"Bone Breakers: The Osteoclasts That Shape Our Skeletons"

DR ANIL MELATH , DR ARJUN MR , DR SWATHI S , ABHIRAMI SANTHOSH , SAGAR

bone, osteoclast

Osteoclasts are specialized, multinucleated cells responsible for bone resorption, playing a crucial role in bone remodeling and calcium homeostasis. Derived from the monocyte/macrophage lineage, these cells adhere to the bone matrix, creating an acidic microenvironment that facilitates the dissolution of mineral components and degradation of the organic matrix, primarily through the secretion of enzymes such as tartrate-resistant acid phosphatase (TRAP) and cathepsin K. The regulation of osteoclast differentiation and activity is mediated by various signaling pathways, including the receptor activator of nuclear factor kappa-B ligand (RANKL) and its decoy receptor osteoprotegerin (OPG). Dysregulation in osteoclast activity is implicated in several bone disorders, such as osteoporosis, where increased bone resorption leads to reduced bone mass and increased fracture risk. This abstract reviews the current understanding of osteoclast biology, emphasizing the molecular mechanisms governing their formation and function, as well as their role in pathological conditions. Further research into osteoclast regulation offers potential therapeutic targets for treating bone-related diseases.

Published Paper   E-Certificate

""Bone Breakers: The Osteoclasts That Shape Our Skeletons"", IJNRD - INTERNATIONAL JOURNAL OF NOVEL RESEARCH AND DEVELOPMENT (www.IJNRD.org), ISSN:2456-4184, Vol.9, Issue 10, page no.a16-a21, October-2024, Available :https://ijnrd.org/papers/IJNRD2410004.pdf

Volume 9 Issue 10, October-2024

Pages : a16-a21

Paper Reg. ID: IJNRD_300921

Published Paper Id: IJNRD2410004

Downloads: 00036

Research Area: Others area

Country: mahe, pondycherry, India

Published Paper PDF: https://ijnrd.org/papers/IJNRD2410004

Published Paper URL: https://ijnrd.org/viewpaperforall?paper=IJNRD2410004

ISSN: 2456-4184 | IMPACT FACTOR: 8.76 Calculated By Google Scholar | ESTD YEAR: 2016

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