The fibroblast is a prominent cellular component of the periodontal ligament. It is believed to play an important role in collagen metabolism in health and disease. The turnover of collagen in the periodontal ligament is believed to be controlled by the balance between collagen synthesis and degradation. The family of matrix metalloproteinases and their inhibitors is one of the mechanisms which regulates this balance. The factors that regulate the synthesis of collagenase and its inhibitor, TIMP-1, by the periodontal ligament cell are poorly understood. The present study was undertaken to assess the effect of interleukin-1 beta (IL-1 beta), platelet-derived growth factor (PDGF), and transforming growth factor-beta 1 (TGF-beta) on the expression of collagenase (MMP-1) and TIMP-1 mRNA in periodontal derived fibroblasts using reverse transcription polymerase chain reaction (RT-PCR). Early passage periodontal ligament derived fibroblasts were treated with IL-1 beta (10 and 100 pg/ml), two isoforms of PDGF, -AA and -BB (4 and 20 ng/ml) and TGF-beta (1 and 10 ng/ml). Treatment with growth factors from 2 to 24 hours revealed that the largest effects on MMP-1 mRNA occurred after 24 hours. IL-1 beta induced a 5 to 9 fold increase in MMP-1 mRNA. The two isoforms of PDGF had less of an effect (3 to 5 fold) on MMP-1 mRNA whereas TGF-beta induced a 25 to 50% decrease in the expression of this message. None of the growth factors had an effect on TIMP-1 mRNA expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous studies have shown that several factors--such as alloxan-induced diabetes, adrenalectomy, or removal of the thyroid-parathyroid gland complex--can influence the flow rate, protein concentration, and protein composition of rat parotid saliva. The present study was undertaken to explore further the influence of glucocorticoids and thyroxine on rat parotid saliva in hormonally intact animals. As compared with untreated animals, adult male rats treated with 10 micrograms dexamethasone per 100 g body weight for eight days demonstrated a 75% reduction in volume of parotid saliva secreted in response to a uniform stimulus. The protein concentration of the saliva was increased three-fold. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed relative decreases in acidic and basic proline-rich proteins and in a protein identified as Fraction V, while amylase was increased. The electron microscopic appearance of the granules was markedly different from that of the control, in that the granules exhibited an electron-dense periphery and core, with the remainder of the granule having an electronlucent appearance. In contrast, rats treated for eight days with 20 micrograms thyroxine per 100 g body weight exhibited a 50% increase in volume of saliva collected in response to a secretory stimulus. Although the concentration of protein was not different from that of the control, gel electrophoresis showed relative increases in acidic and basic proline-rich proteins and a decrease in Fraction V. Amylase was unchanged. The secretory granules of thyroxine-treated rats were electronlucent and amorphous. The granules appeared to coalesce within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to evaluate the effects of chronic subclinical ascorbic acid deficiency on periodontal health in a nonhuman primate model. Young adult Macaca fascicularis monkeys were fed an ascorbic acid free diet for nine weeks followed by a diet with a suboptimal level of ascorbic acid for an additional sixteen weeks. During the 25‐week period, a pair fed control group was fed a nutritionally adequate diet in amounts equivalent to that consumed by the experimental group. From the second week onward, whole blood ascorbic acid levels in the experimental animals but not in pair fed controls were significantly reduced. Experimental animals did not develop clinical signs of ascorbate deficiency, and there was little evidence of spontaneous gingivitis or periodontitis in either group between weeks 0 and 23. At week 23, plaque‐associated periodontitis was experimentally induced to evaluate the response of the periodontal tissues to the underlying subclinical ascorbate deficiency. Gingival index scores and pocket depth measurements were significantly greater in the ascorbate deficient animals than in controls. Preliminary studies of leukocyte function suggested that this susceptibility to periodontitis might be related to impaired polymorphonuclear leukocyte chemotaxis and phagocytosis. This study indicates that the periodontium is vulnerable to chronic inflammation as a consequence of subclinical ascorbic acid deficiency.

Young adult nonhuman primates were initially fed an ascorbic-acid free diet and, subsequently, a diet with a suboptimal level of the vitamin. Following approximately 12 weeks of this dietary regime, five of seven experimental animals developed scorbutic gingivitis. 2 to 3 weeks prior to this stage, the permeability of the gingival sulcular epithelium to ^H-inulin, but not to ^^C-butyric acid or ''C-urea, had increased significantly (+86%, P < 0.01) in the experimental group as compared to ad libitum or pair-fed controls. This defect in the intercellular permeability barrier of the sulcular epithelium could have contributed to the pathogenesis of scorbutic gingivitis.