The present clinical trial was designed to evaluate the regenerative potential of the periodontal tissues in degree II furcation defects at mandibular molars using a surgical treatment technique based on the principles of guided tissue regeneration. The patient sample included 21 subjects, 22-65 years of age. The patients selected had periodontal lesions in the right and left molar regions including advanced periodontal tissue destruction within the interradicular area. After an initial examination, each patient received a series of full-mouth scalings and root planings. 2-3 months later, they were recalled for a baseline examination including assessment of plaque, gingivitis, probing depths and probing attachment levels. The furcation involved molars were randomly assigned in each patient to either a test or a control treatment procedure. The test procedure included the elevation of mucoperiosteal flaps at the buccal and lingual aspect of the alveolar process. The inner surface of each flap was carefully curetted to remove epithelium and granulation tissue. The root surfaces were scaled and planed. A teflon membrane was adjusted to cover the entrance of the furcation area and the adjacent root surfaces as well as a portion of the alveolar bone apical to the crest. The flaps were repositioned and placed on the outer surface of the membrane and secured with interdental sutures which were removed after 10 days of healing. Following surgery, the patients were instructed to rinse the mouth twice daily with chlorhexidine gluconate. A second surgical procedure was performed after a healing period of 1-2 months to remove the teflon membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

The present investigation was designed to evaluate the regenerative potential of the periodontal tissues in degree III furcation defects at mandibular molars using a treatment procedure based on the principle of guided tissue regeneration. The patient sample included 21 patients, 26-65 years of age, who presented periodontal lesions in the right and left molar regions including "through and through" furcation defects. After an initial examination, each patient was subjected to a series of full-mouth scaling and root planing. 2-3 months later, they were recalled for a baseline examination. The furcation-involved molars were randomly assigned in each patient to either a test or a control treatment procedure. The test procedure included the elevation of muco-periosteal flaps at the buccal and lingual aspects of the molars. Granulation tissue was removed and the exposed root surfaces were debrided and planed. The width and the height of the entrance openings to the furcation defects were assessed. A teflon membrane was adjusted to cover the entrances to the defects (buccal and lingual) and was retained in the manner described by Pontoriero et al. (1988). The flaps were repositioned on the outer surface of the membrane and secured by sutures which were removed after 10 days. Following surgery, the patients were instructed to rinse the mouth twice daily for 4 weeks with chlorhexidine gluconate. The membranes were removed after a healing period of 1-2 months. A surgical procedure identical to the test procedure was performed in the control tooth regions with the exception of the placement of membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

The placement of a ligature around the second maxillary molar of the conventional rat caused osteoclastic bone resorption and simultaneously, alveolar bone formation. The number of peripheral mononuclear cells in the blood and lymphoblastic transformation of spleen cells in response to concanavalin A increased. Cyclophosphamide (CY), an immunosuppressive agent, given shortly after placing the ligature suppressed the lymphoid reactions, spleen size, and bone formation and enhanced bone destruction. CY given in higher doses also suppressed the number of PMN cells. Septicemia developed in several of these animals. Pseudomonas aeruginosa, Klebsiella pneumoniae and Escherichia coli were isolated from the blood and/or ligature. Antibiotics prevented bone destruction. Without placing a ligature, the high dose of CY did not result in bone loss. These findings suggest that 1) bone destruction of the ligature‐treated rat is of bacterial origin, 2) CY suppresses proliferation of osteoblasts but does not seem to interfere with the activity of osteoclasts, and 3) suppression of the host defenses greatly facilitates bone destruction.

Oral isolates of Actinobacillus actinomycetemcomitans (strain Y4) release spherical microvesicles in large numbers during normal growth. The biological activities of these products were studied, and it was estimated that approximately 1/10 of their dry weight was made up of heat-and proteolysis-resistant endotoxin. The chicken embryo lethality and bone-resorbing activity of the microvesicles were heat stable but proteolysis sensitive. Other laboratories have reported the presence of a heat-and proteolysis-sensitive leukotoxin in similar preparations. Accordingly, the microvesicles released by strain Y4 may contain, in addition to endotoxin, several potent substances which are highly toxic and active in bone resorption, and these may be significant factors in the pathogenesis of periodontal diseases.