-
MillerPD: Root coverage with the free gingival graft. Factors associatedwith incomplete coverage. J. Periodontol. 58:674-681, 1987.
-
MatterJ. Creeping attachment of free gingival grafts – A five yearfollow-up study. J. Periodontol. 51:681-685, 1980
-
Agudio,G Nieri, M, Rotundo R., Cortellini P, Pini Prato G.: Free gingivalgrafts to increase keratinized tissue: A retrospective long-termevaluation (10-25 years) of outcomes. J Periodontol 2008 Apr; 79(4):587 – 94 (ADD Erratum in : J Periodontol 2008 Jul79(7):1312)
-
FreemanE: Development of the dentogingival junction of the free graft. Ahistologic study. J.Perio Res. 16:140-146, 1981.
-
PasquinelliK. The histology of new attachment utilizing a thick autogenoussoft tissue graft in an area of deep recession; A case report. IntJ Perio Res Dent 1995; 15: 249-57.
Whatare the differences in recipient site preparation? Is there adifference in making a full thickness or split thickness site? Whatwould you expect to see in the healing?
-
DordickB, Coslet JG, Seibert JS. Clinical evaluation of free autogenousgengival grafts placed on alveolar bone. Part I. Clinicalpredictability. J Periodontol. 1976 Oct;47(10):559-67.
-
JamesWC, McFall WT Jr. Placement of free gingival grafts on denudedalveolar bone. Part I: clinical evaluations. J Periodontol. 1978Jun;49(6):283-90.
Whatis a pedicle graft? What are the different ways this can be utilizedto cover recession? How have the classic descriptions been modifiedover time? What is the role of citric acid? How does this type ofprocedure heal? How does this healing compare to the free gingivalgraft? How stable are these grafts?
-
GrupeH, Warren RF. Repair of gingival defects by a sliding flapoperation. J Periodontol 27:92-95, 1956.
-
GrupeHE. Modified technique for sliding flap operation. J Periodontol37:491-495, 1966
-
SmuklerH, Goldman HM : Laterally repositioned “stimulated”osteoperiosteal pedicle grafts in the treatment of denuded roots – apreliminary report. J. Periodontol. 50:379-383, 1979.
-
RobinsonRE. Utilizing an edentulous area as a donor site in the lateralrepositioned flap. Periodontics 2:79- , 1964.
-
CaffesseR, et. al. Lateral sliding flaps with and without citric acid. IntJ Perio Restor Dent 7(6):43-57, 1987.
-
CaffesseRG, Kon S, Castelli WA, Nasjleti CE : Revascularization followingthe lateral sliding flap procedure. J. Periodontol. 55:352-358,1984
-
CommonJ, McFall WT : The effects of citric acid on attachment oflaterally positioned flaps. J.Periodontol. 54:9-18, 1983.
-
CohenDW, Ross S : The double papillae repositioned flap in periodontaltherapy. J Periodontol 39:65-70, 1968.
-
RossS, Crosetti H, Gargiulo A : The double-papillae flap – Analternative. I. Fourteen years in retrospect. Int J Perio RestorDent 6(6):47-59, 1986.
Isthe coronally positioned flap considered a pedicle graft? How usefulis this technique to cover recession? Are there limitations to thistechnique? Histologically, how does this compare with lateral slidingor the double papillae flap? What are some modifications of thistechnique?
-
BernimoulinJP, Luscher B, Muhlemann HR: Coronally repositioned periodontalflaps. J.Clin. Periodontol. 2:1-13,1975.
-
AllenEP, Miller PD: Coronal positioning of existing gingiva: short termresults in the treatment of shallow marginal tissue recession. J. Periodontol. 60:316-319, 1989.
-
HarrisR, Harris A. The coronally positioned pedicle graft with inlaidmargins: A predictable method of obtaining root coverage of shallowdefects. IntJ Perio Rest Dent 1994;14:229-241
-
BaldiC, Pini-Prato G, et al. Coronally advanced flap procedure for rootcoverage. Is flap thickness a relevant predictor to achieve rootcoverage? A 19-case series. J Periodontol. 1999 Sep;70(9):1077-84.
-
LucchesiJA, Santos VR, Amaral CM, Peruzzo DC, Duarte PM. Coronallypositioned flap for treatment of restored root surfaces: a 6-monthclinical evaluation. J Periodontol. Apr;78(4):615-23. 2007
-
GottlowJ, Nyman S, Karring T, Lindhe J: Treatment of localized gingivalrecessions with coronally displaced flaps and citric acid. Anexperimental study in the dog. J. Clin. Periodontol. 13:57-63,1986.
-
ZucchelliG, Sanctis D. Treatment of multiple recession-type defects inpatients with esthetic demands. J Periodontol 71:1506-1514, 2000.
-
ZucchelliG, Mele M, et al. Coronally advanced flap with and without verticalreleasing incisions for the treatment of multiple gingivalrecessions: a comparative controlled randomized clinical trial. JPeriodontol. 2009 Jul;80(7):1083-94.
-
TarnowDP: Semilunar coronally repositioned flap. J. Clin. Periodontol.13:182-185, 1986.
Arethere any techniques to increase keratinized tissue without a pedicleor a free flap? What are the requirements for this?
-
Carnio J, Camargo P, Passanezi: Increasing the apico-coronal dimension ofattached gingival using the modified apically repositioned flaptechnique: A case series with a 6 month follow-up J Periodontol2007Sep 78(9):1825-30
Whatis(are) the known or suspected cause(s) of recession? Do you considerrecession a pathologic or physiologic process? How do we classifyrecession? Is recession progressive? What is it’s relationshipto the underlying bone?
Loe1992 ARTICLE
P:To describe the initiation, pattern of development, and progressionof gingival recession in Norwegian and Sri Lankan population.
M&M:Data presented in this study on recession was obtained throughparallel longitudinal studies of periodontal disease in man conductedin Norway between 1969-1988, and in Sri Lanka between 1970-1990. TheNorwegian group consisted of 565 male high school and non-dental,non-medical university students and junior faculty between 17 and 30+years of age. Norwegian patients reported seeing their dentist on at least an annual basis,owning a toothbrush and brushing their teeth daily. The Sri Lankan group(tea laborers)consisted of 480 male that were healthy but they hadnever received any dental care or any type of instruction on dentalcare. Gingivalrecession was measured on the 4 surfaces of all teeth (except 3rdMolars) from the exposed CEJ.
R:Norwegiangroup: In examsof 20year old subjects, 63% presented recession (between 1-3mm). Itwas confined almost entirely, to the buccal aspects of the maxillaryand mandibular bicuspids and molars. Gingival recession was found inabout 75% of 30year old men, still mainly on the buccal surfaces (13%had rec 1-2mm, 2% had rec 3-7mm). IPx surfaces were still unaffected. In the exams of menbetween 46 and 50 years old, more than 90% had 1 or more sites withgingival recession(26% on buccal surfaces and 4% IPx, 22% of the buccal rec was between1-2mm and 4% between 3-5mm)
SriLankan Group: 29%of men 18 to 19 years old had recession, mainly confined to thebuccal surfaces and did not exceed 4mm. By30 years, 90% had recession on buccal, lingual and IPx surfaces. Byage 40 approximately 100% had recession– 2/3 of which showed recession between 1-2mm and 1/3 between 3-9mm.32% of the lingual surfaces showed recession. At 50 years, recessionoccurred in all teeth types and surfaces with 70% on the buccal, 40%in the IPx, and 50% on the lingual. 50% of the recession measuredbetween 3-9mm.
Forboth groups the distribution of recession was bilaterallysymmetrical.
Conc:
Inboth groups prevalence and severity of gingival recession increasedwith age
Gingivalrecession is something common in both patients with good OH -dentalcare and in patients with poor OH – no dental care.
Severityand extent of gingival recession was higher in tea laborers
Severalfactors determine the initiation and development of recession
Joshipura,1994 ARTICLE
P:To assess the role of poor oral hygiene and forcefultooth-brushing as risk factors for recession.
M+M:298 subjects (42-67 years old) with at least 1 tooth with >1mmrecession examined. Oral hygeine index (debris: 0= no debris;1=debris covering up to a third of the tooth or extrinsic stains;2=debris covering more than a third to less than two-thirds of thetooth surface; 3=debris covering more than two-thirds of the surface;supragingival calculus: 0=no calculus; 1=up to a third of the toothsurface; 2=one third to two-thirds of the tooth surface; 3= more thantwo-thirds of the surface or a continuous band around the tooth), andGI measured . Analyses were performed on buccal surfaces.
R: Analysis of variance on subject means for buccal recession showedboth calculus and presence of buccal root surfaces with abrasion tobe significantly associated with recession after adjusting forage and gender.
59% ofsubjects had buccal abrasion.
Males had morerecession.
Recessionincreased with age.
Premolarshad high amount of recession and abrasion and low levels ofcalculus.
Molarshad high levels of calculus and low levels of abrasion.
BL: OH probably plays an important role on recession in molars (dueto poor OH), and abrasion in PMs (due to forceful brushing).Subjects with poor OH are likely to have more recession due toperiodontal disease; patients who brush with excess vigor haverecession due to trauma; tooth profile can also effect recessionespecially when associated with these two.
Serino 1994 ARTICLE
P: Toevaluate the prevalence and the development/progression of attachmentloss and gingival recession (rec) in a pts with good OH (PI < 30%,BOP < 10%). An additional aim is to study the realationshipbetween ALoss and gingival recession.
M&M:Multi-center study (12 clinics) in Sweden with 225 pts on regulardental care included. Based on age, 4 cohorts were generated: 18-29,30-41, 42-53, 54-65. All subjects had a baseline exam, and thenanother exam at 5 and 12yrs. The exam included PI, GI, PD, PALoss,and rec. FMX was taken at the different exams to determineperiodontal bone support.
R:PALoss (>2mm ALoss on buccal surface) per age group: 18-29 (19%),30-41 (52%), 42-53 (66%), 54-65 (76%).
Rec atbaseline overall was 25%. Over 12 yrs, rec increased in all groupsfrom: 18-29 (7 -> 19%), 30-41 (25 -> 33%), 42-53 (33 ->44%), 54-65 (40 -> 46%). 33% of unaffected sites at baselineshowed rec 12 yrs later, and 87% of sites showing rec at baselinedisplayed an increase in rec from baseline at 12 yrs. Maxillarymolars and PM and mand incisors and PM were the most commonlyaffected at both at baseline and the 12-yr examination. Of the pts<30 yrs of age, 44% displayed rec. Of the pts >41pts of age >90% displayed rec.
Buccalsites with 3mm of ALoss were associated with rec 67% of the time,while 98% of sites with PALoss of 4mm or more had rec. Only 3% ofsites with buccal PALoss of 2mm displayed rec. By including theinterproximal PALoss, interprox bone level, and OH parameters asexplanatory variables, 58% of the variance of the dependentvariable (buccal rec) could be explained.
Only 16% oftth with an intact interproximal periodontium had buccal rec. Tthwith 3mm PALoss and 3mm interprox bone loss had rec 68% of the time.
D: Somebuccal loss of attachment does not necessarily result in recession.Since rec is prevalent in subjects with very good OH and intactinterprox periodontium, it is unlikely that perio dz can account forrec. In fact, rec was uncommon unless the buccal site and had atleast 3mm of ALoss.
BL:Buccal rec was a frequent finding, the proportion of pts with recincreased with age, prevalence and incidence of rec within dentitionshowed different patterns depending on age, sites with rec showedsusceptibility of additional rec, loss of approximal periodontalsupport was associated with rec at the buccal surface.
Hujoel 2005 ARTICLE
Purpose:To distinguish destructive periodontal disease from periodontalatrophy and explore criteria to define when pockets are abnormal.
Discussion:Periodontal atrophy: the gums retain a very healthaspect, are free of pain and inflammation and yet will graduallyrecede. Destructive periodontal disease: presence ofdeepened periodontal pockets and underlying bone loss.
Treatmentand economics:90%of the periodontal procedures would be eliminated if periodontalpocketing disappeared. First, due to the insurance guidelinesrequiring pockets deeper than 4mm. Secondly, because the rationalebehind most (not all) periodontal procedures is the elimination ofdeep pockets. Economic implications of abnormal pocket depth suggestthat its incidence should be tracked as a distinct clinical entity.
Etiology:Osteoporosis, aging , continuous eruption, aggressive oral hygieneprocedures and anatomic periotypes have been suggested as potentialcauses of periodontal atrophy.
Smokingand diabetes are considered the primary driver of destructiveperiodontal disease.
Thebiologic basis for claiming that both phenotypes are the result ofplaque is mostly supported by assumption for the periodontal atrophy,since no such evidence have been presented over the last 30 years.
Theanthropologic and comparative medicine features of destructiveperiodontal disease and periodontal atrophy are different.Studies of 23 different population groups around the world suggestthat age related alveolar bone loss is a normal physiologic process,an observation which is at odds with current thinking that anyattachment loss is pathologic and the result of an inflammatoryprocess caused by plaque.
Authorsbelieve that if pocket-free recession (periodontal atrophy) islabeled a destructive periodontal disease, we will end-up with the“anomalous situation” of being close to 100% ofindividuals with signs of chronic periodontitis.
Isperiodontal atrophy a disease? Attachmentloss is almost universal after the age of 30 and increases with age.Wear-and-tear of aging affects every organ system in the human body.It appears logical that periodontal atrophy is a normal age-relatedprocess.
Abnormalperiodontal pockets: Currently alldefinitions of periodontal diseases are arbitrary, which should because for alarm. Normative values may be superior to arbitraryvalues. These values can be based on parametric or nonparametricpercent of cut-off values.
Diagnosesbased on these values though are irrelevant to underlying factors(diabetes, smoking) and can become disconnected from clinicalrealities (tooth loss, periodontal abscesses, difficulty chewing). Destructive periodontal disease is a complex disease with too muchnatural variability to allow a successful definition based onarbitrary or normative values. The most attractive diagnosis is thetherapeutic diagnosis. A person is screened for the disease only ifthe diagnosis lease to better outcomes. Critical PDs are the exampleof therapeutic reference values in periodontitis, although theshortcoming is that no evidence exists that short term changes inattachment levels relate to clinically relevant outcomes such astooth loss.
Conclusion:Destructive periodontal disease and periodontal atrophy are twophenotypes with distinct clinical features. Different lines ofevidence suggest that the two phenotypes have distinct etiologies,prognosis and are treated differently. The current custom oflabeling both phenotypes as one and the same disease, chronicperiodontitis, merely because they both exhibit attachment loss,needs to be re-evaluated. This will involve evaluating whetherperiodontal atrophy should be labeled as a disease.
Rajapakse2007: ARTICLE
Purpose: The aim of the systematic review was to search for the bestavailable evidence to evaluate potential role of tooth brushing inthe initiation and progression of non-inflammatory, localizedgingival recession.
Materialsand methods:
Thefocused question of the review was” Do factors associated withtooth brushing predict the development and progression ofnon-inflammatory gingival recession in adults?”
Thesearch covered six electronic database b/w Jan 1996-July 2005. Handsearching included searched of J Perio, J of Clin perio, J of PerioReas.
Results:
29papers were read and 18 texts were eligible for inclusion. One wasRCT (Level I evidence) and 17 were observational/cross-sectionalstudy (Level III evidence).
INRCT, author concluded that the toothbrushes significantly reduce the recession on buccal surface of the tooth over 18 months.
Ofremaining 17 studies, 2 concluded that there is no relationship b/wtooth brushing frequency and recession.
8studies concluded with an association b/w brushing frequency andrecession.
Nostudy concluded the potential risk factor like duration, force,frequency of changing of tooth brushes, and brushing technique or theconfounding factors like age, biotype, crowding, ortho TX wascontrolled.
Noneof the observational studies satisfied all the specified criteria forquality appraisal.
Conclusion:
1.Data supporting the association b/w brushing and recession areinconclusive
2.Tooth brushing factors that have been associated with the developmentand progression of the recession are frequency, technique, force, andhardness of the bristles.
3.The limited evidence of one RCT suggests that the tooth brushingeither powered or manual and with standardized instructions intooth brushing technique may reduce the severity of recession.Importantconclusions to remember
Purpose:To assess the prevalence and severity of periodontal and dentalcomplications with the contributing factors of gingival recessionassociated with labial piercing.
M&M:A cross sectional study was performed on 100 (14-28yrs) patients withlower-lip studs. The test and control groups were matched accordingto the gender, age and smoking status. Clinical examination includedplaque and bleeding indices, probing depth, recession, clinicalattachment level, width of keratinized gingiva, periodontal biotype,frenula attachment, evaluation of hard tissues, trauma fromocclusion, stud features, radiographs and photographs of the lowerfront teeth.
R: NSSDwas observed in the mean probing depth, plaque control, and bleedingon probing of the test group compared to the controls. No significantcorrelations were observed with the prevalence of buccal recessions athe distribution of periodontal biotype between groups. Amount ofbuccal recession (occluso-apical and mesio-distal) and avg width ofkeratinized gingiva were significantly higher in test group comparedto the controls. Localized periodontitis was recorded in 4% of testsubjects. There were no significant associations between piercingand abnormal tooth wear. Time since piercing and the position of thestud in relation to the cemento–enamel junction weresignificantly associated with the prevalence of buccal recessions.
BL:Labial piercing was found to be significant factor in thedevelopment of the buccal recession in the mandibular anterior teeth.Narrow width of keratinized gingiva is associated with higher amountsof buccal recession.
P:Cross sectional study to evaluate the periodontal status and riskfactors for gingival recession in individuals with tongue piercings.
M: 60individuals w tongue piercing and 120 w/o were examined from schoolsand universities in Brazil b/t 13 and 28 y/o, entire sampling wastaken from low socioeconomic status. recorded PD, CAL, plaque index,BOP, recession and tooth fracture
R:Thecase group presented with a higher prevalence and severity ofrecession when compared to the control group. The prevalence ofrecession in the anterior lingual mandibular region was associatedwith the use of piercings, male gender and BOP.
Recession inthe lingual of anterior mandible region presence: case: 55% control:10%
case:23% had1-2mm
13% had 3mm
18% had 4mm
control: 10%had 1-2mm
BL: Useof tongue piercings has a strong association with gingival recessionin ant lingual mandibular area.
Side note:prevalence of periodontitis for case: 11.7 and control 4.2
localizedsevere (either man or max: 6.7 and control 1.77
36.7%reported swelling and infection/inflammation
20% reportedfractured teeth
Endo ‘06 NO ARTICLE
Case series:Self inflicted gingival injuries caused by excessive oral hygienepractices
Categorized asNon-plaque induced gingival lesion. Physical injuries are classifiedas: Accidental, Iatrogenic (acute and self-limiting) andSelf-inflicted (SI) (chronic). SI can be deliberate injuries usuallyassociated with emotional disturbances. In kids SI are due damagewith their fingernails and in adults due excessive oral hygienepractice. SI can cause: ulcers, erosions, retractions,hyperkeratosis, CAL and destruction of teeth.
Case I
Female pt,1-month history of pain and bleeding on the buccal gingiva. Marginalgingiva was rolled, horizontal groove in the base of the papilla,linear ulcer #28, white plaque like changes in papilla and marginalgingiva. Brushed teeth 30 min a day due fear to loose more teeth withhard nylon toothbrush (TB), no toothpaste and horizontal motion. Dx:Excessive and improper tooth brushing. Instruction: Use soft TB, 2min, twice a day. Signs disappear within 2 weeks.
Case II
Female pt,3-month history of pain in the gingiva. Horizontal erythematousgroove in the base of the papilla, abrasion, white plaque likechanges in papilla detach with contact. History of 6 Rx fordepression and dry mouth. Brushed teeth 30 min a day/ 3 times becauseshe felt mouth uncomfortable. She used TB and no toothpaste. Dx:Excessive and improper toothbrushing. Instruction: Brush 2 min,twice a day. Use salivary substitute (biotene). Signs disappearwithin 1 week.
Case III
Female pt, 1year hx of painful gingiva in ant mand teeth, loss of tip of papilla.Lesions similar to NUG, lingual ant had lobulated appearance,recession, gingival clefts, white plaque changes, v-shaped gingivalrecessions present. Good medical hx. Pt was concerned withperiodontal disease. Pt used interproximal brush (IB) around 2 hoursa day (she inserted back and forward 100 times in each space b/wteeth, 3 times a day). Dx: Gingival trauma. Instructions: Stop use ofIB, use medium TB twice a day for 2 min. Gingival cleft and whiteplaque lesion disappeared by follow up 1 month later. Lingualgingival enlargements disappeared as well.
Conclusion:
Due fear ofperiodontal disease, these 3 pts practiced excessive tooth brushing.It is important to interview the pts about their oral hygienepractices and ask them to show you. Saliva function as a “blanket”that protects the soft tissue. Pts with xerostomia need to be awareof possibility of tissue damage. Salivary substitute may bebeneficial for them. Abrasion of teeth may be related to toothpaste. No interproximal abrasion in any teeth was noticed on case #3.
Miller,1985 ARTICLE
P: to classify marginal tissue recession.
Disc:
ClassI: Marginal tissuerecession which does not extend to the MGJ. No bone loss ininterdental area & 100% root coverage is expected.
ClassII: Marginal tissuerecession which extends to or beyond the MGJ. No bone loss ininterdental area & 100% root coverage expected.
ClassIII: Marginal tissuerecession which extends to or beyond MGJ. Bone or soft tissue loss ininterdental area is present or there is malpositioning of teeth whichprevents the attempting of 100% root coverage. Partial coverage isexpected.
ClassIV: Marginal tissuerecession to or beyond MGJ. Bone or soft tissue loss in interdentalarea &/or malpositioning of teeth is so severe that root coveragecannot be anticipated.
Rootcoverage is considered to be 100% if the marginal tissue aftercomplete healing is at CEJ & sulcus depth is 2mm or less andthere is no BOP.
Rootcoverage is either primary, which occurs immediately followinggrafting, or secondary, which is known as “creepingattachment.”
Lost,1984 ARTICLE
P:To assess the relationship between bony dehiscence and gingivalrecession.
M&M:Periodontal flap surgery was performed in 50 recession areas, 113affected teeth, in 27 patients (mean age 25.6 years), andpre-operative and intra-operative dehiscence measurements were taken(most apical portionof dehiscence to most apical portion of CEJ).All recessions met thefollowing criteria: located facially, intact interdental papillaeadjacent to area of recession, no interproximal bone loss, absence oftooth mobility, absence of periodontal pockets and no or minimalgingival inflammation.
R:Mean recession and dehiscence depth were 2.67mm and 5.43mmrespectively. The difference between these measurements –2.76mm – consists of 0.82mm sulcus depth, 0.63mm epithelialattachment and 1,22mm connective tissue attachment. Of the 113examined teeth, 16 presented markedly greater distance (4-7.5mm)between the gingival margin and the alveolar bone crest. Acorrelation between dehiscence depth and type of tooth could not befound, but the 1/3 of these 16 teeth presenting 4mm or more betweendehiscence depth and recession were lower canines.
C:In average, a recession depth of 1mm is exceeded by 2.8mm towards theapex of the alveolar bone dehiscence. Almost identical with the valuereported by Gargiulo (2.73mm). Each 1mm increase in recession depthinvolves an average of .98mm in the alveolar bone dehiscence.
Zimmer,2007 ARTICLE
P:To study the effect of orthodontic intrusion on trauma-inducedrecessions
M+M:12 patients (8F, 4M; average age 38 years) with >6 mmoverbite, and recession on at least one incisor caused by directtrauma from contact with opposing dentition. Five had Class 2 Div1and seven had Class 2 Div2. 6 patients had history of periodontaltreatment. All patients received fixed appliances and were treated byintrusion, one patient was taken out of the study due to recurrenceof periodontitis, all were on a 6 week maintenance schedule. 41 teethin total had recession, measured clinical crown lengths intra-orally,on casts and on photographs with an electronic precision slidinggauge. PDs were also measured. Teeth without trauma served ascontrols.
R:Four teeth excluded due to signs of incisal edge abrasion. At the endof treatment the clinical crown measurement of teeth withrecession had SS decreased by an average of -2.05 mm (maxdecrease was –3.2 mm, the min decrease was –0.9 mm; noincreases were observed). The average change in teeth withoutrecession defects was NSS and 0.02 mm (range of -1.2 to +2.4). Nochanges in PDs noted.
BL:Orthodontic treatment is effective in reducing recession caused bytrauma from deep overbite, and in teeth without trauma it can improvegingival marginal contour
Closs 2007 ARTICLE
P:To associate the amount of keratinized gingiva present in adolescentsprior to orthodontic treatment to the development of gingivalrecessions after the end of treatment.
M&M:Retrospective study. The sample consisted of the intra-oralphotographs and orthodontic study models from 209 Caucasian patientswith a mean age of 11.20 +/- 1.83 years on their initial records and14.7 +/- 1.8 years on their final records (28 days or more afterremoval of their appliances). Patients were either Angle Class I orII and were submitted to non-extraction orthodontic treatment. Thespacing or crowding in the lower anterior teeth could not exceed 4mm.Gingival recession was evaluated by visual inspection of the lowerincisors and canines as seen in the initial and final study modelsand intra-oral photographs. The amount of recession was quantifiedusing a digital caliper and the observed post-treatment gingivalmargin alterations were classified as unaltered, coronal migration ofthe gingival margin or apical migration of the gingival margin. Thewidth of the keratinized gingiva was measured from the mucogingivalline to the most apical point of the gingival margin at the center ofthe facial aspect of the teeth on the pre-treatment photographs.
R:The teeth that developed gingival recession and those that did nothave their gingival margin position changed did not differ inrelation to the initial amount of keratinized gingiva (3.00 +/- 0.61and 3.5 +/- 0.86 mm, respectively). Paradoxically, teeth thatpresented a coronal migration of the gingival margin had a smallerinitial amount of keratinized gingiva (2.26 +/- 0.31 mm).
C:The mean amount of initial keratinized gingiva did not predisposelower incisors and canines to gingival recession
CR-Whatmatters more is the direction of the ortho movement: if labially,outside of natural alveolar house, recession will occur.
Whatis the relationship of keratinized tissue and recession? Are patientswho are lacking keratinized tissue more likely to develop recession?Are recessions on teeth with limited KG more likely to progress?
Maynard1979 ARTICLE
Purpose: To present the physiologic dimensions of the periodontium significantto the restorative dentist.
Discussion:Physiologic dimensions have been classified as superficialphysiologic, crevicular physiologic and subcrevicular physiologic.
Intracrevicularmargins are the ones placed into the gingival crevice and aredifferent than subgingival margins that can extent into thejunctional epithelium and connective tissue, which causes gingivitisthat may progress to periodontitis.
Superficialphysiologic dimension extends from MGJ to gingival margin. Ifthere is insufficient attached gingiva restorative procedures mayresult in apical migration of marginal tissue and attachmentapparatus. In these cases preprosthetic surgery should be considered.Adequate band of KG is fundamental to successful restorativedentistry with intracrevicular margins. 2mm of free gingiva and 3mmof attached are required. Thickness of gingiva should also beevaluated. If the probe is visible through the free gingival margin,width should be increased.
When marginaltissue recession is present prior to the restoration twostage approach (increase in KG – root coverage) should beperformed.
Normaldepth of gingival crevice is 0 to 3-4mm. To prepare a toothfor intracrevicular margin a minimum depth of 1.5-2mm should bepresent. If it less than that junctional epithelium will betraumatized during restorative procedures. After periodontal surgeryrestorative procedures should be delayed for at least 6 weeks.Margins of restorations should not be rough and poorly adaptedbecause that will result in mechanical irritation and plaqueretention.
Subcrevicularphysiologic dimensions are on average 0.97mm for JE and1.07mm for connective tissue according to Gargiulo, Wentz and Orban,and violation of these could cause periodontal disease.
Traumafrom occlusion will cause reversible mobility in healthyperiodontium. If inflammation is caused because of the restorations,it will result in more rapid periodontal destruction.
Conclusion:The first and most basic objective of restorative dentistry ispreservation of the teeth. Function, comfort and esthetics are alsoconsidered and margins are intracrevicular although it is widelyaccepted that the best option is supragingival. Daily observation ofthe three physiologic dimensions permits the therapist to restoreteeth with minimal injury to the periodontium.
Wennstrom& Lindhe, 1983 ARTICLE
Purpose:Evaluate the effect of plaque infection on gingiva w or w/o AG andwith different height of the attachment apparatus.
Materialsand methods:
Created4 different dento gingival units in 7 dogs to determine differencesin resistance to inflammation
1. Normal non operated, KG present
2. Normal excised KG and allowed reformationNarrow KG, no AG, n.height of supp. app.
3. Periodontal breakdown – excised – ungrafted. Narrow KG,no AG, low height of supp. app
4. Periodontal breakdown grafted. KG present, AG, low height of supp.app
Theyallowed plaque to accumulate for 40 days
Clinicalexam at day 0, day 20 & day 40 (PI, GI, Gingival Exudate, PD, AL,GM, AG)
2dogs randomly chosen for biopsy and sacrifice to perform histologyprior to plaque accumulation.
Results:
Gingivaregenerated post excision and post grafting is clinically andhistologically similar to normal gingiva.
Unitw/no AG had FG w/ thinner B-L & keratin layer.
3. After 40d of plaque accumulation, there was NSD btw dento gingivalunits regarding size and apical extension of infiltrated portion ofCT or GCF.
4. FG unit supported by alveolar mucosa is not more susceptible toinflammation than a FG unit supported by a wide zone of AG.
BL: The presence or not and the width of AG has an effect on theclinical evaluation of inflammation of the gingival but no effect ina histologic level. Supports Miyasato; Contradicts Lang & Loe,Bowers.
Cr-is 40 days long enough? This supports the clinical observation ofteeth with little or no AG remaining in a steady state for years.
Miyasoto1977 ARTICLE
P: Toevaluate gingival conditions in areas of minimal and appreciablewidth of KG.
M&M: 250 dental, dental hygiene and dental assisting students and dentalfaculty were screened. 16 subjects were selected, age 19-39. 6 ofthem had one lower PM with a width of KG ≤1mm and a PM with widthof KG ≥ 2mm on the opposite side (contralateral pair). Theremaining pts had width of KG ≤ 1mm on one PM and ≥2mm onanother PM on the same side (unilateral pair). Subjects withhigh frenum attach were excluded. Measured GE, GI, sulcusdepth, PI, AG. The 6 pts with contralateral pairs were used forexperimental gingivitis study- asked to cease OH and were re-examinedat 4,7,11,14,18,21,25 days and measured GE, PI, and GI.
R: Mean widthof KG were 0.7mm and 2.3mm for the study pairs. None of the teethwith minimal KG (≤1mm) had any amount of attached gingiva. 0/16showed presence of plaque on mid buccal surface, 2/16 with min widthof KG showed sigs of GI/color change/swelling. No areas showed BOPin either ≤1mm or ≥2mm KG. NSSD between the groups for GE. For the experimental gingivitis, there was a gradual and similarincrease in plaque and GE for both groups. Not until day 25 didbuccal areas show signs of inflammation, 6/6 areas with KG ≤ 1mmshowed inflammation and 4/6 areas of ≥2mm KG showed inflammation.
C: Gingivawith ≤1mm of KG and ≥2mm of KG only exhibit minute amounts ofgingival exudate, which correlated with lack of clinical signs ofinflammation for both types of marginal gingiva. After the 25 dayexperimental gingivitis, there was only a gradual increase in PI.There was no diff in GE in areas with min or appreciable KG. Thismay indicate that areas of min width of KG are no moreprone to the development of plaque-induced inflammatory changes thanareas of appreciable width of KG.
BL: Overthe 25 day period, there was in increase in plaque and GI andclinical inflammation, with no apparent difference between theareas with minimal or appreciable width of KG.
Whatis the theory behind a free gingival graft? How does it heal? Inwhich situations is a free gingival graft appropriate? Describe thetechnique you prefer for a Free Gingival Graft. Is there anydifference if attempting to increase keratinized tissue vs coveringrecession? What are the drawbacks or complications of a free gingivalgraft?
P:report our observation on free gingival grafting and toattempt to correlate the surgical principles previously developed inplastic surgery to the conditions encountered in periodontal
Recipentsite:
The mostimportant is the capacity of the recipient bed to form capillaryoutgrowths for vascularization of the graft.
Adequatehemostasis. Bleeding site will separate the graft and form ahematoma.
Procedurefor recipient site preparation:
Allow adequatetime for hemostasis – control bleeding.
Epithelium,CT, and muscle fibers are sharply dissected down to the periosteum.
Donor site:
Edentulousridge
Avoid visiblepostextraction scars, decreased vascularity
Attachedgingiva
Limited, notsuitable when inflamed and hyperplastic. Requires reshaping.
Palatal mucosa(most common)
Submucosashould be removed wit ha scalped before grafting, it will act as abarrier both to diffusion and vascularization.
Greaterpalatine foramen/vessels – may limit the surgical site.
Graftstypes: Full thickness and intermediate or thick splitthickness gingival grafts.
Thicker graftwill undergo greater immediate contraction upon detachment from thedonor area (higher elastic fiber in the graft)
Secondarycontraction is caused by cicatrization of the tissue, which unitesthe graft and its base.
A thick grafton a rigid bed offers maximum resistance to cicatrix contraction andthus will undergo little secondary contraction.
Graf survivalis enhanced by decreasing the amount of lamina propria in the graft.Thinner graft can be more easily maintained by diffusion and iseasier to vascularize.
However,thicker graft is indicated in area where greater functional demandsare anticipated (it’s resistance to functional stress)
Procedurefor Donor site preparation:
A tin foil orwax template may be made on the recipient bed.
Atraumaticremoval of donor tissue is the most important aspect.
An accessincision is made at a 45 degree angle adjacent to the outline of thegraft. This assists the surgeon in achieving the desired graftthickness.
The donortissue is placed in the recipient bed as soon as possible to mintrauma and dehydration.
Immobilizationof the graft VERY IMPORTANT)
in arealacking vestibular depth at the recipient site – this conditionmay be corrected by performing a vestibular extension in conjunctionwith preparing the recipient site.
The stepsin immobilization
Suturing:
The graft isstretched to conform to the recipient bed. This tension counteractsprimary contraction and aids in vascularization by reopening thegraft’s collapsed vessels.
Minimal numberof sutures is used (author used 5-0 teflon-coated Dacron suture withan atraumatic needle)
Formation of afibrin clot.
Aftersuturing, Pressure is exerted against the graft for 5 mins todisplace blood under it. Fibrin clot anchors the graft to its bed,allow rapid penetration by capillaries, and act as a matrix throughwhich metabolites and waste products diffuse.
Placement ofthe rubber dam – functions as a sliding film btw the dressingand the graft (reduces the shearing forces that preventvascularization.
Dressing –maintains a positive pressure on the the graft and aids in itsimmobilization.
Stages of agraft “Take”
Plasmiccirculation – diffusion of the graft from its host bed andoccurs most efficiently through the fibrin clot.
Vascularization– capillary proliferation (end of 1st day) ->extended into the graft (2-3rd day) ->circulation (3rdday) -> adequate blood supply (8th day)
Organic union(4-5th day) – a fibrous attachment is complete bythe 10th day.
Post-Opcare
Recipientsite:
The first 6days – the pt is instructed to minimize facial movement.
Do not removethe dressing before the 6th day.
If infectionis present, remove hematoma formation or infection- redress for anadditional 5 days.
Donor site:
Protected by adressing until it has epithelized.
Thinnersplit-thickness grafts heal faster
Full thicknessrequire primary closure or coverage.
Problemsand possible limitation
The capacityof the recipient bed to form capillary outgrowths, hemostasis of therecipient bed, atraumatic handling of tissue, rapid vascularizationof the graft, adequate immobilization during healing, and properpost-op care.
Purpose:To measure the root coverage using a free soft tissue autograftfollowing citric acid (CA) application.
M&M:100 consecutive marginal tissue recession on 49 females and 9 males. Width of the recession was constant (around 3mm), but depth (marginaltissue recession + PD) was very variable 2-14mm. Control group wasdiscontinued after recession and sensitivity were present 10 dayspost op in 3 control pts. Technique: CA solution of pH1 mixedwith anhydrous CA crystals (15 min allowed for dissolution) were usedin combination to make the CA super-saturated. CA on a cotton pelletwas used to “burnished” the root surface. The cotton waschange 2-3times a min, and the area was “burnished “for5min. CA was flushed with abundant water. After CA applicationincisions were made. The horizontal incision in made in theinterdental papilla at the level of CEJ. Vertical incisions made atprox line angles of adjacent teeth. Retracted tissue was completelyexcised. Care was taken to maintain intact periosteum. Graft wasremoved from the donor site using a “dry” foil pattern.Most (but not all) of the submucosa (glandular and adipose tissue) isremoved by sharp dissection. The inner surface of the graft was assmooth as possible. Thus avoiding “dead space”.Resorbable sutures were used on each papilla after positioning thebutt joint of the graft close to the butt joint of the papilla. 2additional interrupted sutures were placed in each corner of thegraft and into the periosteum. Coe-pak and adhesive “dry”foil was placed for 2w. Criteria: 100% root coverage (RC) wasconsidered when gingival margin was at CEJ, PD 2mm and no BOP. RC wasconsidered primary if it was found at 10w post-op or secondary ifobtained after 10w. If RC was not 100% at 10w, a recall visit at 1ywas performed to see if 100% RC could be obtained by a secondary RC.Class I recession were included only when were next to a class II orIII, if had been isolated grafting wouldn’t be needed.
Results:100% RC is attainable only in class I and II. In class I and II 100% RC was obtained in 71 of 79 sites 90%, partial in 4 of 79 (5%) andno RC in 4 of 79 sites (5%). Averaged of overall gain was 3.79mm andof probing attachment gain 4.54mm. Class I recession: 100% RC on all13 sites. Class II: 100% RC on 58 of 66 sites (88%). Only 1 toothneed RCT after therapy (it had 5mm recession, 6mm PD, hx of ortho txand vitality was not performed bf sx.
BL:Complete RC can be successful and predictable using soft tissue graftand the right concentration of citric acid as a one stage procedure.
Ctq:Some sites need a 2nd stage for complete RC. No controlgroups.
Miller1987 ARTICLE
Summary:Complete root coverage has been defined according to the followingcriteria:
A)The soft tissue margin must be at the CEJ. B) There is clinicalattachment to the root. C) Sulcus depth is <2mm D) No BOP. Failing to address certain factors can result in incomplete rootcoverage.
Factorsassociated w/ incomplete coverage:
1.Improper classification of marginal tissue recession. First step inpredicting is classifying recession.
2.Inadequate root planing, not creating anatomy conducive to rootcoverage.
3.Failure to treat the planed roots w/ Citric Acid. Surface changesafter conditioning w/ CA include widening of the dentinal tubules,removal of the smear layer, accelerated healing w/ acceleratedre-attachment, inhibition of epithelial migration, and the formationof a CT attachment. Do this prior to preparing recipient site as CAcauses coagulation of blood.
4.Improper prep of the recipient site. The horizontal incision must bemade at the level of the CEJ. If the incision is made apical to theCEJ, complete root coverage should not be contemplated. Authorrecommends creation of a butt joint margin in the papilla to enhancecirculation to the coronal aspect of the graft. Vertical incisionsshould be made at the line angles of adjacent teeth. Recipient siteshould be prepared a minimum of 3 mm apical to the recession.
5.Inadequate size of the interdental papillae. The broader and thickerthe interdental papilla, the greater the blood supply to the coronalaspect of the graft and the easier the suturing.
6.Improperly prepared donor tissue. The undersurface of the graftshould be flat and smooth w/ the graft having the same type of buttjoint margins as those created in the papilla.
7.Inadequate graft size (too much better than too little) / Inadequategraft thickness (thicker better).
8.Dehydration of the graft. Place graft immediately on a bleedingrecipient bed to minimize dehydration.
9.Inadequate adaptation of graft to root and remaining periosteal bed.Failure to stabilize graft.
10.Excess or prolonged pressure in adaptation of sutured graft.
11.Reduction of inflammation prior to grafting. A bleeding papilla mayenhance circulation to the coronal margin of the graft.
12.Trauma to graft during initial healing. Examples include: loosedressing, excessive edema, or stretching or manipulating the lips,and incising foods that can loosen dressing. Give adequate post opinstructions.
Excessivesmoking. 100% correlation b/w failure to obtain root coverage andheavy smoking (in excess of 10 cigs/day). Heavy smokers shouldrefrain from smoking during the 1st 2 post-op wks.
Background: creeping attachment is apost-op migration of the free gingival margin in a coronal directioncovering partially or totally a previously denuded root.
P: To report creeping attachmentsubsequent to placing a free gingival graft in areas of narrowrecession, over a 5 year follow-up period.
M&M: 10 patients (9 Females, 1Male), age 25-45. Isolated narrow recessions, <3 mm inwidth. After OHI and initial th
