Orthodontic treatment in patients with reduced periodontal support, often resulting from a history of periodontitis, presents significant clinical challenges due to the heightened risk of alveolar bone loss and periodontal tissue destruction. This narrative review synthesizes recent evidence from peer-reviewed studies on the cytokine and chemokine profiles during orthodontic tooth movement (OTM) in the context of compromised periodontal health. Cytokines such as interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), and chemokines including C-X-C motif ligand 1 (CXCL1), CXCL2, CXCL5, CXCL8, and CXCL10 play pivotal roles in mediating inflammation, immune cell recruitment, and bone remodeling. In animal models and in vitro studies, bacterial stimuli from periodontopathogens like Fusobacterium nucleatum and Porphyromonas gingivalis upregulate these mediators, exacerbating inflammatory responses. Mechanical forces associated with OTM can further modulate these profiles, sometimes amplifying bacteria-induced expression, as seen in elevated RANKL/OPG ratios leading to enhanced osteoclastogenesis. However, certain studies indicate that biomechanical strain may counteract proinflammatory effects under specific conditions. Key findings highlight protective interventions, such as recombinant irisin or semaphorin 3A, which mitigate bone loss by altering cytokine levels. This review underscores the interplay between microbial and mechanical signals in altering cytokine and chemokine dynamics, offering insights into molecular mechanisms that could inform safer orthodontic strategies for periodontally compromised patients. Understanding these profiles may facilitate targeted therapies to minimize adverse outcomes during treatment.
