H Tal1, D Dayan. 1. Department of Periodontology, The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Israel.
Abstract
BACKGROUND: Spontaneous early exposure of dental implants could interfere with the early healing phase of dental implants. These exposures have been clinically classified according to degree of implant exposure from 0 (intact mucosa) to IV (complete exposure). The characteristics of perforated mucosa (Class I and II) covering submerged dental implants were examined histologically in this study. METHODS: Biopsy specimens of 34 Class I and II perforated mucosa covering submerged dental implants were examined histologically. Serial sections were evaluated from the periphery of the specimen to the center of each perforation lesion. RESULTS: Class I specimens presented hyperplastic epithelium characterized by hyperparakeratosis and acanthosis. Chronic inflammatory cells diffusely infiltrated the connective tissue. Sections closer to the perforation revealed gradual epithelial invagination; in the deepest aspect, there was a cyst-like structure in all Class I specimens examined. A thin layer of connective tissue containing necrotic material and debris formed the "cystic" wall proximal to the implant cover screw. Class II specimens presented the same epithelial patterns; however, the cystic structures were replaced by direct contact between the cover screw and the oral cavity via the perforation. CONCLUSIONS: Spontaneous early perforations are the sequela of either traumatic irritation or failure of the tissue flaps to produce primary healing. Most Class I perforations include epithelial invagination and the formation of a cyst-like structure. Necrosis of the base of the "cyst" or enlargement of the perforation results in direct communication between the oral cavity and the covering screw surface (Class II).
BACKGROUND: Spontaneous early exposure of dental implants could interfere with the early healing phase of dental implants. These exposures have been clinically classified according to degree of implant exposure from 0 (intact mucosa) to IV (complete exposure). The characteristics of perforated mucosa (Class I and II) covering submerged dental implants were examined histologically in this study. METHODS: Biopsy specimens of 34 Class I and II perforated mucosa covering submerged dental implants were examined histologically. Serial sections were evaluated from the periphery of the specimen to the center of each perforation lesion. RESULTS: Class I specimens presented hyperplastic epithelium characterized by hyperparakeratosis and acanthosis. Chronic inflammatory cells diffusely infiltrated the connective tissue. Sections closer to the perforation revealed gradual epithelial invagination; in the deepest aspect, there was a cyst-like structure in all Class I specimens examined. A thin layer of connective tissue containing necrotic material and debris formed the "cystic" wall proximal to the implant cover screw. Class II specimens presented the same epithelial patterns; however, the cystic structures were replaced by direct contact between the cover screw and the oral cavity via the perforation. CONCLUSIONS: Spontaneous early perforations are the sequela of either traumatic irritation or failure of the tissue flaps to produce primary healing. Most Class I perforations include epithelial invagination and the formation of a cyst-like structure. Necrosis of the base of the "cyst" or enlargement of the perforation results in direct communication between the oral cavity and the covering screw surface (Class II).