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

Area of Science:

• Oral Pathology
• Immunology
• Rheumatology

Background:

• Rheumatoid arthritis (RA) is a systemic autoimmune disease.
• Apical periodontitis (AP) is an inflammatory condition of the periapical tissues.
• The interplay between RA and AP requires further investigation.

Purpose of the Study:

• To evaluate the impact of rheumatoid arthritis on the inflammatory and resorptive processes in periapical lesions.
• To investigate the expression of key inflammatory and bone remodeling markers in an animal model.

Main Methods:

• An animal model using Wistar rats was established with four groups: control, AP, RA, and AP+RA.
• Rheumatoid arthritis was induced using methylated bovine albumin (Met-BSA) and Freund's adjuvant.
• Apical periodontitis was induced by pulp exposure; lesions were analyzed via histology, immunohistochemistry (IL-6, IL-17, TNF-α, RANKL, OPG, TRAP), and micro-CT.

Main Results:

• The AP+RA group showed significantly more intense inflammatory infiltrate and exacerbated immune profiles for IL-17 and TNF-α compared to the AP group.
• Micro-CT analysis revealed larger periapical lesions in the AP+RA group.
• Immunostaining indicated greater expression of RANKL and TRAP in the AP+RA group.

Conclusions:

• Rheumatoid arthritis exacerbates periapical inflammation and bone resorption associated with apical periodontitis.
• RA increases the levels of IL-17, TNF-α, TRAP, and RANKL in periapical lesions.