ArticleProceedings of the National Academy of Sciences of the United States of America2025
Inflammasome targeting for periodontitis prevention is sex dependent.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Salivary NLRP3 inflammasome as a promising biomarker for palatal mucosa healing in diabetes mellitus: A pilot study.Journal of periodontology · 2026Article
- NLRP3 inflammasome promotes PAD2/PAD4 release and protein citrullination in rheumatoid arthritis.Communications biology · 2026Article
- Sex differences in immune responses to viruses, bacteria and vaccines.Nature immunology · 2026Review
- Sex-specific variations in subgingival microbiome of elderly patients with moderate periodontitis: an exploratory study.Frontiers in genetics · 2026Article
- Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice.Frontiers in immunology · 2026Article
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Authors and funding
29 authors.
Funding
Abstract
Inflammasome initiates inflammation via the maturation of interleukin-1 beta (IL-1β). Periodontitis is a prevalent, male-biased disease characterized by inflammation-driven bone loss, yet the mechanism(s) of this sex bias is unknown. This study explored whether enhanced inflammasome represents a causal mechanism for this bias. Analyses of three separate human studies (>6,200 samples) show that males have significantly higher IL-1β in the gingival crevicular fluid than females during health and periodontitis. This pattern is experimentally reproduced with different versions of the ligature-induced periodontitis mouse model where males show greater IL-1β secretion than females. The inflammasome drives bone resorption in males but not females as revealed by analyses of inflammasome gene-deletion mice. Pharmacologic treatment with a caspase-1/4 inhibitor reduces inflammatory cell infiltration, dampens osteoclastogenesis signaling (via the receptor activator of nuclear factor-kappa B pathway), and prevents bone resorption in males but not females during experimental periodontitis. While ovariectomized females show no change in their nonresponsiveness to caspase-1/4 inhibition, orchiectomized males no longer respond to the inhibition, suggesting the importance of an intact male reproductive system in the mediation of this inhibition. Thus, our study identifies inflammasome activation as causal for male-biased experimental periodontitis and supports sex-stratified studies to foster future advancement of inflammasome therapeutics in periodontics.
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Registered trials
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