Host response mechanisms in periodontal diseases

Abstract

Periodontal diseases usually refer to common inflammatory disorders known as gingivitis and periodontitis, which are caused by a pathogenic microbiota in the subgingival biofilm, including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Treponema denticola that trigger innate, inflammatory, and adaptive immune responses. These processes result in the destruction of the tissues surrounding and supporting the teeth, and eventually in tissue, bone and finally, tooth loss. The innate immune response constitutes a homeostatic system, which is the first line of defense, and is able to recognize invading microorganisms as non-self, triggering immune responses to eliminate them. In addition to the innate immunity, adaptive immunity cells and characteristic cytokines have been described as important players in the periodontal disease pathogenesis scenario, with a special attention to CD4+ T-cells (T-helper cells). Interestingly, the T cell-mediated adaptive immunity development is highly dependent on innate immunity-associated antigen presenting cells, which after antigen capture undergo into a maturation process and migrate towards the lymph nodes, where they produce distinct patterns of cytokines that will contribute to the subsequent polarization and activation of specific T CD4+ lymphocytes. Skeletal homeostasis depends on a dynamic balance between the activities of the bone-forming osteoblasts (OBLs) and bone-resorbing osteoclasts (OCLs). This balance is tightly controlled by various regulatory systems, such as the endocrine system, and is influenced by the immune system, an osteoimmunological regulation depending on lymphocyte- and macrophage-derived cytokines. All these cytokines and inflammatory mediators are capable of acting alone or in concert, to stimulate periodontal breakdown and collagen destruction via tissue-derived matrix metalloproteinases, a characterization of the progression of periodontitis as a stage that presents a significantly host immune and inflammatory response to the microbial challenge that determine of susceptibility to develop the destructive/progressive periodontitis under the influence of multiple behavioral, environmental and genetic factors.

The Distribution of Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola and Aggregatibacter actinomycetemcomitans in Patients with Alcoholic Disease: A Pilot Study

“…Alcoholics tend to also smoke tobacco that increases their risk for periodontal disease. Numerous studies showed associations between different periopathogens, the immune host response and chronic periodontitis [25]. Present of periopathogens: A. actinomycetemcomitans, P. gingivalis, T. forsythia and T. denticola are considered to be the main periodontal pathogens and strongly associated to the clinical status of periodontal tissues and progression of the periodontal disease [26,27].…”

Probiotics and Periodontal Diseases

“…DC has a central role in directing the T cell response. They can change to T helper cell (Th) 1, Th2, Th17 and T regulatory cells (Treg) [65]. Certain bacterial strains induce the production of Th polarizing key cytokines by DCs, such as IL-10, IL-12 and IL-23 [66,67].…”

“…They represent a family of human zinc-dependent endopeptidases [65]. L. brevis CD2 decreased MMP in saliva [60].…”

“…However, a few bacteria in the subgingival biofilm have been associated with disease. Strong evidence concluded that P. gingivalis, A. actinomycetemcomitans and T. forsythia are periodontal pathogens [65]. Although the tooth-associated biofilm plays a role in the development of periodontitis, it is primarily the host inflammatory response that inflicts the irreversible damage on the periodontium [108].…”

“…Although the tooth-associated biofilm plays a role in the development of periodontitis, it is primarily the host inflammatory response that inflicts the irreversible damage on the periodontium [108]. T helper 1 and Th17 lymphocyte have been described in the pathogenesis of disease [65].…”