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Curr Rheumatol Rep. 2017 Aug;19(8):45. doi: 10.1007/s11926-017-0672-6.

Innate Immune Responses and Osteoarthritis.

Author information

1
University of Kentucky Barnstable Brown Diabetes Center, University of Kentucky College of Medicine, Lexington, KY, 40536, USA.
2
Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
3
University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. Marybeth-humphrey@ouhsc.edu.
4
Veterans Affairs Medical Center, Oklahoma City, OK, 73104, USA. Marybeth-humphrey@ouhsc.edu.

Abstract

PURPOSE OF THE REVIEW:

Osteoarthritis (OA) is a chronic, painful joint disease that affects approximately 40% of adults over 70 year. Age is the strongest predictor of OA, while obesity is considered the primary preventable risk factor for OA. Both conditions are associated with abnormal innate immune inflammatory responses that contribute to OA progression and are the focus of this review.

RECENT FINDINGS:

Recent studies have identified risk factors for OA progression including increased innate immune responses secondary to aging-associated myeloid skewing, obesity-related myeloid activation, and synovial tissue hyperplasia with activated macrophage infiltration. Toll-like receptor (TLR)4-induced catabolic responses also play a significant role in OA. The complex interplay between obesity and aging-associated macrophage activation, pro-inflammatory cytokine production from TLR-driven responses, and adipokines leads to a vicious cycle of synovial hyperplasia, macrophage activation, cartilage catabolism, infrapatellar fat pad fibrosis, and joint destruction.

KEYWORDS:

Cytokines; Inflammation; Obesity; Osteoarthritis; Synovitis; TLR4

PMID:
28718060
DOI:
10.1007/s11926-017-0672-6
[Indexed for MEDLINE]

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