Primate model for testing periodontal treatment procedures: I. Histologic investigation of localized periodontal pockets produced by orthodontic elastics.

Experimental periodontal lesions have been produced in Rhesus monkeys using orthodontic elastics. These lesions are characterized by an irreversible apical positioning of the junctional epithelium and both horizontal and angular bone loss. It was concluded that this lesion is suitable for testing the effect of periodontal treatment.

The attachment between tooth and gingival tissues after periodic root planing and soft tissue curettage.

Utilizing a nonhuman primate model, a study was carried out to determine the nature of the attachment between the tooth and the gingival tissues following periodic root planing and soft tissue curettage. Under the conditions of this investigation, periodic root planing and soft tissue curettage combined with thrice weekly plaque control resulted in the formation of a long junctional epithelium with no new connective tissue attachment. In eight of the 22 experimental pockets, however, this procedure produced discontinuities or "windows" in the junctional epithelium. The coronal attachment of gingival tissues to the root surface (increased resistance to probing) commonly reported following root planing and soft tissue curettage appears to result from the formation of a long junctional epithelium rather than new connective tissue attachment.

Effect of periodontal trauma upon intrabony pockets.

Conflicting results have been reported regarding the effect of periodontal trauma upon progression of periodontitis. In these studies, different initial pocket morphologies were present. This study investigated the effect of trauma superimposed upon existing intrabony pockets. Localized intrabony pockets were produced adjacent to the mesial and distal surfaces of the mandibular third bicuspids in 10 squirrel monkeys. Two animals were killed after 10 weeks of periodontitis. In four (experimental) of the remaining eight animals, mesio-distal jiggling of the third bicuspid was begun 10 weeks after induction of periodontitis, and continued for another 10 weeks. The other four animals (control) were killed 20 weeks after initiation of periodontitis. Step-serial histologic sections were selected from experimental and control specimens and analyzed for loss of connective tissue attachment, loss of crestal alveolar bone and percentage of bone in the coronal interproximal periodontium. When corresponding dimensions from experimental and control surfaces were compared statistically, there were no differences in loss of connective tissue attachment but a greater loss of bone had occurred in specimens with the combination of periodontitis and trauma. In addition, there was a marked difference in osseous morphology between the experimental and control specimens. It was concluded that trauma superimposed upon existing intrabony pockets increased loss of alveolar bone and altered osseous morphology, but did not affect the loss of connective tissue attachment.

Alveolar bone regeneration after removal of inflammatory and traumatic factors.

In this investigation periodontal destruction was produced by a combination of inflammatory and traumatic factors. After the inflammation was resolved and the trama stopped, a significant amount of alveolar bone regeneration took place. The implications of these findings for the management of advanced periodontal disease are discussed.

Conversion of chronic gingivitis to periodontitis in squirrel monkeys.

1. Acute exacerbation of gingivitis can lead to destructive periodontitis. 2. Such periods of acute inflammation may be associated with epithelial ulceration. 3. Bone loss in periodontal disease may occur in bursts of osteoclastic activity triggered by cells or factors generated during an acute phase. 4. Partial repair can follow an acute episode and a "stable lesion" may become re-established.

Interproximal and buccal cell populations apical to the sulcus before and during experimental periodontitis in squirrel monkeys.

The purpose of this investigation was to study inflammatory cell populations apical to the buccal and interproximal gingival sulcus during destructive experimental marginal periodontitis in squirrel monkeys. Specimens were obtained of the clinically healthy periodontium, and (after 2 and 10 weeks) of experimental periodontitis induced by the placement of plaque-retentive silk ligatures at the gingival margin. Cell populations were characterized and quantitated in a standard area of connective tissue immediately subjacent to the most apical cells of the junctional epithelium in buccal and interproximal locations. Comparisons of periodontitis cell populations showed there were no differences between the regions in relation to either total numbers of cells, or in the percentages of inflammatory cell types. The inflammatory cells consisted primarily of granulocytes and macrophages, with only small percentages of lymphoid and plasma cells. Mechanisms and consequences of these cell types relative to periodontal tissue destruction are discussed.

Cell populations in the transseptal fiber region before, during and after experimental periodontitis in squirrel monkeys.

A study was designed to enumerate cell populations before, during and after experimentally induced periodontitis in squirrel monkeys. The clinically healthy gingival connective tissue adjacent to the sulcus contained populations of macrophages, plasma cells, lymphoid cells, and granulocytes, indicating that immune responses were probably in operation. Although these cell populations have been associated with tissue destruction, it is possible that they may serve to confine the antigens to the tissue adjacent to the sulcus, and reduce their spread apically. Active periodontitis was associated with the presence of granulocytes and macrophages in the transseptal fiber region. These cells are capable of causing the localized collagen degradation and bone resorption that occur during the destructive phase of the disease. Eight weeks after etiologic agents were removed, the cell populations in the transseptal fiber area returned to a level comparable with those in the pre-experimental, clinically healthy. This indicates that active periodontitis within the transseptal fiber region had ceased and repair had occurred.