Clinical Cases in Periodontics. Группа авторов

Figure 1.4.4 Periapical radiographs depicting the interproximal bone levels.

Discussion

      Most patients who have gingival enlargement present with the chief complaint of an unesthetic smile. Comprehensive medical and dental histories (A) as well as a complete periodontal examination are needed to come to the appropriate diagnosis. Most commonly, gingival enlargement is a dental plaque‐induced gingival condition modified by medications such as phenytoin, cyclosporine, or calcium channel blockers [1]. In some rare cases, a non‐plaque‐induced gingival enlargement called hereditary gingival fibromatosis (A) may be seen.

      Once the diagnosis is determined, the treatment plan includes oral hygiene instructions, an initial phase of treatment (scaling and polishing), and communication with the primary care physician for potential alternative medication to address the systemic condition (G). Phase 1 therapy is followed by periodontal reevaluation at four to six weeks. If the gingival enlargement persists at this visit, surgical excision of excessive gingiva is recommended with subsequent reinforcement of home care oral hygiene and a periodontal maintenance every three months is instituted (G).

      In a recent case report, Capodiferro et al. [2] showed that nonsurgical periodontal treatment by an Er:YAG laser also promoted regression of gingival overgrowth in patients taking cyclosporine.

      Self-Study Questions

      1 What is the etiology for gingival enlargement? What questions in a dental history might help you begin to form a differential diagnosis?

      2 What are the characteristics of drug-induced gingival enlargement?

      3 How would you differentiate between a “true” periodontal pocket and a “pseudo-pocket”?

      4 D. What are the clinical characteristics that distinguish gingival enlargement versus periodontitis?

      5 What is the pathogenesis of gingival enlargement?

      6 What is another reason for a short clinical crown?

      7 What is the current treatment for patients with drug-induced gingival enlargement? What is the long-term prognosis with treatment for these patients?

      Answers located at the end of the chapter.

References

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      2 2. Capodiferro S, Tempesta A, Limongelli L, et al. Nonsurgical periodontal treatment by erbium:YAG laser promotes regression of gingival overgrowth in patient taking cyclosporine A: a case report. Photobiomodul Photomed Laser Surg 2019; 37:53–56.

      3 3. Caton JG Jr, Rees T, Pack A, et al. Consensus report: Non‐plaque‐induced gingival lesions. Ann Periodontol 1999; 4:30–31.

      4 4. Hart TC, Pallos D, Bozzo L, et al. Evidence of genetic heterogeneity for hereditary gingival fibromatosis. J Dent Res 2000; 79:1758–1764.

      5 5. Hart TC, Zhang Y, Gorry MC, et al. A mutation in the SOS1 gene causes hereditary gingival fibromatosis type 1. Am J Hum Genet 2002; 70:943–954.

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      7 7. Dreizen S, McCredie KB, Keating MJ. Chemotherapy‐associated oral hemorrhages in adults with acute leukemia. Oral Surg Oral Med Oral Pathol 1984; 57:494–498.

      8 8. Mariotti A. Dental plaque‐induced gingival diseases. Ann Periodontol 1999; 4:7–19.

      9 9. Listgarten MA. Periodontal probing: what does it mean? [review]. J Clin Periodontol 1980; 7:165–176.

      10 10. Trackman PC, Kantarci A. Connective tissue metabolism and gingival overgrowth. Crit Rev Oral Biol Med 2004; 15;165–175.

      11 11. Black SA Jr, Palamakumbura AH, Stan M, Trackman PC. Tissue‐specific mechanisms for CCN2/CTGF persistence in fibrotic gingiva: interactions between cAMP and MAPK signaling pathways, and prostaglandin E2‐EP3 receptor mediated activation of the c‐JUN N‐terminal kinase. J Biol Chem 2007; 282:15416–15429.

      12 12. Kantarci A, Black SA, Xydas CE, et al. Epithelial and connective tissue cell CTGF/CCN2 expression in gingival fibrosis. J Pathol 2006; 210:59–66.

      13 13. Uzel MI, Kantarci A, Hong HH, et al. Connective tissue growth factor in drug‐induced gingival overgrowth. J Periodontol 2001; 72:921–931.

      14 14. Kantarci A, Augustin P, Firatli E, et al. Apoptosis in gingival overgrowth tissues. J Dent Res 2007; 86:888–892.

      15 15. Volchansky A, Cleaton‐Jones P. Delayed passive eruption: a predisposing factor to Vincent’s infection. J Dent Assoc S Africa 1974; 29:291–294.

      16 16. Volchansky A, Cleaton‐Jones P. The position of the gingival margin as expressed by clinical crown height in children ages 6–16 years. J Dent 1975; 4:116–122.

      17 17. Goldman HM, Cohen DW. Periodontal Therapy, 4th edn. St. Louis, MO: Mosby, 1968.

      18 18. Marshall RI, Bartold PM. A clinical review of drug‐induced gingival overgrowths. Aust Dent J 1999; 44:219–232.

      19 19. Hall EE. Prevention and treatment considerations in patients with drug‐induced gingival enlargement. Curr Opin Periodontol 1997; 4:59–63.

      20 20. Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal therapy in patients with drug‐induced gingival overgrowth. Long‐term results. J Periodontol 1999; 70:967–972.

      21 21. Ciancio SG, Bartz NW Jr, Lauciello FR. Cyclosporine‐induced gingival hyperplasia and chlorhexidine: a case report. Int J Periodontics Restorative Dent 1991; 11:241–245.

      22 22. Prasad VN, Chawla HS, Goyal A, et al. Folic acid and phenytoin induced gingival overgrowth: is there a preventive effect? J Indian Soc Pedod Prev Dent 2004; 22:82–91.

      23 23. Chand DH, Quattrocchi J, Poe SA, et al. Trial of metronidazole vs. azithromycin for treatment of cyclosporine‐induced gingival overgrowth. Pediatr Transplant 2004; 8:60–64.

      TAKE‐HOME POINTS

      A. Gingival overgrowth or enlargement is a common side effect and unwanted outcome of certain systemic medications. Drug‐influenced gingival enlargement refers to an abnormal growth of the gingiva secondary to use of systemic medication and is classified by the 2017 World Workshop as a form of dental plaque‐induced gingival disease modified by medications [1]. Currently three pharmaceutical categories of medication (anticonvulsants, immunosuppressants, and calcium channel blockers) are associated with gingival enlargement. However, a strong association has been noted only with phenytoin (when used in a chronic regimen to control epileptic seizures), cyclosporine (powerful immunoregulator drug primarily used in the prevention of organ transplant rejection), and nifedipine (commonly prescribed as an antihypertensive, antiarrhythmic, and antianginal agent). The prevalence of gingival overgrowth varies widely: the prevalence related to use of phenytoin is approximately 50%, whereas cyclosporine and nifedipine produce significant gingival changes in about 25% of the patients treated.

      Among the non‐plaque‐induced gingival lesions, gingival fibromatosis of genetic origin has been also described as associated with gingival overgrowth [3]. Hereditary gingival fibromatosis (HGF) is an uncommon disorder that can occur as an isolated finding or as part of a genetic syndrome. HGF is most frequently reported to be transmitted as an autosomal dominant trait, but autosomal recessive inheritance has also been reported [4]. The clinical presentation of HGF is variable, both in the distribution (number of teeth involved)