Aspects of adaptive host response in periodontitis

Abstract

In periodontitis lesions, plasma cells are the most common cell type and represent about 50% of all cells, while B cells comprise about 18%. The proportion of B cells is larger than that of T cells and Th cells occur in larger numbers than T cytotoxic cells. Polymorphonuclear cells and macrophages are found in fractions of less than 5% of all cells. Lesions in aggressive and chronic forms of periodontitis exhibit similar cellular composition. Differences in disease severity, however, may reflect increases in plasma cell and B cell densities. B cells serve as important antigen-presenting cells in periodontitis. The periodontitis lesion expresses a unique TCR gene repertoire that is different from that in blood. The role of superantigens in periodontitis is unclear. There are few studies using comparative designs and unbiased quantitative methods regarding Th-1 and Th-2 cells in periodontitis. The relative dominance of B cells and plasma cells in periodontitis lesions cannot entirely be explained by enhanced Th-2 functions but maybe because of an imbalance between Th-1 and Th-2. Autoimmune reactions are evident in periodontitis lesions. The role of auto-antibodies in the regulation of host response in periodontitis, however, needs to be clarified. Auto-reactive B cells occur in larger proportions in subjects with periodontitis than in healthy controls.

Host‐response: understanding the cellular and molecular mechanisms of host‐microbial interactions – Consensus of the Seventh European Workshop on Periodontology

“…The essential difference between periodontitis and RA is that RA is an autoimmune disease, while periodontitis is an infectious disease. Nevertheless, in periodontitis there are autoimmune responses against tissue breakdown components (reviewed in Berglundh & Donati 2005).…”

“…T regulatory cells (Treg) are also implicated in RA; a lower activity has been found in active lesions, while after successful treatment of RA, Treg activity is increased. In periodontal diseases, the development of gingivitis involves Th1 cells, while in periodontitis there is a shift towards Th2 cells (reviewed in Berglundh & Donati 2005). The number of Treg cells is increased in periodontitis compared with gingivitis tissues (Nakajima et al 2005).…”

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

“…In gingivitis the host innate and adaptive immune system are able to control the bacterial infection. In periodontitis however, the balance between bacteria and host response is disturbed, resulting in an uncontrolled inflammation characterized by the production of high levels of inflammatory mediators such as IL-1, IL-6, IL-17 and TNF-α, and low levels of anti-inflammatory molecules such as IL-10 [9,57]. These molecules act in concert to amplify the inflammatory reaction and activate the effector mechanisms responsible for tissue destruction in PDs (Fig.…”

Mucosal Langerhans Cells Promote Differentiation of Th17 Cells in a Murine Model of Periodontitis but Are Not Required for Porphyromonas gingivalis–Driven Alveolar Bone Destruction

“…Infiltration of these immune cells leads to hostmediated destruction of alveolar bone and loss of connective tissue attachment to the tooth (3)(4)(5)(6). In this regard, periodontitis resembles other inflammatory-driven bone destructive diseases where proinflammatory cytokines IL-1, IL-6, IL-17A, receptor activator for NF-kB ligand (RANKL), and TNF-a are important mediators of osteoclast differentiation, activation, and survival (7).…”