Toll-like receptors and their dual role in periodontitis: a review

Abstract

Innate immunity is the first line of host defense and represents inherited resistance to infection. Innate immunity works through toll-like receptors (TLRs), which recognize the conserved molecular patterns on pathogenic bacteria known as pathogen-associated molecular patterns. The periodontium is a unique environment in which oral microorganisms are in constant contact with the host immune system. The TLRs present on gingival epithelial cells are continuously stimulated, resulting in production of cytokines and defensins that help to maintain oral health. If the epithelial barrier is breached, allowing invasion of bacteria into the underlying connective tissue, the TLRs on other resident and non-resident cells of the periodontium become activated. This leads to an exaggerated release of pro-inflammatory cytokines and other biological mediators, which may cause host tissue destruction. The present review examines the role of TLRs and their signaling in periodontal health and disease.

Role of the Hypoxia-Inducible Factor in Periodontal Inflammation

“…Bacterial components, such as LPS and peptidoglycans, released by bacteria recognized by TLRs on the surface of host cells could instigate the inlammatory reaction cascade [38]. Under steady-state conditions, activation of TLRs by commensal bacteria is critical for the maintenance of oral health [73]. Thus, TLRs provide the irst line of defense in periodontal health maintenance.…”

“…TLRs on the periodontal/gingival epithelial cells recognize the conserved molecular paterns on pathogenic bacteria that are also known as PAMP, limiting invasion of the microbes, and help to maintain oral health [73]. Other than providing a physical barrier to the outside world, the skin and mucosal membrane produce a number of antimicrobial peptides (AMPs).…”

Local and systemic immune responses in gingivitis and periodontitis

“…The data of Wang et al (2000) indicated that P. gingivalis LPS bound the toll-like receptor-4 in gingival fibroblast [8]. The resident cells involved in the innate host response are many, including epithelial cells, gingival and periodontal ligament I Barzdziukaite et al fibroblasts, osteoblasts, and dendritic cells [9]. Once TLR S on the surface of the resident cells recognize pathogen-associated molecular patterns, they initiate the activation of several transcription factors including activator protein 1 and the receptor activator of nuclear factor kappa β ligand (RANKL) through the mitogenactivated proteinkinase cascade [9,10].…”

“…The resident cells involved in the innate host response are many, including epithelial cells, gingival and periodontal ligament I Barzdziukaite et al fibroblasts, osteoblasts, and dendritic cells [9]. Once TLR S on the surface of the resident cells recognize pathogen-associated molecular patterns, they initiate the activation of several transcription factors including activator protein 1 and the receptor activator of nuclear factor kappa β ligand (RANKL) through the mitogenactivated proteinkinase cascade [9,10]. These, in turn, activate different innate immunity pathways -including cytokine and chemokine production -that recruit nonresident leukocytes to the periodontal space.…”

Sexual dimorphism in periodontitis in a mouse model.

“…The innate component is mediated by pattern recognition receptors (PRRs). These pattern-recognition receptors are transmembrane proteins which detect unique structures pertaining to a pathogen, known as pathogen-associated molecular patterns (PAMPs) 37,38 . PAMPs of microorganisms include LPS, peptidoglycan, and lipoproteins 38 .…”