Inflammatory mediators and the destruction of bone

Journal of Periodontal Research - Tập 26 Số 3 - Trang 213-217 - 1991
Gregory R. Mundy1
1University of Texas Health Science Center San Antonio, Texas USA

Tóm tắt

Bone is remodelled by the coordinated actions of osteoclasts and osteoblasts. Cellular remodelling occurs in discrete packets of bone, and is regulated by local cytokines produced in the environment of the remodelling cells. These cytokines are secreted by immune cells and by bone cells. In addition, some growth regulatory factors are incorporated into the noncollagenous bone matrix and are released in an active form when bone is stimulated to resorb. Complex interactions between these cytokines and their target cells are responsible for the normal delicate balance between bone resorption and bone formation, and disorders of bone loss are due to imbalances between the rates of resorption and formation.

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Tài liệu tham khảo

10.1073/pnas.85.15.5683

10.1172/JCI113647

10.1073/pnas.87.8.3023

10.1210/endo-126-6-3069

10.1016/0006-291X(89)91143-1

YatesAJ OreffoROC MayorK MundyGR.Inorganic phosphate inhibits osteoclast formation and the activity of mature osteoclasts.J Bone Min Res1990(in press).

10.1016/S0021-9258(18)67143-1

10.1073/pnas.82.8.2267

Seyedin SM, 1986, Cartilage‐inducing factor A: Apparent identity to transforming growth factor beta, J Biol Chem, 261, 5693, 10.1016/S0021-9258(17)38436-3

10.1210/endo-124-6-2991

Marcelli C, 1990, In vivo effects of human recombinant transforming growth factor beta on bone turnover in normal mice, Calcif Tiss Int, 46, A40

10.1172/JCI113318

10.1210/endo-118-1-74

10.1210/endo-125-3-1142

10.1210/endo-125-5-2780

Obberghen‐Schilling E, 1988, Transforming growth factor‐β positively regulates its own expression in normal and transformed cells, J Biol Chem, 263, 7741, 10.1016/S0021-9258(18)68561-8

10.1126/science.3969553

10.1111/j.1600-051X.1989.tb02334.x

10.1073/pnas.84.13.4616

10.1073/pnas.86.7.2398

10.1056/NEJM198708273170902

10.1182/blood.V73.8.2145.2145

10.1182/blood.V74.1.380.380

10.1172/JCI114392

BlackKS MundyGR GarrettIR.Interleukin‐6 causes hypercalcemia in vivo and enhances the bone resorbing potency of interleukin‐1 and tumor necrosis factor by two orders of magnitude in vitro.J Bone Min Res1990(in press).

Sato K, 1989, Paraneoplastic syndrome of hypercalcemia and leukocytosis caused by squamous carcinoma cells (T3M‐1) producing parathyroid hormone‐related protein, interleukin‐1‐alpha, and granulocyte colony‐stimulating factor, Cancer Res, 49, 4740

10.1210/endo-124-5-2172

Sabatini M., 1990, Stimulation of tumor necrosis factor release from monocytic cells by the A375 human melanoma via granulocyte‐macrophage colony stimulating factor, Cancer Res, 50, 2673

Sabatini M, 1990, Increased production of tumor necrosis factor by normal immune cells in a model of the humoral hypercalcemia of malignancy, Lab Invest, 63, 676

Yoneda T., 1989, Hypercalcemia in a human tumor is due to tumor necrosis factor production by host immune cells, J Bone Min Res, 4, 826