Guided bone regeneration of a pronounced gingivo-alveolar cleft due to orthodontic space closure.

BACKGROUND: Gingival invagination is a relatively common occurrence following orthodontic closure of extraction sites. The present paper reports a combined periodontal and orthodontic treatment in a patient with a severe gingivo-alveolar cleft due to orthodontic closure of maxillary central incisor extraction space. METHODS: A definite interdental gingival cleft, extending 8 mm into the alveolar bone, required the correction of the gingival deformity as a first step, followed by guided bone regeneration (GBR). The GBR approach included the emptying of the incisive foramen to approximately 5 mm in depth followed by the insertion of bioabsorbable hydroxyapatite and covering with a bioabsorbable barrier membrane. Six months afterward, the orthodontic therapy was resumed. RESULTS: Radiographs and clinical examination 4 years after the completion of therapy indicates functionally and aesthetically satisfactory and stable results. CONCLUSION: The present paper illustrates an additional application for the guided bone regeneration technique.

Quantification and localization of platelet-derived growth factor in gingiva of periodontitis patients.

BACKGROUND: Platelet-derived growth factor (PDGF) is a mitogen and chemoattractant for cells of mesenchymal origin. Over-expression of PDGF-B can promote formation of inflammatory lesions in the lungs of transgenic mice. Moreover, continuous exposure to PDGF inhibits collagen production by osteoblastic cells. Thus, the expression of mitogenic factors in an inflammatory context may limit the differentiated function of cells, and thereby limit repair following periodontal attachment and bone loss. The goals of the present study were to test whether PDGF is present at increased levels in inflamed gingiva and to localize its expression in gingival biopsies from individuals with chronic periodontitis. METHODS: Tissues obtained during therapeutic procedures from inflamed and control sites of 9 patients were subjected to protein extraction, descriptive histology by hematoxylin and eosin, or immunohistochemistry assays. Quantification was calculated with an enzyme-linked immunosorbent assay (ELISA) kit specific for PDGF-AB. For the immunolocalization, anti-PDGF-A and -B antibodies were employed. RESULTS: PDGF concentration in the total protein extract was approximately 3 times higher in the inflamed sites (0.60 +/- 0.18 ng/mg versus 0.20 +/- 0.05 ng/mg; P = 0.03). Immunohistochemistry revealed prominent expression of PDGF in the pocket epithelial cells as well as the adjacent connective tissue. In contrast, little or no expression was detected in control biopsies devoid of the pocket epithelium and granulation tissue. CONCLUSIONS: PDGF is present in increased levels in the human inflamed gingiva and is mainly localized to the pocket epithelium. It is possible that chronic expression of PDGF contributes to the inflammatory changes that occur during periodontal diseases.