ArticleJDR clinical and translational research2018
Periodontitis in Chédiak-Higashi Syndrome: An Altered Immunoinflammatory Response.
Article in JDR clinical and translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Global Salivary Proteomic Profiling of Individuals with the Co-Occurrence of Type 2 Diabetes Mellitus, Dyslipidemia, and Periodontitis.International journal of molecular sciences · 2025Article
- Monoallelic mutations in MMD2 cause autosomal dominant aggressive periodontitis.The Journal of experimental medicine · 2025Article
- Genetic risk variants implicate impaired maintenance and repair of periodontal tissues as causal for periodontitis-A synthesis of recent findings.Periodontology 2000 · 2025Review
- Inborn errors of immunity-related immunological mechanisms and pharmacological therapy alternatives in periodontitis.Clinical and experimental immunology · 2025Review
- Toward Digital Periodontal Health: Recent Advances and Future Perspectives.Bioengineering (Basel, Switzerland) · 2024Review
- Oral Management of a Haematopoietic Stem Cell Transplant Recipient with Chédiak-Higashi Syndrome.Case reports in dentistry · 2021Article
- Characterization of Cytokines and Proliferation Marker Ki67 in Cleft Affected Lip Tissue.Medicina (Kaunas, Lithuania) · 2019Article
- Primary immunodeficiencies reveal the essential role of tissue neutrophils in periodontitis.Immunological reviews · 2019Review
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Chédiak-Higashi syndrome (CHS), a rare autosomal recessive disorder caused by mutations in the lysosomal trafficking regulator gene (LYST), is associated with aggressive periodontitis. It is suggested that LYST mutations affect the toll-like receptor (TLR)-mediated immunoinflammatory response, leading to frequent infections. This study sought to determine the periodontal status of patients with classic (severe) and atypical (milder) forms of CHS and the immunoregulatory functions of gingival fibroblasts in CHS patients. In contrast to aged-matched healthy controls, atypical (n = 4) and classic (n = 3) CHS patients presented with mild chronic periodontitis with no evidence of gingival ulceration, severe tooth mobility, or premature exfoliation of teeth. As a standard of care, all classic CHS patients had undergone bone marrow transplantation (BMT). Primary gingival fibroblasts obtained from atypical and BMT classic CHS patients displayed higher protein expression of TLR-2 (1.81-fold and 1.56-fold, respectively) and decreased expression of TLR-4 (-2.5-fold and -3.85-fold, respectively) at baseline when compared with healthy control gingival fibroblasts. When challenged with whole bacterial extract of Fusobacterium nucleatum, both atypical and classic CHS gingival fibroblasts failed to up-regulate TLR-2 and TLR-4 expression when compared with their respective untreated groups and control cells. Cytokine multiplex analysis following F. nucleatum challenge showed that atypical CHS gingival fibroblasts featured significantly increased cytokine expression (interleukin [IL]-2, IL-4, IL-5, IL-6, IL-10, IL-12, interferon-γ, tumor necrosis factor-α), whereas classic CHS cells featured similar/decreased cytokine expression when compared with treated control cells. Collectively, these results suggest that LYST mutations in CHS patients affect TLR-2 and TLR-4 expression/function, leading to dysregulated immunoinflammatory response, which in turn may influence the periodontal phenotype noted in CHS patients. Furthermore, our results suggest that atypical CHS patients and classic CHS patients who undergo BMT early in life are less susceptible to aggressive periodontitis and that hematopoietic cells play a critical role in mitigating the risk of aggressive periodontitis in CHS.
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