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 is a complication that could account for significant interference during the early healing phase of dental implants. Spontaneous perforations of the mucosa covering implants have been classified according to the degree of implant exposure from 0 (no perforation) to IV (complete exposure). In this study, the characteristics of the epithelium and connective tissue of clinically non-perforated mucosa over submerged implants are histologically and histomorphometrically evaluated. METHODS: Ten randomly selected tissue disks of intact (Class [Cl]-0) mucosa covering submerged implants were removed using a biopsy punch. Identical mucosal punch specimens were obtained from edentulous sites treated by non-submerged (1-stage) implants for use as controls. Specimens were histopathologically examined. The epithelial width and inflammatory infiltrate adjacent to the epithelium were histomorphometrically measured and the data statistically analyzed. RESULTS: Non-perforated mucosa covering the submerged implants (Cl-0) was characterized by an inflammatory fibro-epithelial hyperplasia. In 70% of Cl-0 hematoxylin and eosin-stained sections, there was mineralized material in the connective tissue, mostly sequestra. The epithelial width was 1.5 times higher (0.553 +/- 0.187 mm) when compared to controls (0.345 +/- 0.129 mm; P <0.0001). Concomitantly, the chronic inflammatory infiltrate was almost double in Cl-0 specimens (1,411 +/- 617 cell/mm2) when compared to controls (833 +/- 275 cells/mm2; P<0.001). A positive correlation between the linear combination of the epithelial width and the linear combination of the inflammatory cell concentration was found in both groups: Cl-0: r = 0.669, P= 0.0001; control: r = 0.541, P= 0.005. CONCLUSIONS: Different factors may result in the formation of spontaneous early perforation, most of which are associated with mechanical trauma to the mucosa or tension in the tissue flaps covering the implants. Bone debris produced during the osteotomy could act as an additional predisposing factor; these are sequestrated and accompanied by chronic inflammatory cell infiltration as well as epithelial-covering reaction. Since this study focused only on specimens from intact mucosa, until further investigation of this phenomenon in spontaneously perforated sites is conducted, no conclusions on the role of these histopathological findings can be made.
BACKGROUND: Spontaneous early exposure is a complication that could account for significant interference during the early healing phase of dental implants. Spontaneous perforations of the mucosa covering implants have been classified according to the degree of implant exposure from 0 (no perforation) to IV (complete exposure). In this study, the characteristics of the epithelium and connective tissue of clinically non-perforated mucosa over submerged implants are histologically and histomorphometrically evaluated. METHODS: Ten randomly selected tissue disks of intact (Class [Cl]-0) mucosa covering submerged implants were removed using a biopsy punch. Identical mucosal punch specimens were obtained from edentulous sites treated by non-submerged (1-stage) implants for use as controls. Specimens were histopathologically examined. The epithelial width and inflammatory infiltrate adjacent to the epithelium were histomorphometrically measured and the data statistically analyzed. RESULTS: Non-perforated mucosa covering the submerged implants (Cl-0) was characterized by an inflammatory fibro-epithelial hyperplasia. In 70% of Cl-0hematoxylin and eosin-stained sections, there was mineralized material in the connective tissue, mostly sequestra. The epithelial width was 1.5 times higher (0.553 +/- 0.187 mm) when compared to controls (0.345 +/- 0.129 mm; P <0.0001). Concomitantly, the chronic inflammatory infiltrate was almost double in Cl-0 specimens (1,411 +/- 617 cell/mm2) when compared to controls (833 +/- 275 cells/mm2; P<0.001). A positive correlation between the linear combination of the epithelial width and the linear combination of the inflammatory cell concentration was found in both groups: Cl-0: r = 0.669, P= 0.0001; control: r = 0.541, P= 0.005. CONCLUSIONS: Different factors may result in the formation of spontaneous early perforation, most of which are associated with mechanical trauma to the mucosa or tension in the tissue flaps covering the implants. Bone debris produced during the osteotomy could act as an additional predisposing factor; these are sequestrated and accompanied by chronic inflammatory cell infiltration as well as epithelial-covering reaction. Since this study focused only on specimens from intact mucosa, until further investigation of this phenomenon in spontaneously perforated sites is conducted, no conclusions on the role of these histopathological findings can be made.