Hyperocclusion up-regulates CCL3 expression in CCL2- and CCR2-deficient mice.

UNLABELLED: Excessive mechanical stress (MS) during hyperocclusion is known to result in disappearance of the alveolar hard line, enlargement of the periodontal ligament (PDL) space, and destruction of alveolar bone, leading to occlusal traumatism. We have recently reported that MS induces predominantly C-C chemokine ligand (CCL) 2 expression in PDL tissues, leading, via C-C chemokine receptor (CCR) 2, to MS-dependent osteoclastogenesis in alveolar bone. Thus, we hypothesize that ablation of the CCL2/CCR2 signaling pathway should suppress MS-induced osteoclastogenesis-associated chemokines and alleviate occlusal traumatism. We examined the effect of MS on chemokine expression and osteoclastogenesis using in vivo and in vitro hyperocclusion models with CCL2-deficient (CCL2((-/-))) and CCR2-deficient (CCR2((-/-))) mice. Compared with that in wild-type mice, expression of CCL3 in PDL cells and TRAP-positive cells in alveolar bone from CCL2((-/-)) and CCR2((-/-)) mice was up-regulated, even in the absence of MS. Furthermore, the expression of CCL3 and TRAP-positive cells was significantly increased after both 4 and 7 days of hyperocclusal MS loading in CCL2((-/-)) and CCR2((-/-)) mice. Hyperocclusion induced compensatory CCL3 expression and promoted osteoclastogenesis to counterbalance deficient CCL2/CCR2 signaling, suggesting that co-expression of CCL3 with CCL2 may precipitate synergistic, MS-dependent alveolar bone destruction during occlusal traumatism. ABBREVIATIONS: MS, mechanical stress; PDL, periodontal ligament; CCL2, CC chemokine ligand 2 (MCP-1; monocyte chemoattractant protein-1); CCR2, CC chemokine receptor 2; CCL3, CC chemokine ligand 3 (MIP-1α); CCL5, CC chemokine ligand 5 (RANTES).

Alterations in the masseter muscle and plasma IL-6 level following experimentally induced occlusal interference and chronic stress--a study in rats.

This study was undertaken to examine the alteration of masseter and plasma interleukin-6 after inducing occlusal interference and chronic stress. Male Wistar rats were submitted to chronic stress procedure, exposed to occlusal interference, or exposed to both mentioned procedures. Whole blood and masseter tissue were collected to determine interleukin-6 level, measured by means of ELISA. Masseter pain was evaluated using the orofacial formalin test. Masseter interleukin-6 level was significantly higher in animals submitted to combination of occlusal interference and chronic stress than in the control group (p<0.05). There was positive and significant correlation between pain response and masseter interleukin-6 level (r=0.5741; p<0.0003). No significant differences in plasma interleukin-6 level were found between groups (p>0.05), as well as no correlation with pain (p>0.05). Combination of occlusal interference and chronic stress leads to strong local reaction characterized by high levels of masseter interleukine-6. High concentrations of muscle interleukin-6 and its correlation with pain point to inflammatory background of masticatory muscle pain.

Saliva components reestablish the basal production of IL-6 by mononuclear cells, 72 hours after nitinol archiwire placement: a preliminary study.

The purpose of the study was to evaluate interleukin-6 production, in saliva-activated mononuclear cell cultures from malocclusion patients, before and after placement of .014 NiTi archwires.Four patients receiving .014 Nitinol archwire to correct malocclusion participated in this study. Samples of their blood and saliva were collected before and after placement of the apparatus. Mononuclear cells were obtained from the blood using the Ficoll-Paque (1.077 g/ml) density gradient separation method. Mononuclear Cells were activated with saliva from each patient and were cultured in 96-well plates for 72 hours. Samples were collected at 24 hours before apparatus placement, and at 24 hours and 72 hours after placement. IL-6 expression levels in the cell culture supernatants were quantified by ELISA. An increase in IL-6 levels in the cell culture supernatants was observed 24 hours after placement of the orthodontic apparatus relative to the negative control (p = 0.002) and IL-6 came to basal limits 72 hours after apparatus placement.IL-6 quantification may be useful as a biomarker to estimate the inflammatory response caused by forces applied during orthodontic treatment and their levels came to basal limits 72 hours after apparatus placement in patients without systemic diseases. The isolation of saliva components involved in such effects is important to study the mechanisms to control the acute inflammation in oral cavity after apparatus placement.