80 research outputs found
Unraveling the Link between Periodontitis and Inflammatory Bowel Disease: Challenges and Outlook
Periodontitis and Inflammatory Bowel Disease (IBD) are chronic inflammatory
conditions, characterized by microbial dysbiosis and hyper-immunoinflammatory
responses. Growing evidence suggest an interconnection between periodontitis
and IBD, implying a shift from the traditional concept of independent diseases
to a complex, reciprocal cycle. This review outlines the evidence supporting an
Oral-Gut axis, marked by a higher prevalence of periodontitis in IBD patients
and vice versa. The specific mechanisms linking periodontitis and IBD remain to
be fully elucidated, but emerging evidence points to the ectopic colonization
of the gut by oral bacteria, which promote intestinal inflammation by
activating host immune responses. This review presents an in-depth examination
of the interconnection between periodontitis and IBD, highlighting the shared
microbiological and immunological pathways, and proposing a multi-hit
hypothesis in the pathogenesis of periodontitis-mediated intestinal
inflammation. Furthermore, the review underscores the critical need for a
collaborative approach between dentists and gastroenterologists to provide
holistic oral-systemic healthcare.Comment: Total Words: 7,016 Figures: 3 Tables: 2 Reference: 34
The characteristics of bisphosphonate patients developing bisphosphonate-related osteonecrosis of the jaw attending an OMFS department
Serum Markers of Bone Turnover and Angiogenesis in Patients With Bisphosphonate-Related Osteonecrosis of the Jaw After Discontinuation of Long-Term Intravenous Bisphosphonate Therapy
M2a macrophages facilitate resolution of chemically-induced colitis in TLR4-SNP mice
ABSTRACT Toll-like receptor 4 (TLR4) is an innate immune receptor responsive to lipopolysaccharide (LPS). Single nucleotide polymorphisms (SNPs) in human TLR4 that encode an A896G transition at SNP rs4986790 (D299G) and a C1196T transition at SNP rs4986791 (T399I) render individuals hyporesponsive to LPS. In humans, these SNPs are also associated with increased susceptibility to inflammatory bowel diseases (IBDs). Using knock-in mice engineered to express the murine homologs of these human TLR4 mutations (“TLR4-SNP” mice), we have shown that TLR4-SNP mice develop significantly more severe colitis induced by dextran sodium sulfate (DSS) than wild-type (WT) mice, similar to IBD in humans expressing these SNPs. Previous studies have provided indirect evidence for “tissue repair” M2 macrophages (Mφ) in the resolution of colitis. Signaling through the IL-4/IL-13 receptor, IL-4Rα, and the transcription factor, peroxisome proliferator-activated receptor (PPARγ), have been shown to be required for induction of M2a Mφ, and our data provide direct evidence for the involvement of both in the repair of DSS-induced colonic damage. In response to DSS, colons of TLR4-SNP mice produced reduced levels of M2a Mφ marker mRNA and protein, including PPARγ, and therapeutic administration of the PPARγ agonist ligand, rosiglitazone, resolved colitis in TLR4-SNP mice, and increased expression of the M2a protein, Ym1. Together, these data indicate that the failure of TLR4-SNP mice to resolve DSS-induced colitis may be secondary to their failure to induce “tissue repair” M2a Mφ. Importance Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, impacts millions of individuals worldwide and severely impairs the quality of life for patients. Dysregulation of innate immune signaling pathways reduces barrier function and exacerbates disease progression. Macrophage (Mφ) signaling pathways are potential targets for IBD therapies. While multiple treatments are available for IBD, (i) not all patients respond, (ii) responses may diminish over time, and (iii) treatments often have undesirable side effects. Genetic studies have shown that the inheritance of two co-segregating SNPs expressed in the innate immune receptor, TLR4, is associated with human IBD. Mice expressing homologous SNPs (“TLR4-SNP” mice) exhibited more severe colitis than WT mice in a DSS-induced colonic inflammation/repair model. We identified a critical role for M2a “tissue repair” Mφ in the resolution of colitis. Our findings provide insight into potential development of novel therapies targeting Mφ signaling pathways that aim to alleviate the debilitating symptoms experienced by individuals with IBD
Treatment of Amalgam Tattoo With a New Technique: Mucoabrasion and Free Connective Tissue Graft
Medication-related osteonecrosis of the jaws caused lethal sepsis in an edentulous patient with multiple systemic factors
Resource utilization in cancer patients with bisphosphonate-associated osteonecrosis of the jaw
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