Rheumatoid arthritis exacerbates apical periodontitis in Wistar rats, increasing IL-17, TNF-α, TRAP, and RANKL levels.

This study aimed to evaluate the influence of rheumatoid arthritis on the inflammatory and resorptive process of periapical lesions in an animal model. Forty Wistar rats were divided into four groups (n = 10): control (C), apical periodontitis (AP), rheumatoid arthritis (RA), and AP + RA. RA was induced by two injections into the caudal subcutaneous tissue containing 50 µL volume of methylated bovine albumin (Met-BSA, 40 mg/mL) and 5% glucose emulsified with CFA/complete Freund's adjuvant (Mycobacterium sp), and a third intra-articular injection in the right knee with half of the same solution. The right knee width was measured throughout the experimental period. AP was induced by pulp exposure of the right upper and lower first and second molars. After 30 days, the animals were euthanized, and the joints were processed for descriptive analysis using hematoxylin-eosin (H&E) staining. The hemi-mandibles were also removed and the inflammatory infiltrate was analyzed by H&E and immunohistochemistry for IL-6, IL-17, TNF-α, and the resorptive process by RANKL, OPG, TRAP, and micro-CT analysis. Statistical tests were applied (p < 0.05). The periapical lesions of the AP + RA group exhibited a more intense inflammatory infiltrate and a more exacerbated immune profile for IL-17 and TNF-α compared to the AP group (p < 0.05). Micro-CT analysis revealed larger lesions in the AP + RA group and greater immunostaining for RANKL and TRAP compared to the AP group (p < 0.05). It can be concluded that RA exacerbates periapical inflammation and bone resorption of AP, increasing the levels of IL-17, TNF-α, TRAP, and RANKL.