Dietary-induced hyperparathyroidism affects serum and gingival proinflammatory cytokine levels in rats.

BACKGROUND: Poor diet and inadequate nutrition are suggested to affect the periodontium as well as impair the systemic health. This study investigated the systemic and periodontal effects of dietary-induced hyperparathyroidism (dHPT) by evaluating serum and gingival proinflammatory cytokine levels. METHODS: Twenty-four Sprague-Dawley rats were used in the study. dHPT was induced in 12 rats by calcium/phosphorus imbalance, and 12 rats were fed a standard diet (SD). Afterward, endotoxin-induced periodontitis was induced on the right mandibular molar teeth (mmt). Four study groups were created: dHPT + mmt without periodontitis (group 1), dHPT + mmt with periodontitis (group 2), SD + mmt with periodontitis (group 3), and SD + mmt without periodontitis (group 4). Interleukin (IL)-1beta and tumor necrosis factor-alpha (TNF-alpha) levels were measured by enzyme-linked immunosorbent assay to evaluate the proinflammatory cytokine profiles. Serum cytokines were analyzed in the blood samples collected prior to periodontitis induction, whereas gingival cytokines were analyzed in the gingival supernatants of the four groups. RESULTS: Serum cytokines were higher in dHPT rats than in SD rats (P <0.001), with a positive correlation between parathormone and the cytokines (P <0.001). Gingival cytokines were highest in group 2 and lowest in group 4 (group 2 > group 3 > group 1) (P <0.001). There was a positive correlation between parathormone and the gingival cytokines in group 1 (P <0.001 for IL-1beta; P <0.01 for TNF-alpha). CONCLUSION: The results suggested that increased serum proinflammatory cytokine production may be a complication of dHPT, and this may affect healthy and diseased periodontia by increasing gingival proinflammatory cytokine levels.

Osmotic pressure and vasculature of gingiva in periodontal disease: an experimental study in rats.

Alterations in vascularisation, vasodilatation and tissue osmotic pressure (OP) are inevitable aspects of the inflammatory process that have an adverse effect on the fluid dynamics of the tissue involved. The aim of this study was to investigate tissue OP and its relationship with the vasculature in inflammed gingival tissues, in order to reveal the possible effects of vascular changes on OP in the fluid dynamics of periodontal soft tissues during periodontal disease. The parameters of fluid dynamics assessed in this study were OP, vascularisation and vasodilatation. Ligature-induced periodontitis was performed in 10 rats (test group), and gingival biopsies taken from the diseased teeth were utilised for the test procedures. These biopsies were compared with biopsies of the same teeth from 10 periodontally healthy rats (control group). OP was measured in mosmol/kg using a semi-micro digital osmometer. Vascularisation and vasodilatation were examined histopathologically; the number of vessels (VN) was quantified and the micrometric changes in vessel diameters (VD) were calculated as the alterations in the vasculature. OP, VN and VD were found to be higher in the test group (84.3+/-37.1 mosmol/kg, 13.2+/-3.2 and 19.5+/-1.3 microm, respectively) than the control group (11.6+/-3.8 mosmol/kg, 6.8+/-1.1 and 15.5+/-2.4 microm, respectively) (P<0.000). There was a strong, positive correlation between OP and VN (r=0.55, P<0.000) and a weak, negative correlation between OP and VD (r=0.1, P>0.05) in the test group. These results confirm that the OP of periodontal soft tissues does change during inflammatory conditions. The increase in OP during this process may be affected by increased vascularisation in the inflammed tissue.