Gingival recession: Narrow perception - erroneous; wider canvass - out-of-focus!

作者
Ashish Kumar
出处
期刊:Journal of Indian Society of Periodontology [Medknow]
卷期号:27 (3): 227-229 被引量:2
标识
DOI:10.4103/jisp.jisp_118_23
摘要

The exposure of the root surface technically and scientifically called gingival recession is one of the most common conditions observed in people affected with periodontal diseases. The gingival recession has been found to be associated with increasing age in epidemiologic studies. Most of the loss of periodontal tissues seen approximately after the age of 45 years as a result of periodontitis is in the form of gingival recession. A common pattern was observed and identified in the data from population of two countries, United States - National Health and Nutrition Examination Survey (NHANES), for years 2009 to 2014 and from Germany- The Study of Health in Pomerania (SHIP-Trend) for years 2008 to 2012. The linear association of clinical attachment loss (CAL) with age was clearly spotted.[1] Another interesting observation was that pocket depth (PD) emerged to be the main factor responsible for CAL up to 44 years, but beyond that, in older age groups, gingival recession was the major contributor to CAL.[1] These observations also have huge implications on the status of overemphasized importance of gingival recession treatment limited to anterior labial region pertaining to aesthetic dentistry The gingival recession is widely spread across age groups and across all regions of mouth but most of the literature about the treatment of gingival recession revolves around the anterior sextant of jaws. The fact that periodontal disease (periodontitis) remains the main contributor of gingival recession, also points to the fact that most of these recessions remain difficult or almost impossible to treat and achieve root coverage due to their association with interproximal attachment loss. Also the age at which gingival recession becomes a prominent feature, the demand for aesthetics is very less in majority of the population, barring a very small proportion of highly motivated and aesthetic conscious population. The fact that periodontal destruction phenotypes has historically being either in form of “destructive periodontal disease” associated with deep periodontal pockets and bone loss or “periodontal atrophy,” where the gingiva is free of inflammation, is very healthy and still gradually demonstrates gingival recession.[2] There is not only marked difference in phenotype of the destructive periodontal disease and periodontal atrophy but may also differs in terms of aetiology and treatments.[2] The only cases which fit within the successful treatment bracket and most periodontal plastic surgical procedures pertaining to root coverage are attempted, belong to younger age cohort where in gingival recession is generally of Cairo’s recession type 1 (RT1)[3] or older Miller’s Class I or II type of gingival recession.[4] Most of these cases of gingival recession may be due to aggressive oral hygiene practices, e.g. tooth brush trauma, phenotypic issues of gingiva or teeth malpositions. Even in these situations, most of gingival recessions are asymptomatic or not perceived by patients limiting the number of the people seeking treatment.[5] Most of our treatment in periodontal arena is based on the pocket reduction/elimination procedures and thus related to treatment of “destructive periodontal disease”. As mentioned earlier, more of periodontal atrophic features are seen in higher age group, leading to more prevalence of gingival recession in aging population. But the fact that both of the disease forms (destructive as well as atrophic) at this age group are termed periodontitis.[2] The difficult/untreatable situation of the atrophic changes at this age, because of the interproximal loss, also puts a question mark on the lack of attempt to find a solution to gingival recessions in the areas other than anterior regions. Gingival recession in 2017 classification was defined as “an apical shift of the gingival margin caused by different conditions/pathologies. It is associated with clinical attachment loss. This may apply to all surfaces (buccal/lingual/interproximal).”[6] The 2017 classification of periodontal diseases endorsed Cairo’s classification of gingival recession.[6] The new definition of gingival recession identifies and accepts the presence of recession on all aspects of teeth but very astoundingly endorsed a new classification which only records labial/buccal recessions and ignores the gingival recessions present on surfaces other than labial/buccal. The requirement of new gingival recession classification was based on the fact that drawbacks of the most followed classification of gingival recession (Miller’s) had become loud and clear.[7,8] Miller’s classification also had limited application (labial/buccal recessions) and could not be applied to the recessions on other surfaces with gingival recession.[7-9] There were issues with the Miller’s classification application even on the labial/buccal recessions which had inter-proximal bone loss but did not extend to the mucogingival junction (MGJ) could not be categorized.[7,8] However, the recent classification endorsed in 2017[6] has many similar drawbacks as Miller’s classification. The explorative and reliability study carried out by Cairo et al.[3] had inclusion of only labial/facial recessions and after the completion of Phase I therapy. Also the full-mouth plaque score and bleeding scores were less than 15% when recorded at four sites/tooth and detectable cementoenamel junction (CEJ) at the tooth with a recession. It implies this classification can be applied only when the gingival status is healthy and has a detectable CEJ. This also means that at an initial examination of a patient with inflamed gingival tissues, and while recording periodontal parameters, it would be difficult to classify gingival recession. Also, the classification is heavily based on the presence and detection of CEJ and measurement of CAL. Also is the fact that CEJ is not easily noticeable in large number of cases of gingival recessions (because of presences of non-carious cervical lesions) on labial/buccal surfaces and detection of CEJ on proximal aspects may not be a easy proposition. In such a situation where CEJ is not visible, classification of recession with Cairo’s classification becomes extremely challenging. A diagnostic 4X5 matrix was proposed along classification and included the recording of recession type, recession depth, keratinized tissue width, gingival thickness, CEJ (detectable/undetectable), and root surface concavity (presence/absence of cervical step).[6] The interesting aspect is that the consensus report adopts a classification of gingival recession based on the clinical attachment loss[6] but proposes a diagnostic matrix where CEJ detectable or not option has to be recorded. In absence of detectable CEJ, how does one bring this classification under universal and precise applicability? The most important concern and, very difficult to understand, is of limited applicability i.e. only on labial/buccal surfaces. The recession defects can also be associated with interdental papilla only, and can also involve the palatal/lingual aspects. How can the recession observed on surfaces other than labial/buccal be ignored? Not marking recession and only recording attachment loss on surfaces other than labial/buccal can be hugely misleading. Furthermore, attachment loss can also be seen in true pockets without recession. Therefore marking attachment loss without recession can adversely affect the correct determination of prognosis and treatment planning. Cortellini and Bissada[10] state that suboptimal oral hygiene, thin periodontal biotypes and requirement of orthodontic or restorative treatment increases the probability of development or progression of gingival recession. Are these factors which put the patient at risk, only create risk on labial/buccal aspect? Dentin hypersensitivity and carious/non-carious cervical lesions on the exposed root surface are of very common occurrence. Hypersensitivity and root caries may occur on any surface and are not limited only on labial/buccal surfaces. If patients have thin gingival biotypes and mucogingival deformities which puts them at risk of further recession, should that not be recorded on other surfaces? All the concerns and problems seen in patients of gingival recession (aesthetic concern, dentin hypersensitivity, cervical lesions, thin gingival biotypes and mucogingival deformities) are best treated by mucogingival surgical intervention whenever required.[10] Just because the palatal/lingual defects do not cause any aesthetic problems and very many successful treatment modalities have not been developed because of inherent anatomical issues, that does not mean we should ignore recording of gingival recessions on palatal/lingual sides and endorse classifications which only record labial/buccal recessions. The presence of palatal/lingual recession can change the diagnosis, prognosis and treatment plan of a case. The mindset to see gingival recession from only treatment outcome point of view and whether the treatment will result in complete coverage led to incorporation of standard prognostic prediction, depending on the class of recession, is another major shortcoming. The 2017 classification[6] added phenotype descriptions such as gingival thickness, keratinized tissue (KT) width and root surface characteristics, such as, detectability of the CEJ or presence of root steps in the classification system for prognostic prediction. Detection of CEJ is a hugely challenging aspect in most of the cases, especially with the presence of non-carious cervical lesions. The prediction of prognosis incorporated in new classification has drawn its roots from Miller’s classification. The literature has proved beyond doubt that Miller’s prognostic prediction on the basis of type of recession was not successful. The academic expectancy of 100% root coverage does not mean that it will occur. The results of Miller’s classification in periodontal literature have shown that coverage in Classes I and II, range from 9% to 90%.[7] Why every classification of gingival recession should be associated with prediction mechanism? Are all the disease classifications in periodontal literature associated with result prediction? The tendency to include the prognostic prediction of amount of coverage depending upon the type of classification, would have been an excellent idea if all the factors on which treatment prognosis was based on, could be factored in the classification. A lot of adjunctive factors (tooth position, local frenum insertion, to name a few) are related to mucogingival deformities and conditions.[10] All the factors included in the list of “Mucogingival Deformities and Conditions” play a significant role in determining the treatment modality.[10] Other than these factors, patient motivation, maintenance, surgical skills of operator, and many factors which are difficult to incorporate but affect the treatment outcome. Without factoring in all the aspects which affect treatment, how wise is it to predict the treatment outcome just on the basis of a classification? A classification should have the ability to categorize maximium number of cases. A classification which when applied cannot classify majority of the recession defects, is incomplete and will never project the real clinical scenario. A classification of recession should be able to, at least, record maximum number of the recession defects present in the mouth and should not get into the area of speculation and prediction of results till all the factors which can modify results can be assessed. The original and complete information recorded are vitally important for the clinicians to provide better patient care and prevent further loss. The undeniable statistic, that most of the gingival recession occurs as a result of destructive periodontal disease and remains beyond the realm of focus for the reasons known to everyone, should not be forgotten. One has to think critically about the growing overemphasis on the treatment of gingival recession for a very small cohort of patients limited to anterior regions. Efforts should also get directed to manage gingival recessions for nonaesthetic reasons and in non-aesthetic areas. We need to keep in mind that the economics of periodontal therapy, as of now, is primarily reliant on abnormal pocket depth and not gingival recession, as most of the treatments are aimed at reducing pocket depths. Creating successful treatment options for gingival recessions in areas other than anterior regions, could open up another channel of economics for periodontal therapy.

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