acid-phosphatase and Dental-Occlusion--Traumatic

Occlusal trauma (OT) and smoking are both factors that alter alveolar bone metabolism and therefore could synergistically act on alveolar bone loss. The aim of this experimental study was to evaluate the influence of short-term cigarette smoke inhalation (CSI) on inter-radicular alveolar bone loss promoted by primary OT in a rat model.. Forty-eight animals were randomly assigned to one of three groups based on treatment type: OT + CSI (n = 16), animals were exposed to CSI three times per day, for 8 min per exposure, and they concomitantly received unilateral vertical augmentation creating an occlusal interference inducing experimental OT; OT (n = 16), animals received only unilateral vertical augmentation; negative control (NC; n = 16), animals maintained for equal periods to achieve periodontal baseline values of periodontal ligament dimension. Each group was divided into two subgroups (n = 8) based on treatment length: 7 or 14 d.. After 7 d, the OT + CSI group exhibited significantly higher bone loss compared to the NC group (p = 0.0022). After 14 d, the OT (p < 0.0001) and OT + CSI (p < 0.0001) groups presented significantly higher bone loss compared to the NC group, and OT + CSI resulted in significantly higher bone loss than OT alone (p = 0.0241). The number of tartrate-resistant acid phosphatase-positive cells on the linear surface of the bone crest after 7 d was significantly higher in the OT + CSI group as compared to the NC and OT groups (p < 0.0001 and p = 0.0045, respectively) and remained significantly higher in the OT + CSI group after 14 d, compared to the OT group (p < 0.0001).. Short-term CSI increases early bone loss in association with OT after 7 d, and this worsens in severity after 14 d of exposure.

Topics: Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomarkers; Dental Occlusion, Traumatic; Disease Models, Animal; Disease Progression; Furcation Defects; Isoenzymes; Male; Random Allocation; Rats; Rats, Wistar; Smoking; Tartrate-Resistant Acid Phosphatase; Time Factors

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.. 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).

Topics: Acid Phosphatase; Alveolar Bone Loss; Alveolar Process; Animals; Biomechanical Phenomena; Cell Culture Techniques; Chemokine CCL2; Chemokine CCL3; Chemokine CCL5; Dental Occlusion, Traumatic; Isoenzymes; Malocclusion; Mice; Mice, Inbred C57BL; Mice, Knockout; Osteoclasts; Periodontal Ligament; Receptors, CCR1; Receptors, CCR2; Signal Transduction; Stress, Mechanical; Tartrate-Resistant Acid Phosphatase; Time Factors; Up-Regulation

This histochemical study showed that experimentally arteriosclerotic rats, subjected to an occlusal stress of six weeks' duration, showed an inflammation-related increase of chloride-activated arginine aminopeptidase and acid phosphatase activity in the basal cells of the gingival epithelium. The activity of chloride-activated arginine aminopeptidase and acid and alkaline phosphatase in the gingival connective tissue was slight and suggestive of chronic inflammation. Biochemical comparison of gingival specimens from the stressed and unstressed sides of the jaw in the experimental animals failed to reveal any difference in the rate of N-L-arginyl-2-naphthylamide hydrolysis induced by the C1-ion in connection with occlusal disorder. On the other hand, the mean value of the enzyme activity was lower in the experimental animals than the controls (p less than 0.5). The difference was assumed to be associated with degenerative tissue changes. The hydrolysis of p-nitrophenyl phosphate at acidic and alkaline pH in the gingiva was higher in the experimental animals than in the controls, and in the alkaline pH range the difference between the mean values was statistically significant (p less than 0.01). This finding, which may be associated not only with gingival inflammation but also with other tissue changes, requires further investigation.

Topics: Acid Phosphatase; Alkaline Phosphatase; Aminopeptidases; Animals; Arteriosclerosis; Dental Occlusion, Traumatic; Female; Gingivitis; Male; Rats