This study evaluated the use of tricalcium phosphate (TCP) ceramic implant material in periodontal osseous defects. Thirteen defects in two patients were treated with mucoperiosteal flaps and placement of TCP. The defects were evaluated clinically and radiographically utilizing standardized probe placement and radiographic technique. Clinically, there was a mean probing pocket reduction of 4.5 mm as a result of a mean gain of clinical probing attachment level of 2.0 mm and a mean gingival recession of 2.5 mm. Radiographically, there was a mean "fill" of 1.8 mm. Six teeth were removed by block biopsy for histologic analysis, three at 3 months, one at 6 months and two a 9 months. The TCP particles were well tolerated and encapsulated by fibrous connective tissue, but the particles did not stimulate new bone growth. The junctional epithelium ended 1.62 mm coronal to the apical extent of a reference notch placed at the base of the defect. Although new cementum was observed, there was limited evidence of new attachment.

Twenty-four patients receiving comprehensive orthognathic care including genioplasty were studied to evaluate the effect of orthognathic treatment on the mucogingival complex in the mandibular anterior region. Parameters measured prior to and after therapy were: width of keratinized gingiva, width of attached gingiva and gingival recession. A subjective assessment of tissue thickness was accomplished. A statistically significant decrease in width of both keratinized and attached gingiva was noted following orthognathic therapy in the mandibular anterior area. In six of 24 patients, gingival recession was a clinically significant finding. The actual pretreatment width of keratinized and/or attached tissue did not seem to be the critical factor in development of recession. Risk of recession appeared to increase when genioplasty was combined with mandibular advancement and tended to occur at sites in which the keratinized gingiva and underlying bone appeared thin.

T his study examined the histopathologic features of advanced periodontitis lesions tentatively classified as active or inactive by the selected clinical criteria of bleeding or bleeding and suppuration within 15 seconds of probing or the absence thereof. The Gingival Index, Plaque Index, and pocket fluid flow also were assessed. From 12 human subjects, a total of nine bleeding and five nonbleeding periodontitis lesions were obtained. The biopsies consisted of an extracted tooth and the portion of attached soft tissue which formed the pocket wall at the location where the clinical evaluation was performed. The soft tissue included the entire pocket and junctional epithelia as well as the adjacent normal and infiltrated connective tissue (ICT) and oral epithelium. Major histologic differences were found between the two lesion types. Morphometric point counting using grid intersections revealed that the mean percentage of ICT was consistently much larger in bleeding (55.1 ± (5.1) than in nonbleeding lesions (30.5 ± 7.8). In comparing the composition of the ICT of the two lesion types, significant differences were found between the mean percent volume occupied by plasma cells (68% versus 24%), mononuclear cells (5.5% versus 22%), and extracellular space/connective tissue (18% versus 48%) in the bleeding versus nonbleeding lesions. Nonsignificant differences were present in the volume occupied by polymorphonuclear leukocytes, unidentifiable cells, and vessels in the two lesion types. The pocket epithelium of bleeding lesions consistently demonstrated thinned or ulcerated areas and long, tortuous strands of rete pegs extending deep into the ICT. While showing definite regional variations in polymorphonuclear and mononuclear leukocyte infiltration, the pocket and junctional epithelia of bleeding lesions always contained greater numbers of leukocytes. Bleeding or bleeding combined with suppuration upon probing is therefore indicative of characteristic histopathologic changes in lesions of advanced inflammatory periodontal disease. These changes may relate to the state of activity or inactivity of the disease process in the advanced lesion.