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Background: Annexin A1 (ANXA1) and the NOD‐like receptor family pyrin domain‐containing protein 3 (NLRP3) inflammasome play important roles in bone remodeling. However, expression profiles of these factors in bone cells under diabetes mellitus (DM) and estrogen‐deficient conditions are poorly understood. This study investigated the immunoexpression of ANXA1 and its formyl peptide receptor 2 (FPR2), as well as NLRP3 inflammasome mediators, during remodeling of the alveolar process in diabetic and estrogen‐deficient rats. Methods: Twenty adult female Wistar rats were divided into four groups (n = 5): Sham‐operated (SHAM) and ovariectomized (OVX) rats received a vehicle solution, and SHAM and OVX rats were intraperitoneally administered 60 mg/kg/body weight (BW) of streptozotocin (STZ) to induce DM (SHAM‐Di and OVX‐Di groups). After 7 weeks, the rats were euthanized and their maxillae were fixed in phosphate‐buffered 4% formaldehyde and embedded in paraffin. Sections were stained with hematoxylin/eosin (H&E) and picrosirius red or subjected to immunohistochemical detection of ANXA1, FPR2, NLRP3, interleukin‐1β (IL‐1β), and cyclooxygenase‐2 (COX2). Results: Estrogen deficiency and DM were associated with deleterious effects in bone tissue, as evidenced by a lower number of osteocytes and higher number of empty lacunae in the SHAM‐Di and OVX‐Di groups compared to the nondiabetic groups. Both diabetic groups showed a smaller vascular area and weaker collagen fiber birefringence intensity in alveolar bone tissue. A significantly higher number of ANXA1/FPR2‐positive osteoblasts, osteocytes, and osteoclasts was accompanied by a significantly higher number of these cells immunolabeled for COX2, NLRP3, and IL‐1β in the diabetic and OVX groups, especially in both estrogen‐deficient and diabetic rats. Conclusion: These results indicate a possible role for the ANXA1/FPR2 pathway as a fine‐tuning/anti‐inflammatory regulator to counterbalance exacerbated COX2/NLRP3/IL‐1β activation in bone cells during bone remodeling under estrogen deficiency and DM. [ABSTRACT FROM AUTHOR]

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