Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Why Does Inflammation Result in Resorptive Bone Loss?

Version 1 : Received: 17 May 2022 / Approved: 20 May 2022 / Online: 20 May 2022 (04:01:33 CEST)

A peer-reviewed article of this Preprint also exists.

Klein, G.L. Why Does Inflammation Result in Resorptive Bone Loss? What the Study of Burns Teaches Us. Endocrines 2022, 3, 452-459. Klein, G.L. Why Does Inflammation Result in Resorptive Bone Loss? What the Study of Burns Teaches Us. Endocrines 2022, 3, 452-459.

Journal reference: Endocrines 2022, 3, 36
DOI: 10.3390/endocrines3030036

Abstract

Burn injury serves as an example of a condition with a robust inflammatory response. The elevation of circulating interleukins (IL)- 1 beta and -6 in children with severe burn injury up-regulate the parathyroid calcium sensing receptor (CaSR) resulting in hypocalcemic hypoparathyroidism with urinary calcium wasting. This effect protects the body from the hypercalcemia resulting from bone resorption liberating calcium into the circulation. Extracellular calcium can exacerbate and prolong the inflammatory response by stimulating mononuclear cell chemokine production as well as the NLRP3 inflammasome of the innate immune system, resulting in increased IL-1 production by monocytes and macrophages. Interestingly, the CaSR response to inflammatory cytokines disappears with age, potentially trapping calcium from bone resorption in the circulation and allowing it to contribute to increased inflammation and possibly increased calcium deposition in small arteries, , such as the coronaries, as conditions with increased chronic inflammation, such as spinal cord injury, osteoarthritis and rheumatoid arthritis have an incidence of cardiovascular disease and coronary artery calcium deposition significantly higher than the unaffected age-matched population.

Keywords

inflammation; calcium-sensing receptor; burns; chemokines; NLRP3 inflammasome

Subject

MEDICINE & PHARMACOLOGY, Other

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