The capacity of collagen membranes to support guided regeneration of periodontal tissues in the dog was assessed. The mesiolabial, labial and distolabial aspects of the mesial root of the second and third mandibular premolar were surgically exposed in three beagle dogs. Collagen membranes, 0.5 to 0.7 mm thick, prepared from a purified solution of rat-Type I collagen were interposed between the gingival flap and the exposed root surfaces of the right premolars. The left premolars were sham-operated without the use of collagen membranes. Animals were killed one month after surgery. Tissue blocks, including the surgical sites, were removed and prepared for histological and histometric examination. Long epithelial attachment was the modality of healing in the control sites. The apical level of the junctional epithelium was located either at, or close to, the apical level of the defect. The experimental sites exhibited a combination of three healing modalities: (1) partial regeneration of periodontal tissues (new bone, periodontal ligament and cementum) occurred in the apical half of the defect, (2) long epithelial attachment developed in the coronal quarter of the defect and (3) connective tissue adhesion developed between the two. Pocket depth was similar in both the control and experimental sites. Collagen membranes could not be identified at the time of examination. The results indicate that: (1) collagen membranes have the capacity to support regeneration of periodontal tissues and (2) collagen membranes are either incorporated within the healing tissues or degraded by these during the healing process. These findings suggest that collagen membranes may be of value in reconstructive periodontal therapy.

The capacity of collagen membranes to prevent the apical migration of epithelium and to support new connective tissue attachment was assessed in experimental periodontal defects in dogs. Experimental periodontal defects were produced in 8 mongrel dogs by removing the alveolar bone and the periodontal ligament over the most coronal 5 mm of the labial aspect of the maxillary canines. Experimental defects associated with the right canine and its surrounding bone were covered by collagen membranes prepared by air drying gels of rat type I fibrillar collagen. Flaps were repositioned and sutured. The contralateral control defects were sham-operated without using collagen membranes. Animals were killed, 10 and 30 days after surgery, 4 at each time point. The experimental and control sites were processed for histologic and histomorphometric evaluation. At 10 d, the average distance between the apical margin of the epithelium and the apical level of the defect (EA) sites was 3.20 +/- 0.55 mm for the experimental sites and 0.73 +/- 0.18 mm for the controls. The experimental root surfaces apical to the epithelium and the collagen membranes were covered by connective tissue cells. At 30 d, the EA for experimental and control sites were 2.55 +/- 0.36 mm and 0.47 +/- 0.30 mm, respectively. In the experimental sites healing by long junctional epithelium was observed in the coronal 40% of apico-occlusal dimension of the defect and new connective tissue attachment with inserting fibers in the apical 55% of the defect length. No new bone formation was observed. In the control sites, pocket formation was found in the most coronal one-third of the defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Collagen membranes were interposed between full thickness periodontal flaps and denuded root surfaces of right upper canines in 3 mongrel dogs; the left canines were sham‐operated without the use of collagen membranes. Animals were killed 10 d after surgery. Tissue blocks were removed, and experimental and control sites were processed for histometric and histologic examination. The results indicate that collagen membranes: (i) prevent apical migration of the epithelium during initial stages of healing; and (ii) are colonized by connective tissue cells and incorporated within the healing connective tissue.

The combined length of the supracrestal connective tissue attachment and the junctional epithelium is referred to as the "biologic width". The long-term (1-year) effect of complete violation of the supracrestal connective tissue attachment was examined in beagle dogs. Full thickness periodontal flaps were elevated, exposing the buccal bony crests of the maxillary and mandibular canines of 3 beagle dogs. The roots of the experimental teeth were planed and class V cavities were prepared. The apical border of each cavity was located at the alveolar bone crest. The cavities were restored with amalgam and the flaps were repositioned and sutured. In the control sites, a notch was prepared at the CEJ and the distance between the notch and the bony crest was measured. The dogs were sacrificed 57 weeks after the operation and the experimental and control sites prepared for histologic analysis. Every 5th section was examined and measurements were taken of the amount of gingival and bone recession, the length of the connective tissue and the epithelial attachment. Control sites healed uneventfully. Gingival recession averaged only 0.5 mm; bone loss was minimal and averaged 0.15 mm. The combined length of the supracrestal connective tissue and epithelial attachment measured 4.47 mm. In experimental sites, the gingiva receded 3.16 mm on average. Moderate bone loss (mean = 1.17 mm) was noted, but no signs of bone resorption were seen at the time of sacrifice. After bone loss, root surfaces which were previously attached to alveolar bone by periodontal ligament were mainly (0.90 mm) attached to connective tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to assess the effect of endotoxin adsorbed to dental surfaces and to collagen type I on the migration, attachment, and orientation of human gingival fibroblasts (HGF). Transversely cut porcine tooth root slices (RS), 200 micron thick, were prepared. Half of the RS obtained were partially demineralized in EDTA. Half of the demineralized and non-demineralized RS were incubated with 400 micrograms/mL of endotoxin for 24 hr, whereas the other half were maintained in PBS and served as controls. Experimental and control RS were placed on confluent layers of HFG and cultured for six days. Cell migration toward and cell attachment to the periphery of the RS and the formation of oriented cell sheets were assessed by means of photographic techniques. Additionally, six-day-old cultures were fixed and processed for SEM observation. In separate experiments, the effect of endotoxin on cell attachment to collagen type I and on contraction of three-dimensional collagen gels was assessed. It was found that: (i) bacterial endotoxin inhibited migration and attachment of HGF to both demineralized and non-demineralized cementum and interfered with the development of oriented cellular structure: (ii) the inhibitory effect was significantly more pronounced for non-demineralized than for demineralized cementum: (iii) the morphology of HGF attached to endotoxin-treated dental surfaces was altered compared with that of their controls: and (iv) bacterial endotoxin inhibited cell attachment to collagen type I and delayed the contraction of collagen gel.