Search

The purpose of this study was to determine the effect of bisphosphonate on alveolar bone resorption in experimentally-induced peri-implantitis in beagle dogs. Experimental peri-implantitis was induced by ligation around the abutments, 6 months after placement of a fixture. Pamidronate (0.6 mg/kg) was injected intramuscularly every 3 days into each of 5 dogs. Another 5 dogs served as the control group and were injected with saline only. Peripheral blood and urine samples were collected every week up to 12 weeks after placement of the ligature. Standard X-rays were taken every week. Urinary deoxypyridinoline (DPD) and serum osteocalcin (OC) were evaluated by ELISA as markers of alveolar bone remodeling. X-ray films were analyzed with a computer image analyzer. After 12 weeks, the bone level was measured after removal of the gingival flap. The distance between the top surface of the fixture and the fundus of the defect was significantly lower in the Pamidronate group (1.59+/-0.55 mm, mean+/-SD) than in the control group (2.41+/-0.48 mm). Bone density analyzed from the X-ray films was significantly higher in the bisphosphonate group (69.2+/-8.7%, mean+/-SD) than in the control group (50.3+/-12.8%) after 2 to 8 weeks compared with the baseline value (100%). OC and DPD levels fluctuated during the experimental period. These findings suggest that bisphosphonate inhibits the progression of alveolar bone resorption during ligature-induced peri-implantitis in dogs.

Chediak-Higashi syndrome (CHS) is an extremely rare hereditary disease characterized by leukocyte dysfunction. We report on a 21-year-old woman who presented at the age 9 years with CHS and serious periodontal tissue destruction around erupted teeth. The patient had received systemic, radiographic, immunological, microbial, and clinical periodontal examinations since childhood. The chemotactic activity of neutrophils in the Boyden chamber assay was 22% of the control, and leukocyte bactericidal activity was one-third of the control. Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia were isolated from periodontal pockets. Periodontal treatment including oral hygiene was provided, followed by professional tooth cleaning from the age of 12 to 21 years. However, the mobility of teeth and the inflammation of periodontal tissue progressed. This CHS patient presented with periodontal disease of extremely early onset, which was resistant to periodontal treatment.

This study was designed to demonstrate, by use of biotin-labeled hyaluronic acid binding protein (HABP) and an avidin-enzyme system, the localization of hyaluronan (HA) in periodontal tissue of beagle dogs during experimentally induced periodontitis. Experimental periodontitis was induced in the dogs by ligation of the gingival sulcus. Experimental tissue was collected at 0, 3, 7 and 21 days after ligation. HA was revealed by strong staining in the intercellular space around epithelial cells and periodontal ligament, and by light staining in the gingival connective tissue. According to the progression of periodontal tissue breakdown, HA was detected in a small number of leukocytes and monocytes, on the surface of osteoclasts, the surface of alveolar bone, thickened endothelium and in epithelial cells related to rete peg formation. Streptomyces hyaluronidase-treated specimens gave negative staining. This study suggests that HA may be associated with the inflammatory reaction in experimental periodontitis tissue.

This study was undertaken to observe osteoclast differentiation related to inflammatory progression in aggressive periodontitis induced in beagle dogs by ligature of the gingival sulcus. To monitor osteoclastic activity, we used histochemical methods (staining for tartrate-resistant acid phosphatase [TRAP]) to visualize osteoclasts and their TRAP-positive precursors and biochemical methods (ELISA assay of pyridinium crosslinks) to detect bone matrix degradation products in gingival crevicular fluid (GCF), serum, and urine. For histochemical study, tissue specimens were prepared from 3 adult female beagle dogs induced with experimental periodontitis by silk ligature placement below the gingival margin of mandibular molars ligated for 3, 7, and 21 days. For biochemical study for pyridinoline measurement, the 24 mandibular molars of 4 male beagle dogs were ligated. GCF, urine, and serum were collected at day 0 and at 3, 7, 14, and 21 days after ligation. In the early inflammatory phase of ligature-induced periodontitis (day 3), TRAP+ mononuclear and TRAP+ multinucleated cells were present in the gingival connective tissue, and active bone-resorbing cells were found in excavated lacunae at the alveolar crest, but osteoclasts were not infiltrating the periodontal ligament during this early phase. During later stages of the inflammatory process (7 and 21 days), osteoclasts appeared at both the gingival and ligament side of the alveolar bone. Osteoclastic bone resorption appeared to be more severe on the bone surface at the gingival side than on the bone surface of the periodontal ligament side. Measurement of pyridinoline significantly increased in GCF and urine 3 days after ligation. The results suggested that bone at the crest of the alveolar bone is rapidly resorbed within 3 days of inducing experimental periodontitis.

The purpose of this study was to develop an ELISA method to detect chondroitin sulfate isomer-linked proteoglycans in gingival crevicular fluid (GCF), and to elucidate the role played by the glycosaminoglycans (GAGs) in GCF during experimentally-induced periodontitis in dogs. Experimental periodontitis was induced by placement of a silk ligature below the gingival margin of the molar teeth in 3 mongrel dogs. GCF was collected using microcapillary tubes at 0, 7, 21 and 60 days after ligature placement. To compare with GAG in GCF, bovine nasal cartilage proteoglycan monomer, dog's serum and supernatant of homogenized gingival tissue were prepared. Combination of monoclonal antibodies, 3B3 and 9A2, and specific enzymatic digestion made possible the identification of chondroitin 4 sulfate (C4S), chondroitin 6 sulfate (C6S) and dermatan sulfate (DS). The ELISA method detected very small amount of chondroitin sulfate (CS) isomers (15-1000 ng/ml of bovine nasal cartilage proteoglycan). The ELISA value of CS isomers in GCF was lower than that of homogenized gingival tissue but higher than that of the serum. The ELISA value of C4S, C6S and DS, although fluctuating, increased in proportion to the severity of the inflammation.

There are many reports showing a close relationship between polyamine metabolism and tissue growth or the recovery of damaged tissues, such as that occurring after partial hepatectomy. Therefore, it was proposed that the metabolism of polyamines might change in periodontitis induced by attaching surgical ligatures below the gingival margin of dog molars. One to two days after fixing the ligatures, the putrescine content and activity of ornithine decarboxylase in the tissue rose to about twice the control levels and then decreased gradually to control levels on day 7. No significant change in spermidine or spermine concentration was observed during this period. When the ligatures were removed on day 7, the putrescine content increased to about 2.5 times the normal level within 12 h. Ornithine decarboxylase activity changed in parallel with the change in putrescine content. Clinical and histopathological indications of periodontitis then started to decrease and had almost disappeared 2 weeks after removal of the ligatures. On the other hand, when the ligatures were removed on day 14, no significant increase in putrescine content was observed within 36 h and the rate of recovery from periodontitis was significantly slower than when the ligatures were removed on day 7. However, application of putrescine to the periodontal pocket immediately after removal of the ligatures on day 14 increased the rate of recovery, as determined by histological criteria. These findings suggest that putrescine or its metabolites are important in the process of recovery from periodontitis.

The lymphocyte subsets in the peripheral blood of 8 individuals, aged 25 to 57 yr, with moderate to advanced adult periodontitis were analyzed before and after treatment by means of flow cytometry, and then compared with the findings in 20 normal adults (aged 30 to 45 yr). The results were as follows: the percentage of OKT-8+ (CD 8) in the patients (20.25 +/- 7.15%) was lower than that in normal individuals (31.50 +/- 6.03%, P less than 0.01) while the OKT-4/OKT-8 ratio (2.34 +/- 1.18) was higher than the corresponding ratio in the controls (1.23 +/- 0.37); however, there was no significant difference in the percentages of OKT-3+ (CD 3), OKT-4+ (CD 4) and Leu-12+ (CD 19) between patients and normal subjects. The percentages of OKT-3+, OKT-4+, OKT-8+, Leu-12+ and OKT-4/OKT-8 after the periodontal therapy did not show a significant difference compared with the data obtained before treatment. These results indicate that the decrease in suppressor/cytotoxic T-cell population may be a kind of pathological disposition of the initiation and/or course of adult periodontitis.

The purpose of this study was to investigate the changes in glycosaminoglycans (GAGs) of the gingiva during a period of experimental periodontitis induced by placing a silk ligature below the gingival margin of dog molars. Incorporation of 3H-glucosamine into the gingiva was determined autoradiographically. The gingiva was collected at 0, 7, 21, 60 and 90 days and cultured in vitro in the presence of 3H-glucosamine. The autoradiographs showed a predominantly epithelial location of the silver grains in all gingival epithelia. The location was intercellular in all epithelia. The results suggest greater 3H-glucosamine incorporation by the epithelium compared with the connective tissue and markedly more rapid metabolic turnover of epithelial GAGs.

The purpose of this study was to develop an ELISA method to detect chondroitin sulfate isomer-linked proteoglycans in gingival crevicular fluid (GCF), and to elucidate the role played by the glycosaminoglycans (GAGs) in GCF during experimentally-induced periodontitis in dogs. experimental periodontitis was induced by placement of a silk ligature below the gingival margin of the molar teeth in 3 mongrel dogs. GCF was collected using microcapillary tubes at 0, 7, 21 and 60 days after ligature placement. To compare with GAG in GCF, bovine nasal cartilage proteoglycan monomer, dog's serum and supernatant of homogenized gingival tissuw were prepared. Combination of monoclonal antibodies, 3B3 and 9A2, and specific enzymatic digestion made possible the identification of chondroitin 4 sulfate (C4S), chondroitin 6 sulfate (C6S) and dermatan sulfate(DS). The ELISA method detected very small amounts of chondroitin sulfate (CS) isomers (15-1000 ng/ml of bovine nasal cartilage proteoglycan). The ELISA value of CS isomers in GCF was lower than that of homogenized gingival tissue but higher than that of the serum. The ELISA value of C4S, C6S and DS, although fluctuating, increased in proportion to the severity of the inflammation. [ABSTRACT FROM AUTHOR]