Clinical Cases in Periodontics. Группа авторов

      The treatment plan for a typical case of molar/incisor pattern periodontitis consists of the following phases.

       The diagnostic phase consists of a comprehensive periodontal examination, radiographs and study models. In some cases, microbial testing and genetic testing can be performed.

       The disease control phase includes oral hygiene instruction, splinting of mandibular incisors and scaling/root planing of all the affected areas with adjunctive systemic antibiotics (amoxicillin and metronidazole combination). Extractions of all the third molars can be included in this phase.

       The reevaluation phase consists of revisiting her probing pocket depths and her overall periodontal condition plus treatment planning for sites that did not improve after the initial phase of therapy or those that warrant further treatment.

       The sites that need further treatment can be treated surgically.

       Guided tissue regeneration or bone grafts with enamel matrix protein is commonly employed to treat the intrabony defects associated with molars.

       After surgical phase, the sites will again be evaluated for improvement in the periodontal condition.

       Once the periodontal condition is stabilized, patient will be placed on a three‐ to six‐month maintenance protocol.

Discussion

Following the 2017 World Workshop on the Classification of Periodontal and Peri‐implant Diseases and Conditions, the previous classification of chronic periodontitis and aggressive periodontitis was amended so that now they are grouped under a single category – “periodontitis” [1]. With the new 2017 classification system, grading estimates the aggressiveness of the disease by focusing on the factors contributing to progression rather than previously focusing on the identification of a form of periodontitis. The characteristic clinical and radiographic features associated with molar/incisor pattern periodontitis allow the oral healthcare provider to diagnose the condition without much difficulty. The case that we present in this book chapter exhibited the classical clinical and radiographic features of molar/incisor pattern periodontitis, including age of onset of disease, the pattern of disease progression and aggressiveness in clinical attachment loss. Stage III was determined after considering both severity (including interdental attachment loss ≥5 mm and bone loss beyond more than middle third of root) and complexity (including probing depths ≥6 mm with vertical bone loss ≥3 mm). Grade C was due to the high risk of progression. Therefore a diagnosis of molar/incisor pattern stage III grade C periodontitis was made. In some cases, microbiological and immunological tests can be used as an adjunct to diagnose this disease. Increased levels of Aggregatibacter actinomycetemcomitans (especially serotype b) microbes and a robust antibiotic response to the same microorganism are expected in such testing. After completing phase 1 therapy consisting of scaling and root planing with adjunctive use of systemic antibiotics, a drastic improvement in probing depth reduction and clinical attachment gain are expected in deeper pockets. Residual pockets (>6 mm) remaining after phase 1 therapy will be usually treated with surgical periodontal therapy. Adequate oral hygiene is critical in the successful outcome of any periodontal therapy. Usually patients with molar/incisor pattern periodontitis tend to exhibit insignificant amounts of local factors such as plaque and calculus and tend to have good oral hygiene. In the case described in this chapter, the patient had insignificant amounts of local factors (Figures 1.5.1–1.5.5). With respect to outcomes of surgeries performed in patients with molar/incisor pattern periodontitis, long‐term stability after regenerative therapy has been shown. The success rates of dental implants in patients with molar/incisor pattern periodontitis are inconclusive. Some studies have indicated that the success rates in these patients are slightly lower (<10%) than in patients with grade A or B periodontitis [2,3].

      Self-Study Questions

      1 How do you define molar/incisor pattern periodontitis and how do you classify it?

      2 What are the other terms used to describe molar/incisor pattern periodontitis?

      3 What are the characteristic presentations common to molar/incisor pattern grade C periodontitis and generalized grade C periodontitis?

      4 What are the features that distinguish molar/incisor pattern grade C periodontitis from generalized grade C periodontitis?

      5 How common is molar/incisor pattern periodontitis and which sector of the population is more susceptible to this disease?

      6 What are the etiologic agents responsible for molar/incisor pattern periodontitis?

      7 How do you treat patients with molar/incisor pattern periodontitis?

      8 In molar/incisor pattern periodontitis patients what will be the prognosis after treatment?

References

      1 1. Caton JG, Armitage G, Berglundh T, et al. A new classification scheme for periodontal and peri-implant diseases and conditions. Introduction and key changes from the 1999 classification. J Periodontol 2018; 89(Suppl 1):S1–S8.

      2 2. De Boever AL, Quirynen M, Coucke W, et al. Clinical and radiographic study of implant treatment outcome in periodontally susceptible and non-susceptible patients: a prospective long-term study. Clin Oral Implants Res 2009; 20:1341–1350.

      3 3. Al-Zahrani MS. Implant therapy in aggressive periodontitis patients: a systematic review and clinical implications. Quintessence Int 2008; 39:211–215.

      4 4. Meng H, Xu L, Li Q, et al. Determinants of host susceptibility in aggressive periodontitis. Periodontol 2000 2007; 43:133–159.

      5 5. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999; 4:1–6.

      6 6. Brown LJ, Albandar JM, Brunelle JA, Loe H. Early-onset periodontitis: progression of attachment loss during 6 years. J Periodontol 1996; 67:968–975.

      7 7. Orban B. A diffuse atrophy of the alveolar bone (periodontosis). J Periodontol 1942; 13:31.

      8 8. Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971; 42:516–520.

      9 9. Lang N, Bartold PM, Cullinan M, et al. Consensus report: aggressive periodontitis. Ann Periodontol 1999; 4:53.

      10 10. Benjamin SD, Baer PN. Familial patterns of advanced alveolar bone loss in adolescence (periodontosis). Periodontics 1967; 5:82–88.

      11 11. Kantarci A, Oyaizu K, Van Dyke TE. Neutrophil‐mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis. J Periodontol 2003; 74:66–75.

      12 12. Fredman G, Oh SF, Ayilavarapu S, et al. Impaired phagocytosis in localized aggressive periodontitis: rescue by Resolvin E1. PLoS One 2011; 6:e24422.

      13 13. Shaddox L, Wiedey J, Bimstein E, et al. Hyper‐responsive phenotype in localized aggressive periodontitis. J Dent Res 2010; 89:143–148.

      14 14. Fine DH, Armitage GC, Genco RJ, et al. Unique etiologic, demographic, and pathologic characteristics of localized aggressive periodontitis support classification as a distinct subcategory of periodontitis. J Am Dent Assoc 2019; 150:922–931.

      15 15. Loe H, Brown LJ. Early onset periodontitis in the United States of America. J Periodontol 1991; 62:608–616.

      16 16. Albandar JM, Muranga MB, Rams TE. Prevalence of aggressive periodontitis in school attendees in Uganda. J Clin Periodontol 2002; 29:823–831.

      17 17. Miller K, Treloar T, Guelmann M, et al. Clinical characteristics of localized aggressive periodontitis in primary dentition. J Clin Pediatr Dent 2018; 42:95–102.

      18 18. Merchant SN, Vovk A, Kalash D, et al. Localized aggressive periodontitis treatment response in primary and permanent dentitions. J Periodontol