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Innate Immune Responses and Osteoarthritis
被引:94
|作者:
Kalaitzoglou, Evangelia
[1
]
Griffin, Timothy M.
[2
]
Humphrey, Mary Beth
[3
,4
]
机构:
[1] Univ Kentucky, Coll Med, Barnstable Brown Diabet Ctr, Lexington, KY 40536 USA
[2] Oklahoma Med Res Fdn, 825 NE 13th St, Oklahoma City, OK 73104 USA
[3] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73104 USA
[4] Vet Affairs Med Ctr, Oklahoma City, OK 73104 USA
关键词:
Synovitis;
Osteoarthritis;
TLR4;
Obesity;
Inflammation;
Cytokines;
INFRAPATELLAR FAT PAD;
KNEE OSTEOARTHRITIS;
SYNOVIAL-FLUID;
ADIPOSE-TISSUE;
INFLAMMATORY MEDIATORS;
JOINT OSTEOARTHRITIS;
BODY-WEIGHT;
OBESITY;
RISK;
ASSOCIATION;
D O I:
10.1007/s11926-017-0672-6
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
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. Summary 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.
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