We determined the hyaluronic acid disaccharides, ΔDi-HA, in the gingival crevicular fluid(GCF)and whole saliva of patients with periodontal disease, and in the peri-implant sulcus fluid(PISF)from sites around titanium osseointegrated implants, and compared these values with those in the GCF and whole saliva of controls. We also determined values for chondroitin sulfate disaccharide isomers at the same time. Glycosaminoglycans were extracted by digestion with Pronase E, followed by digestion of GAGs with hyaluronidase SD and chondroitinase ACII. Unsaturated disaccharide isomers produced from hyaluronic acid and chondroitin sulfate were analyzed by high-performance liquid chromatography(HPLC).
The hyaluronic acid disaccharide ΔDi-HA was found in all samples of GCF, PISF and whole saliva. The concentration of ΔDi-HA in both GCF and whole saliva of the periodontitis group was greater than that in the controls. There was no difference in the concentration of ΔDi-HA between the PISF and GCF of the controls. The ratios of hyaluronic acid to chondroitin sulfate in the GCF and in the whole saliva of the periodontitis group were significantly lower than that of the controls. There was no difference between the ratios in PISF and those in GCF of the controls.
These results indicate that checking hyaluronic acid in GCF and whole saliva using HPLC is a useful means of assessing the condition of periodontal tissues, and that assaying hyaluronic acid in PISF may also be effective for monitoring the condition of tissues around dental implants.

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Many antibiotics are used to treat infection in clinical practice. Actions of these drugs involve specific immune enhancement and improved overall phagocytic and bactericidal capacities of polymorphonuclear leukocytes and macrophages at the site of infection.
In this study, we examined the effects of antibiotics on chemotaxis and phagocytosis by reacting macrophages with 7 different antibiotics, specifically ampicillin(ABPC), cephalexin(CEX), cefotiam(CTM), amikacin(AMK), clindamycin(CLDM), tetracycline(TC)and bleomycin(BLM). At 1μg/ml, there were significant differences in chemotaxis between control and experimental groups treated with agents other than ABPC and CEX(CLDM : p<0.05, AMK : p<0.01, CTM, TC and BLM : p<0.001). At 10μg/ml, there were significant differences in chemotaxis between the control group and all treated groups(ABPC and CLDM : p<0.01, CEX, CTM, AMK, TC and BLM : p<0.001). At 100μg/ml, all antibiotics significantly inhibited chemotaxis(p<0.001). Phagocytosis was evaluated by determining both the ratio and index of phagocytosis. There was a significant difference in the phagocytosis ratio between the control group and the group treated with 10μg/ml of BLM(p<0.001). At 100μg/ml, all agents but ABPC significantly reduced phagocytosis in a dose-dependent manner. Agents other than ABPC similarly reduced the phagocytosis index. Significant differences were noted between the control group and groups treated with BLM or AMK(BLM : 10μg/ml : p<0.01, 100μg/ml : p<0.001, AMK : 100μg/ml : p<0.01). (J Osaka Dent Univ 1998 ; 32 : 9-15)

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The effects of intravenous morphine on responses of feline thalamic nociceptive neurons receiving afferent input from the tooth pulp(TP)were investigated. Morphine suppressed responses to TP stimulation in both tooth pulp specific(TPS)and wide dynamic range(WDR)neurons with TP input recorded from the nucleus ventralis posteromedialis(VPM). However, there was scant morphine effect on responses to stimulation of trigeminothalamic tract(TTT)fibers in the trigeminal medial lemniscus. Furthermore, in nociceptive neurons with TP input recorded from nucleus centralis lateralis(CL)and parafascicularis(Pf)of the intralaminar nuclei, intravenous morphine suppressed responses both to stimulation of the mesencephalic reticular formation(MRF)as well as TP stimulation. The suppressive action of morphine on responses elicited by TP stimulation of VPM, CL and Pf neurons was antagonized by intravenous naloxone(1mg/kg). Results suggest that intravenous morphine suppresses synaptic transmission of nociceptive impulses in the intralaminar nuclei as well as in the lower brain stem but not in the VPM. (J Osaka Dent Univ 1998 Apr ; 32 : 17-26)

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BMP-HAP complex was implanted into a bone defect in the femur of Wister-strain rats, and animals were allowed to heal for one to 8 weeks prior to sacrifice. Similar bone defects without BMP-HAP complex served as controls. Osseous healing and microvascular changes, as revealed by plastic microcorrosion castings, were subsequently examined under a scanning electron microscope. One week after implantation, sproutings and congregate sinusoidal capillary plexuses and primary bone trabeculae(woven bone)were observed around and between the BMP-HAP complexes. Control specimens revealed a fine and immature sinusoidal capillary plexus arising from sproutings and elongations of pre-existing blood vessels, but bone formation was not observed. At two weeks, newly-formed trabeculae were observed around and on the surface of the HAPs, and a network of thick, newly-formed vessels was observed in intervening space. At three weeks, networks of newly-formed vessels were observed on the surface of the HAPs, and surrounding newly-formed trabeculae had become thickened. At four weeks, bone defects were filled, and HAP was completely embedded in new bone. At eight weeks, the HAP was fused with new bone, and the boundary between the HAP and new bone was unclear. In comparison with comparable surgically created control bone defects without implanted BMP-HAP complex, BMP apparently stimulates new vascularization. Further, implanted BMP-HAP apparently stimulates undifferentiated mesenchymal cells to differentiate into angioblasts and osteoblasts, or vice versa (dedifferentiation). (J Osaka Dent Univ 1998 Apr ; 32 : 27-34)

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