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T and B cell Mediated Bone Resorption through RANK-RANK-L Activation in Periodontal Disease.

This is a very recent paper that I have written!

T and B cell Mediated Bone Resorption through RANK-RANK-L Activation in Periodontal Disease.

Bone remodeling, which is vital in maintaining a constant bone mass, involves synthesis of bone matrix by osteoblasts and bone resorption by osteoclasts. Osteoblasts are known to arise from mesenchymal stem cells and osteoclasts from the hemopoietic monocyte-macrophage cell line. The disturbance in the balance maintained by the osteoblast and the osteoclast could lead to increased bone formation (osteopetrosis) or decreased bone mass (osteoporosis). Various cytokines are known to influence in vitro osteoclastogenesis, which indicate close interactions between osteoclasts and the immune system. Cytokines such as interleukin 1 (IL-1), IL-6, IL-11, IL-7 and TNF-α stimulate osteoclast formation and bone resorption, while, IL-4, IL-10, IL-13, and INF-γ inhibited osteoclastogenesis and/or osteoclast activities (1).

In recent years the involvement of humoral and cell mediated immune response in bone remodeling and bone loss has been better understood. Periodontitis which is an inflammation of the periodontal structures around the teeth is a polymicrobial infection causing inflammation of periodontal structures and alveolar bone resorption. This paper will attempt at reviewing the role of host immune response in alveolar bone destruction by periodontal disease.

Immune Response In Periodontal Disease:

Periodontal disease is a multi-pathogenic disease with approximately 300 different types of microorganisms found in periodontal sites with only few among them having been implicated to cause the actual disease. Host response to these bacteria can be detected as elevated levels of serum IgG antibody to the bacteria colonizing the periodontal site (2), which is a proof of a humoral immune response. Cellular response is seen in the form of a prominent infiltration of B cells, T cells, and higher number of CD3+ and CD20+ lymphocytes as compared to the healthy gingival tissue. T cell subsets, which are found in the gingival tissue with periodontal disease, are comprised of T cells which bear T-cell antigen receptor (γδ-TCR and αβ-TCR). The subset of αβ T-cells is subdivided into CD4- and CD8+ cells (3). The CD4+ T-cells (Th1 and Th2 type T-cells) play a important role in periodontal bone resorption (3) and CD 8+ cells seems to suppress osteoclastogenesis(1).

RANK, RANKL and OPG:

Receptor activator of NF-κB ligand (RANKL) and Receptor activator of NF-κB (RANK), and a soluble decoy receptor osteoprotegerin (OPG), are the three players that regulate osteoclast recruitment and function (4).The balance of the osteoclast differentiation regulation is based on the RANKL/OPG ratio expressed in the microenvironment surrounding the osteoclast precursor cells (2).

(a)RANK and RANK-L:

RANK and its ligand RANKL which is also known as osteoprotegerin ligand (OPGL), TNF-related activation-induced cytokine (TRANCE), osteoclast differentiating factor (ODF), belong to the tumor necrosis factor (TNF) family (2, 5). RANK is expressed on chondrocytes, osteoclast precursors and mature osteoclasts. RANKL is expressed on T cells, B cells, osteoblasts, and bone marrow stromal cells. Also, RANKL is known to regulate lymph node organogenesis, lymphocyte development and interactions between T cells and dendritic cells in the immune system (2, 5). RANK-L expression in T cells is induced by antigen receptor engagement and is regulated by protein kinase C (PKC), phosphoinositide 3-kinase (PI3K) and calcineurin-mediated signaling pathways (5). It is the interaction between the RANKL and the RANK that causes the differentiation of the osteoclast precursors to their mature form (2). It has been previously reported that RANKL produced by plasma cells is responsible for the development of the bone resorption in multiple myeloma.

(b)OPG:

OPG, a secreted member of the TNF receptor family, is expressed ubiquitously by many types of cells and tissues. OPG acts as a decoy receptor and binds to the RANK-L, thereby preventing osteoclast differentiation and excessive bone resorption. Kawai et al. (2) found that exclusive production of RANKL and the lack of production of OPG by lymphocytes contributed to increase RANKL to OPG ratio in bone resorptive periodontitis lesions. Similar to the findings in the periodontitis patients, an increased concentration of soluble form of RANK-L (sRANKL) and a decreased concentration of OPG were detected in synovial fluid from rheumatoid arthritis patients(6). Results of Kong et al. (5) show that RANK-L is a key regulator of bone metabolism and that inhibition of the RANK-L activity by OPG can prevent cartilage destruction, a critical irreversible step in the pathogenesis of arthritis.

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