Background: Periodontitis is a chronic immune-inflammatory disease associated with microbial dysbiosis and
dysregulated host response, leading to irreversible destruction of the periodontal apparatus and alveolar bone.
Conventional treatments primarily target bacterial reduction but do not actively resolve inflammation or restore tissue
homeostasis. Specialized pro-resolving mediators (SPMs), such as resolvin E1 (RvE1), derived from omega-3 fatty
acids, have emerged as potent modulators of inflammation resolution through interaction with the chemerin receptor
CHEMR23.
Objective: This study aimed to evaluate the effects of RvE1 on alveolar bone loss and inflammatory response in ligatureinduced experimental periodontitis in rats, using histopathological, immunohistochemical, and molecular genetic approaches, and to identify CHEMR23-expressing cells as potential RvE1 targets.
Material and methods: Thirty male Wistar rats were randomly divided into five groups (n=6 per group): control (I),
periodontitis (II), vehicle (III), early RvE1 treatment (IV; administration from Day 1), and late RvE1 treatment (V;
administration from Day 7). Alveolar bone loss was assessed by measuring the cemento-enamel junction to alveolar
bone crest distance. Histological evaluation and TRAP staining were used to assess inflammation and osteoclastic
activity. Expression of CHEMR23 was examined immunohistochemically. Relative mRNA levels of TNF-α, IL-1β,
RANK, and OPG in gingival tissues were determined by qPCR method.
Results: Ligature-induced periodontitis caused pronounced inflammatory infiltration, alveolar bone resorption, and
increased numbers of TRAP+ osteoclasts, accompanied by up-regulation of TNF-α, IL-1β, and RANK. RvE1
administration significantly reduced the cemento-enamel junction to alveolar bone crest distance and inflammatory
scores. Early RvE1 treatment showed stronger protection than late treatment, restoring near-normal bone architecture
and cytokine expression profiles. CHEMR23 immunoreactivity was detected predominantly in osteoclasts,
macrophages, and lymphocytes, suggesting these as primary RvE1-responsive cell populations.
Conclusion: Resolvin E1 effectively attenuates inflammation and bone resorption in experimental periodontitis, acting
partly through CHEMR23-expressing osteoclasts and immune cells. Early intervention yields superior outcomes,
highlighting the importance of timely modulation of inflammatory and osteoclastogenic pathways. These findings
support RvE1 as a promising therapeutic candidate for host-modulatory management of periodontitis
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