Oral rinse MMP-8 together with TIMP-1 analysis may have potential in complementary periodontal diagnostics. dentoELISA can be applied in quantitative oral rinse chair side biomarker diagnostics.
Three teeth from each of 14 adult patients with advanced periodontitis were included in this study. The Test Tooth was an incisor or canine with increased mobility associated with an occlusal interference and a ≥ 5 mm deep pathologic pocket. The Infected Control Tooth was a non‐mobile incisor or canine with a ≥ 5 mm pocket. A non‐mobile incisor or canine with pockets ≤3 mm served as the Healthy Control Tooth. At least 7 d prior to Day 0 the patients were taught an effective oral hygiene regimen and received a supragingival prophylaxis. At Day 0, sulcular fluid for assay of protein content and Collagenase activity was collected from each chosen pocket. Immediately thereafter the Test Teeth of 7 subjects were scaled and root planed and the Test Teeth of 7 subjects occlusally adjusted. At Day 14, the treatments were reversed for the two groups. Sulcular fluid for the assays was again collected at Days 14 and 28. The protein content and collagenase activity in deep pockets was elevated during periodontitis in both mobile and immobile teeth. After establishment of a supragingivally clean oral environment, a rapid decrease of the collagenase activity took place following scaling and root planing of the root surfaces within the periodontal pockets (p≤0.05). Also, occlusal adjustment of the hypermobile teeth with deep pathological pockets reduced the protein content and collagenase activity in sulcular fluid (p ≤ 0.02). There was a further reduction of collagenase activity when occlu‐sally adjusted teeth were scaled and root planed (p≤0.02). No change in the protein content or collagenase activity was observed in the deep pockets of the untreated Control Teeth in the same patients.
Periodontal epithelium plays a critical role in protection, destruction and repair of human periodontium. During optimal repair, epithelium migrates and covers the wound surface to prevent infection and damage of the vulnerable underlying connective tissue. During periodontal destruction, junctional epithelium undergoes transformation to pocket epithelium that has quite different characteristics from junctional epithelium. In the course of periodontal disease the epithelial attachment to the tooth surface is lost and the epithelium proliferates and extends pseudo‐rete ridges deep into the inflamed connective tissue. Both scenarios, repair and destruction, involve active epithelial migration either in the wound provisional matrix or in the inflamed connective tissue matrix, respectively. This review covers recent research data on cellular receptors, integrins, that mediate epithelial cell migration during wound healing and destruction of human periodontiurn.
Larjava H, Uitto V-J, Haapasalo M, Heino J, Vuento M: Fibronectin fragmentation induced by dental plaque and Bacteroides gingivalis. ScandJ Dent Res 1987; 95: 308-14.Ahstract -Degradation of fihronectin (FN) by subgingival and supragingival plaque and Bacteroides gingivalis (Bg] was studied in vitro. The degradation .of FN by both types of plaque was relatively rapid, continuous but incomplete. Some difTerences were found between supraand suhgingival samples. Supragingival plaque extracts produced .several FN fragments oi 110-180 kd during short incubations of 15-60 min. The predominant fragment after overnight incubation was a 110 id poiypeptide. With subgingival plaque extract a more extensive degradation of FN was noted. The main degradation product was a 120 kd fragment after overnight incubation. Several peptide fragments were released from fibronectin by Bg extracts. Their molecular size was different from those produced by trj-psin, elastase or dental plaque. When cell extracts of Bg were fractionated by high performance liquid chromatography, three separate peaks of fibronectin degrading activity were obtained. Two of those peaks also contained trypsinlike enzyme activity. The degradation of fibronectin and the subsequent formation of biologically active peptides may have many effects in periodontal pockets. These may include modifying effects on plaque growth and wound healing.
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