Role of inflammation in the process of clinical Kashin-Beck disease: latest findings and interpretations

Abstract

Kashin-Beck disease (KBD), a particular type of osteoarthritis (OA), and an endemic disease with articular cartilage damage and chondrocytes apoptosis, can affect many joints, and the most commonly affected joints are the knee, ankle, and hand. KBD has traditionally been classified as a non-inflammatory OA. However, recent studies have shown that inflammation has played an important role in the development of KBD. Nowadays, clinical KBD is not only an endemic disease, but also a combined result of many other non-endemic factors, which contains age, altered biomechanics, joint trauma and secondary OA. The characteristics of the developmental joint failure of advanced KBD, because of the biochemical and mechanical processes, are tightly linked with the interaction of joint damage and its immune response, as well as the subsequent state of chronic inflammation leading to KBD progression. In this review, we focus on the epidemiology, pathology, imaging, cytokines and transduction pathways investigating the association of inflammation with KBD; meanwhile, a wide range of data will be discussed to elicit our current hypotheses considering the role of inflammation and immune activation in KBD development.

Selection and Investigation of a Primate Model of Spontaneous Degenerative Knee Osteoarthritis, the Cynomolgus Monkey (Macaca Fascicularis)

“…Therefore, it is possible that the identification of serum or joint biomarkers could reflect the state and symptoms of joint function and predict the progress of KOA, and may be more sensitive than traditional imaging tests [ 33 ]. Also, according to the pathophysiological processes of osteoarthritis, a reliable biomarker might more accurately predict the severity of the disease [ 34 – 36 ].…”

Proteomic analysis of knee cartilage reveals potential signaling pathways in pathological mechanism of Kashin-Beck disease compared with osteoarthritis

“…NF-κB is a vital protein in cartilage metabolism. NF-κB-regulated gene products are involved in inflammation and cartilage degradation 11,38 . Moreover, NF-κB pathway enhances the articular damage by promoting the synthesis of catabolic factors, cartilage inflammation and apoptosis of chondrocyte 39,40 .…”

“…OA occurs mainly in the middle aged and elderly population 1 . The pathologic changes in OA joints include degradation of the articular cartilage, especially at the superficial zones, thickening of the subchondral bone, osteophyte formation, and variable degrees of synovial inflammation 11 . KBD occurs mostly in children aged 3-12 years old in endemic regions 4 .…”

“…Most of the deformities were established at the age of 15, then subsequently become symptomatic in adults 7,12,13 . A typical distinction of KBD from OA or other bone and joint diseases is the damage of epiphyseal cartilage and hyaline cartilage in the deep zones of cartilage 11,14 . This distinction might explain the occurrence of severe joint deformities during development in young people with KBD 15 .…”

Inhibition of Carrageenan/Kaolin-Induced Arthritis in Rats and of Inflammatory Cytokine Expressions in Human IL-1β-Stimulated Fibroblast-like Synoviocytes by a Benzylideneacetophenone Derivative

“…In fact, consequent inflammation in synovial membranes and joint fluid are important symptoms of osteoarthritis, and eventually result in synovitis and synovial hyperplasia. Synovitis is a symptom of inflammatory and degenerative arthritis, and in RA, synovitis and synovial fibroblast activation are key stages in the development of invasive rheumatoid pannus [ 9 ].…”