mobic and Mandibular-Diseases

To assess whether the administration of meloxicam before head and neck radiotherapy reduces the risk of mandibular osteoradionecrosis in rats.. Sixty male Wistar rats were randomly divided into 6 groups (n = 10) according to the meloxicam administration and radiation therapy: control (C), irradiated (I), single dose of meloxicam (M1), single dose of meloxicam and irradiated (M1I), triple dose of meloxicam (M3), triple dose of meloxicam and irradiated (M3I). Meloxicam was administrated (20 mg/kg per dose) 1 h before the radiation therapy (single dose of 20 Gy) and 24 h and 48 h after the radiation therapy for groups with two additional doses. Ten days after the radiation therapy, the three right mandibular molars were extracted from all rats, who were euthanatized after 21 or 35 days (n = 5 per group). The mandibles were assessed by macroscopic evaluation and micro-CT analysis.. The right hemimandibles of the irradiated groups revealed macroscopic signs of osteoradionecrosis, and those of the non-irradiated groups revealed complete gingival healing. A significant delay in alveolar socket healing in all irradiated groups was observed in the micro-CT assessment regardless meloxicam treatment.. The administration of meloxicam before head and neck radiotherapy does not reduce the risk of mandibular osteoradionecrosis when associated to dental extractions.. Since meloxicam has been shown to be a potential radiation-protective agent, and osteoradionecrosis physiopathology is believed to be related to an inflammatory process, possible interactions are relevant to be investigated.

Topics: Animals; Head and Neck Neoplasms; Male; Mandible; Mandibular Diseases; Meloxicam; Osteoradionecrosis; Rats; Rats, Wistar; X-Ray Microtomography

To elucidate the pathogenesis of periapical lesion-associated bone resorption, a disease model of Wistar rat molar was employed. After lesion induction, the mRNAs encoding for matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2) in the developing lesions were detected by in situ hybridization at day 5, 10, 15 and 20, respectively. At day 5, MMP-1, IL-6 and COX-2 mRNAs appeared predominantly in macrophages. During day 15 to day 20, increased expressions of these mediators were also found in osteoblasts but to a lesser extent compared with those in macrophages. MMP-1 mRNA was also detected in osteoclasts. In contrast, expression of the TIMP-1 gene was noted primarily in osteoblasts and was less pronounced compared with that of MMP-1. The mediator-expressing cells aggregated in the vicinity of bone resorption areas and their numbers increased with time. These data suggest that macrophages and osteoblasts are involved in the development of periapical lesions, and that they promote bone resorption by producing MMP-1, IL-6 and COX-2. In addition, administration of a specific COX-2 inhibitor, meloxicam, reduced the extent of periapical bone resorption by 43% and simultaneously diminished the numbers of cells synthesizing MMP-1 and IL-6 mRNAs. These results further elucidate the significance of COX-2 in disease progression of periapical lesions as it modulates indirectly the production of MMP-1 and IL-6.

Topics: Animals; Bone Resorption; Cell Count; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Disease Models, Animal; Disease Progression; Gene Expression; In Situ Hybridization; Injections, Intraperitoneal; Interleukin-6; Isoenzymes; Macrophages; Mandibular Diseases; Matrix Metalloproteinase 1; Meloxicam; Osteoblasts; Periapical Diseases; Peroxidases; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Wistar; RNA, Messenger; Thiazines; Thiazoles; Time Factors; Tissue Inhibitor of Metalloproteinase-1