Immunoporosis: the Role of Immune Cells in Osteoporosis

Osteoporosis, the age-related loss of bone mass and strength, is a serious condition. Bone is constantly remodeled, created by osteoblasts and removed by osteoclasts. With age, the balance of these activities tips towards favoring the osteoclasts, and bone mineral density declines over time as a consequence. It is becoming clear that inflammatory signaling is an important contributing factor in this dysregulation of the normal balance. The chronic inflammation that accompanies aging, the consequence of rising numbers of senescent cells, as well as of the presence of molecular damage that provokes the immune system, can be blamed for a great deal of the burden of aging.

Osteoporosis or porous bone disorder is the result of an imbalance in an otherwise highly balanced physiological process known as 'bone remodeling'. The immune system is intricately involved in bone physiology as well as pathologies. Inflammatory diseases are often correlated with osteoporosis. Inflammatory mediators such as reactive oxygen species (ROS), and pro-inflammatory cytokines and chemokines directly or indirectly act on the bone cells and play a role in the pathogenesis of osteoporosis.

Recently, researchers have coined the term "immunoporosis" to emphasize the role of immune cells in the pathology of osteoporosis. Accumulated evidence suggests both innate and adaptive immune cells contribute to osteoporosis. However, innate cells are the major effectors of inflammation. They sense various triggers to inflammation such as pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), cellular stress, etc., thus producing pro-inflammatory mediators that play a critical role in the pathogenesis of osteoporosis.

Cells of the myeloid lineage, including macrophages, monocytes, and dendritic cells, explicitly influences the skeletal system by the action of production of pro-inflammatory cytokines and can transdifferentiate into osteoclasts. Other cells of the myeloid lineage, such as neutrophils, eosinophils, and mast cells, largely impact osteoporosis via the production of pro-inflammatory cytokines. Further, cells of the lymphoid lineage, including natural killer cells and innate lymphoid cells, share innate-like properties and play a role in osteoporosis.


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