T AND B CELL SUBSETS IN PERIODONTITIS

Jose R, GonzalesPERIODONTOLOGY 2000,2015;69:181-200

GUIDED BY: PRESENTED BY:DR. AMIT GOEL DR. VIRSHALI GUPTA PG 1ST YEAR APPROVED ON: 11/04/16

INTRODUCTION

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Periodontitis is an inflammatory disease characterised by the interactions between oral microorganisms organised in biofilms and immune cell response against them, which leads to periodontal tissue breakdown.

However, subsequent disease progression and severity is determined by the host immune response which is governed by activating various cells like PMN’S, FIBROBLASTS, MONOCYTES, MACROPHAGES.

NK CELL

• NK cells are called natural because they do not need to recognize a specific antigen.

• NK cells kill on contact, binds with target aims its weapons and then deliver some toxins that produce holes in target cell membrane and cleaves DNA into pieces in a programmed cell death (apoptosis).

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NATURAL KILLER CELLS AND PERIODONTITS

• Only a few investigators have studied the role of NK cells in the pathogenesis of periodontitis:

1. Interferon-gamma has been suggested as one of the main cytokines in the pathogenesis of periodontitis.

• Mice lacking interferon-gamma demonstrate decreased bone loss following infection of the oral cavity with P. gingivalis, suggesting that interferon-gamma is a central mediator in this process.

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2. Impaired natural killer-cell cytotoxicity has been described in several genetic and acquired conditions associated with periodontal involvement.

3. Deficiency in the antimicrobial peptide, LL37, has been found in Morbus Kostmann syndrome (a genetic disorder associated with severe periodontitis).

• The expression of CD1 isoforms and Valpha 24(+) invariant NK cells ass with gingivitis and periodontitis was investigated.

• Investigations showed that CD1d expressing B cells could activate NK cells and this activation of NK cells may play a role in the pathogenesis of periodontal disease.

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• Recently, decreased numbers of T-helper cells and increased numbers of NK cells have been detected in chronic periodontitis.

• The predominant NK cell-activating molecule in periodontitis was CD2-like receptor activating cytotoxic cells.

• Additional results showed that infection with A. actinomycetemcomitans induce NK cells activation and infection with P. gingivalis did not induce NK cell activation.

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B- CELLS SUBSETS AND THEIR ROLE IN PERIODONTITIS

• B-cells initiate immune protection by producing antibody molecules, also known as immunoglobulin's which can recognize antigen through either low or high affinity binging domains.

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MECHANISM FOR B CELLS ACTIVATION

Antigens initiate antibody responses in

the follicular cells thus creating environment

for interaction T and B cells.

After interaction naïve B cell receptor, migrate to the boundary between

follicular and outer T cell zone.

1) follicular pathway generates Bc16 positive germinal center B cells that differentiate into long lived memory

B cell and plasma cells producing high affinity antibodies.

2) Extra follicular pathway generates Bc16 negative which differentiate to

produce short lived plasma cells secreting low affinity antibodies.

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• Activated B cells can serve as antigen presenting cells for both CD4+ and CD8+T cells.

• Recently, 3 types of antigen presenting cells (dendritic cells, monocytes and B cells) were analyzed in biopsies of patients with chronic periodontitis.

• CD68+ monocyte like cells, CD20+ B cells and strong T helper 17 cells was observed in the lower regions of chronic periodontitis, whereas CD1a+ dendritic cells were only detected in the coronal regions.

• Only a few studies have analyzed the functional role of B cells and B cell subsets in the pathogenesis of periodontitis.

• More recently, B cell subtype, B1a is found at high proportions in periodontitis lesions.

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INTERACTIONS OF T AND B CELL SUBSETS IN PERIODONTITS

lymphocytes functions association

T and B cells Reduction of soluble RANKL release

Osteoclastic bone resorption

T helper 17 cells Expressed in the alveolar bone of diseased patients

Chronic periodontitis.

CD3+ T cells & CD4+& CD8+ subpopulations & CD19+ B cells

More periodontal breakdown in smoking pts

Smoking & periodontitis

CD4+ T cells RANKL mRNA levels were higher in pts with periodontitis. CD4+ T cells were predominant infiltrate cell subset present in gingival tissues of pts with periodontitis.

Levels of RANKL with CD4+ T cells activity present in gingival tissues of pts with chronic periodontitis.

T and B cells High levels of interferon gamma & minimal interleukin 5

Severe periodontitis tissues

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CELLULAR AND MOLECULAR MODEL OF THE SUSCEPITIBILITY TO

PERIODONTITITS

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CONCLUSION

• In view of the current evidence base, it is not possible to define completely the mechanisms that are under the control of T- and B cells in periodontitis.

• The dominance of b-cells and plasma cells in periodontitis lesions is not dependent on either enhanced or decreased activities of T helper, T-cytokine, regulatory T, natural killer cell and/or b-cell subsets, including their cytokine networks.

• As with other inflammatory diseases, as imbalance in the regulatory immune mechanisms appears to be responsible for the onset and progression of periodontal disease.

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