T Cells Support Osteoclastogenesis in an In Vitro Model Derived From Human Periodontitis Patients

Brunetti, Giacomina; Colucci, Silvia; Pignataro, Patrizia; Coricciati, M; Mori, Giorgio; Cirulli, Nunzio; Zallone, Alberta; Grassi, Felice Roberto; Grano, Maria

doi:10.1902/jop.2005.76.10.1675

Cited by 77 publications

(99 citation statements)

References 25 publications

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“…This could probably be associated with migrations of these cells to periodontal tissues. Our results indirectly support previous authors' histological research data about extensive plasma cell infiltration in periodontal tissues of patients with periodontal disease [57], and also show that the B cells are responsible for T cell-dependent osteoclastogenesis in periodontitis patients through the involvement of IL-6 and IL-7, and via RANKL and TNF-α over-expression [58,59]. It is noteworthy that the severity of the disease does not correlate with ALC levels in GMB.…”

Section: Discussionsupporting

confidence: 91%

Local and systemic immune responses in gingivitis and periodontitis

et al. 2014

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Section: Discussionsupporting

confidence: 91%

Local and systemic immune responses in gingivitis and periodontitis

et al. 2014

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“…The increased spontaneous osteoclastogenesis in vitro in PBMCs from patients with metastatic cancers (5), periodontitis (6), and PsA (7) has been demonstrated to be T cell-dependent, since it was completely abrogated by T cell depletion. Our findings are consistent with this concept, since T cell depletion abrogated spontaneous osteoclastogenesis in vitro and could be partially compensated for by exogenous RANKL in cultures of PBMCs from healthy donors.…”

Section: Discussionmentioning

confidence: 99%

“…Studies using the TNFtransgenic mouse model as well as clinical trials with TNF blockers indicate that enhanced spontaneous osteoclastogenesis in vitro is related to a TNF-mediated increase in myeloid precursor cells (2,4,8,9). Other studies, however, have emphasized the crucial role of activated T lymphocytes in this process (3,6,7). In the present study, we reassessed the mechanisms of spontaneous osteoclastogenesis in vitro with special focus on the role of T lymphocytes.…”

mentioning

confidence: 89%

In vitro spontaneous osteoclastogenesis of human peripheral blood mononuclear cells is not crucially dependent on T lymphocytes

Vandooren¹,

Melis²,

Veys³

et al. 2009

Arthritis & Rheumatism

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Objective. In vitro spontaneous osteoclastogenesis from peripheral blood mononuclear cells (PBMCs) is increased in diseases with excessive bone loss. The purpose of this study was to reassess the role of T lymphocytes in this process.Methods. Fresh or cryopreserved PBMCs obtained from healthy subjects and from patients with rheumatoid arthritis, psoriatic arthritis, and nonpsoriatic spondylarthritis were cultured at high density and stained for tartrate-resistant acid phosphatase (TRAP). Resorption of mineralized matrix was assessed by a dentin disc assay. CD14؉ monocytes and CD3؉ T cells were selected using magnetically labeled antibodies.Results. Numerous multinucleated, TRAP؉, dentin-resorbing osteoclasts developed spontaneously from fresh PBMCs from healthy individuals. This process was abrogated by T cell depletion and was restored by exogenous macrophage colony-stimulating factor (M-CSF) and RANKL, indicating the important role of T cells in spontaneous osteoclastogenesis in vitro. Using physiologic freezing and thawing as a model for the activation of PBMCs, spontaneous osteoclastogenesis was significantly increased in cryopreserved versus fresh cells. Under these conditions, spontaneous osteoclastogenesis was not dependent on T lymphocytes, since it was not influenced by T cell depletion and persisted in purified CD14؉ cell cultures supplemented with M-CSF and RANKL. In contrast to studies with fresh PBMCs, spontaneous osteoclastogenesis under these conditions did not appear to be clearly different between healthy subjects and patients with arthritis.Conclusion. Spontaneous osteoclastogenesis in vitro is dependent on T lymphocytes or on the direct activation of monocytic cells, depending on the test conditions. This variability warrants better validation of the relevance of this functional test for in vivo osteoclastogenesis.

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“…2 Although in physiological conditions RANKL is the main cytokine driving OC formation, and is principally expressed by mesenchymal cells of the osteoblast lineage, the osteoclastogenic cytokine is produced in abundance by T cells in states of destructive osteolytic bone disease associated with MM, as well as other pathologies with bone involvement. [3][4][5][6][7] It has long been recognized that infection, inflammation and auto-immune disorder are associated with systemic and local bone loss, [5][6][7] and recently several groups have shown a link between T cells and the development of osteolysis associated with malignancy. 3,4,8 Consistently, we showed earlier an important role of T cells in supporting the formation and survival of OCs in peripheral blood mononuclear cells (PBMCs) from MM patients with osteolysis.…”

Section: Introductionmentioning

confidence: 99%

Soluble decoy receptor 3 modulates the survival and formation of osteoclasts from multiple myeloma bone disease patients

et al. 2009

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Decoy receptor 3 (DcR3), a member of the tumor necrosis factor (TNF) receptor superfamily, is known to be involved in cell survival and osteoclast (OC) formation. In this study, we show that malignant plasma cells and T lymphocytes from multiple myeloma (MM) bone disease patients, as well as Karpas 909, a human myeloma cell line, directly produce DcR3. By interacting with FasL, this molecule could inhibit OC apoptosis. In fact, the use of a neutralizing anti-DcR3 antibody induces a reduction of cell viability with a consequent increase of apoptotic cell number, the activation of caspase-8 and -3, and DNA fragmentation. Furthermore, we show that DcR3 supports OC formation in samples from MM patients through the upregulation of RANKL and TNFa by T lymphocytes and only TNFa by CD14 þ cells. In conclusion, our data provide the first evidence of the expression of DcR3 in MM, and the involvement of this molecule in supporting the survival and formation of OCs from MM bone disease patients. The production of DcR3 by T lymphocytes confers these cells a role in the pathogenesis of bone disease associated with MM.

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T Cells Support Osteoclastogenesis in an In Vitro Model Derived From Human Periodontitis Patients

Abstract: Our data suggest that T cells support spontaneous osteoclastogenesis in PP via RANKL and TNF-alpha overexpression.

Cited by 77 publications

References 25 publications

Local and systemic immune responses in gingivitis and periodontitis

Local and systemic immune responses in gingivitis and periodontitis

In vitro spontaneous osteoclastogenesis of human peripheral blood mononuclear cells is not crucially dependent on T lymphocytes

Soluble decoy receptor 3 modulates the survival and formation of osteoclasts from multiple myeloma bone disease patients

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