Periodontics. Fernando Suarez

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      Fig 3-4 (a to f) Periodontitis (formerly referred to as aggressive periodontitis).

      Nevertheless, chronic and aggressive periodontitis share many similarities, and the latest classification from the 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions refuted the presence of enough evidence to support the distinction between aggressive and chronic periodontitis as two separate diseases. This recent report emphasized the phenotypic differences between both entities, and more specifically, between chronic and localized aggressive periodontitis (including age of onset, location of initial lesions, and rate of progression). However, it also reiterated that both represent inflammatory diseases responding to biofilm accumulation, and it is premature to describe pathophysiologic differences until further data in larger and more controlled studies is available. In addition, both chronic and localized aggressive periodontitis have a common end result.⁶² Hence, it was concluded that while there are significant variations with regard to clinical presentations, the currently available evidence does not support the distinction between chronic and aggressive periodontitis as two separate diseases.¹

      Periodontitis as a Manifestation of Systemic Diseases

      Several systemic diseases and conditions can affect the periodontium and cause its destruction. Most of these disorders or conditions are secondary to innate mechanisms, although some are acquired through lifestyles or environmental factors. The periodontal effects of these systemic diseases and conditions are mainly through their influence on the immune and inflammatory responses. In addition, these can affect the periodontium by either influencing the course of periodontitis or by affecting the supporting tissues independently of plaque-induced inflammation.⁷⁵ Albandar et al⁷⁵ classified those diseases and conditions into three main categories. The first includes systemic disorders with a major impact on the loss of periodontal tissue by influencing periodontal inflammation. These disorders include genetic disorders (eg, Down syndrome), acquired immunodeficiency diseases (eg, HIV infection), and inflammatory diseases (eg, arthritis). The second category describes systemic disorders that influence the pathogenesis of periodontal diseases contributing to periodontal tissue loss (eg, smoking, depression). Last, the third category describes disorders that can cause destruction of the periodontal attachment independent of plaque-induced periodontitis (eg, neoplasms).⁷⁵

      Most of these conditions are determined by the genotype of the host, and they may be modified by environmental and behavioral factors. In addition, periodontitis and certain systemic disorders may share similar genetic and/or environmental risk factors. Consequently, loss of periodontal attachment is a common manifestation of several systemic disorders, which could have an important therapeutic and diagnostic value.

      Necrotizing Periodontal Diseases

      Necrotizing periodontal diseases belong to a group of acute lesions occurring in the periodontium and can be divided into necrotizing gingivitis (formerly referred to as necrotizing ulcerative gingivitis) and necrotizing periodontitis (formerly referred to as necrotizing ulcerative periodontitis).⁷⁶ Currently available evidence suggests that given the similar etiology, clinical features, and treatment, these entities may represent different stages of the same disease and may even progress to more severe forms such as necrotizing stomatitis and noma.⁷⁶

      Necrotizing periodontal diseases are associated with impairment in the host immune response and typically present with three clinical features: papilla necrosis, pain, and bleeding. Other signs and symptoms may include halitosis, pseudomembranes, regional lymphadenopathy, fever, sialorrhea, and rapid bone loss in cases of necrotizing periodontitis. Necrotizing stomatitis is a more severe inflammatory condition that courses with soft tissue necrosis beyond the gingiva, osteitis, and bone sequestrum.¹

      Similar to other forms of periodontitis, the etiology of necrotizing periodontal diseases is a bacterial infection; however, several other predisposing factors and immune-related conditions play a role in the pathogenesis.⁷⁶

      References

      1. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol 2018;89(suppl 1):S173–S182.

      2. Lilienfeld DE. Definitions of epidemiology. Am J Epidemiol 1978;107:87–90.

      3. Trombelli L, Farina R, Silva CO, Tatakis DN. Plaque-induced gingivitis: Case definition and diagnostic considerations. J Periodontol 2018;89(suppl 1):S46–S73.

      4. American Academy of Periodontology. Glossary of Periodontal Terms. American Academy of Periodontology, 2001.

      5. Lang NP, Bartold PM. Periodontal health. J Periodontol 2018;89(suppl 1):S9–S16.

      6. Russell AL. Epidemiology and the rational base of dental public health and dental practice. In: Young WO (ed). The Dentist, His Practice, and His Community, ed 2. Philadelphia: Saunders, 1969.

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      9. Burt BA, Eklund SA. The methods of oral epidemiology. In: Burt BA, Eklund SA (eds). Dentistry, Dental Practice, and the Community, ed 4. Philadelphia: Saunders, 1992.

      10. Löe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533–551.

      11. Ainamo J, Bay I. Problems and proposals for recording gingivitis and plaque. Int Dent J 1975;25:229–235.

      12. Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condtion. Acta Odontol Scand 1964;22:121–135.

      13. O’Leary TJ, Drake RB, Naylor JE. The plaque control record. J Periodontol 1972;43:38.

      14. Russell AL. A system of classification and scoring for prevalence surveys of periodontal disease. J Dent Res 1956;35:350–359.

      15. Ramfjord SP. Indices for prevalence and incidence of periodontal disease. J Periodontol 1959;30:51–59.

      16. Schei O, Waerhaug J, Lovdal A, Arno A. Alveolar bone loss as related to oral hygiene and age. J Periodontol 1959;30:7–16.

      17. Ainamo J, Barmes D, Beagrie G, Cutress T, Martin J, Sardo-Infirri J. Development of the World Health Organization (WHO) community periodontal index of treatment needs (CPITN). Int Dent J 1982;32:281–291.

      18. Eke PI, Thornton-Evans GO, Wei L, Borgnakke WS, Dye BA, Genco RJ. Periodontitis in US Adults: National Health and Nutrition Examination Survey 2009–2014. J Am Dent Assoc 2018;149:576–588.

      19. Albandar JM, Brown LJ, Brunelle JA, Löe H. Gingival state and dental calculus in early-onset periodontitis. J Periodontol 1996;67:953–959.

      20. Kingman A, Albandar JM. Methodological aspects of epidemiological studies of periodontal diseases. Periodontology 2000 2002;29:11–30.