periodontal staging and grading system as a prognostic factor for future tooth loss: a long‐term retrospective study. J Periodontol 2020; 91(4):454–461.
7 7. Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri‐implant Diseases and Conditions. J Clin Periodontolol 2018; 45(Suppl 20):S68–S77.
8 8. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: framework and proposal of a new classification and case definition. J Periodontol 2018; 89(Suppl 1):S159–S172.
9 9. Duarte PM, Bastos MF, Fermiano D, et al. Do subjects with aggressive and chronic periodontitis exhibit a different cytokine/chemokine profile in the gingival crevicular fluid? A systematic review. J Periodontal Res 2015; 50(1):18–27.
10 10. Montenegro SCL, Retamal‐Valdes B, Bueno‐Silva B, et al. Do patients with aggressive and chronic periodontitis exhibit specific differences in the subgingival microbial composition? A systematic review. J Periodontol 2020; 91(11):1503–1520.
11 11. Claffey N, Nylund K, Kiger R, et al. Diagnostic predictability of scores of plaque, bleeding, suppuration and probing depth for probing attachment loss: 3½ years of observation following initial periodontal therapy. J Clin Periodontol 1990; 17:108–114.
12 12. Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding on probing. An indicator of periodontal stability. J Clin Periodontol 1990; 17:714–721.
13 13. Matuliene G, Pjetursson BE, Salvi GE, et al. Influence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance. J Clin Periodontol 2008; 35(8):685–695.
14 14. Feres M, Retamal‐Valdes B, Faveri M, et al. Proposal of a clinical endpoint for periodontal trials: the treat‐to‐target approach. J Int Acad Periodontol 2020; 22(2):41–53.
15 15. Loos BG, Needleman I. Endpoints of active periodontal therapy. J Clin Periodontol 2020; 47(Suppl 22):61–71.
16 16. Hung HC, Douglass CW. Meta‐analysis of the effect of scaling and root planing, surgical treatment and antibiotic therapies on periodontal probing depth and attachment loss. J Clin Periodontol 2002; 29:975–986.
17 17. Heitz‐Mayfield LJ, Trombelli L, Heitz F, et al. A systematic review of the effect of surgical debridement vs non‐surgical debridement for the treatment of chronic periodontitis. J Clin Periodontol 2002; 29(Suppl 3):92–102; discussion 160–162.
18 18. Jepsen S, Caton JG, Albandar JM, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: consensus report of workgroup 3 of the 2018 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions. J Clin Periodontol 2018; 45(Suppl 20):S219–S229.
19 19. Mongardini C, van Steenberghe D, Dekeyser C, Quirynen M. One stage full‐versus partial‐mouth disinfection in the treatment of chronic adult or generalized early‐onset periodontitis. I. Long‐term clinical observations. J Periodontol 1999; 70:632–645.
20 20. Claffey N, Egelberg J. Clinical indicators of probing attachment loss following initial periodontal treatment in advanced periodontitis patients. J Clin Periodontol 1995; 22:690–696.
21 21. Nyman S, Rosling B, Lindhe J. Effect of professional tooth cleaning on healing after periodontal surgery. J Clin Periodontol 1975; 2:80–86.
TAKE‐HOME POINTS
A. Incidental loss of attachment associated with mechanical trauma has distinct clinical features that make it clearly distinguishable from infection/inflammation‐induced attachment loss. It tends to be circumscribed to buccal surfaces, particularly in areas of a very thin soft tissue, and the neighboring papilla present normal height. The tissue surrounding the recession has a very healthy appearance, and it is not uncommon to have toothbrush abrasion associated with the gingival recession. The collapse of gingival tissues on buccal surfaces can also be associated with marginal gingival inflammation, but in this case the presence of plaque and calculus is not an uncommon finding and the tissues surrounding the gingival recession tend to show clinical signs of inflammation.
B. The distinction between the two diagnoses can be difficult at times. The differences are typically determined by the age of onset, rate of progression, and the patterns of bone loss. In general, periodontitis starts at age 30–35 years and progresses in random bursts in different sites throughout life. If the disease presents in younger patients or can be documented to have occurred in a short period, it tends to be classified as of more aggressive nature, increasing the grading of the case for periodontitis, or considering the possibility of a systemic disease that may have major impact on periodontal tissues. Both forms of periodontitis can occur in a localized or generalized pattern. Familial aggregation is one of the features of many forms of aggressive patterns of periodontitis; therefore, if this is suspected, the clinician should inquire about the periodontal status of close relatives or suggest they receive an oral examination. Many common chronic diseases, such as diabetes, may affect the course of periodontitis, or at least are intrinsically associated with it, but do not necessarily have a distinguishable phenotype, and thus the diagnosis still is of periodontitis. However, a careful review of the medical history is imperative, including referral for further evaluations or consultations for any systemic comorbidities, including rare medical disorders that may have major impact on the periodontal tissues. Those medical evaluations should confirm the periodontal diagnosis and direct the treatment plan. Because of the much higher prevalence of periodontitis compared with other aggressive forms associated with rare systemic diseases, this will be the most prevalent diagnosis, but the potential for the latter should not be dismissed [18].
C. Although it is not the intent here to address therapy, which is discussed extensively in other chapters of the book, the relevance of the distinction between different aggressive forms of periodontitis, especially considering the grading system of the new classification, depends on the assumption that these clinical forms of the disease would require specific types of treatment. Classical literature has indicated that subjects with different aggressive forms of periodontitis (aggressive forms compared to “chronic periodontitis” in previous classifications) with comparable extent and severity of the conditions tend to respond similarly to periodontal therapy [19]. This would imply that the prognosis of the case would depend more on the extent and severity (staging) of the periodontal disease, and also the progression and risk factors associated with it (grading). Therefore, the new classification system could be helpful in establishing different treatment protocols according to the combination of the findings already discussed. A general dentist should be especially mindful in consulting a periodontist whenever the diagnosis reaches stage III or grade B, and potentially other dental and healthcare providers the diagnosis reaches stage IV or grade C, or if the case presents with other signs of potential aggressiveness or major complexity.
D. In these circumstances, the clinician should confirm the grading of the case, ruling out any systemic causes for the disease (risk factors such as smoking or uncontrolled diabetes, immunocompromise, endocrine disorders, or syndromes). The next thing to check is the efficiency of the patient’s plaque control. This can be easily ascertained by the gingival and plaque indices. In the presence of large amounts of plaque, reinfection of pockets occurs fast and healing is compromised. Once the level of oral hygiene of the patient has been assessed, provided it was not the problem, the next steps will depend greatly on the level of periodontal training of the therapist. If the clinician is an experienced periodontist, the chances are that therapy was properly executed and there is very little room for improvement. The clinician might be dealing with a rare case of refractory periodontitis, where the subject does not respond to conventional therapy. The next step would be to consider adjunctive or complementary approaches such as systemic antibiotics and/or periodontal surgery. If a less experienced clinician is involved, the fair assumption is there was failure in calculus removal to a level compatible with resolution of the periodontal condition. Particularly for severe generalized forms (higher staging) of the disease this should not be a surprise because subgingival debridement