Osteoarthritis in the XXIst century: risk factors and behaviours that influence disease onset and progression

Abstract

Osteoarthritis (OA) is a growing public health problem across the globe, affecting more than half of the over 65 population. In the past, OA was considered a wear and tear disease, leading to the loss of articular cartilage and joint disability. Nowadays, thanks to advancements in molecular biology, OA is believed to be a very complex multifactorial disease. OA is a degenerative disease characterized by "low-grade inflammation" in cartilage and synovium, resulting in the loss of joint structure and progressive deterioration of cartilage. Although the disease can be dependent on genetic and epigenetic factors, sex, ethnicity, and age (cellular senescence, apoptosis and lubricin), it is also associated with obesity and overweight, dietary factors, sedentary lifestyle and sport injuries. The aim of this review is to highlight how certain behaviors, habits and lifestyles may be involved in the onset and progression of OA and to summarize the principal risk factors involved in the development of this complicated joint disorder.

Figure 1

This figure shows the alterations that occur in the joints during the onset of osteoarthritis (OA).

Figure 2

The scheme represents the major risk factors that lead to the increased susceptibility and predisposition to develop OA.

Figure 3

This figure shows 5 different lifestyles. (A) Pictograph A shows a person who leads a healthy life choosing a controlled diet, rich in nutrients and vitamins, and moderate physical activity. This subject reduces the risk to develop OA, both in cartilage alterations and inflammation; (B) Pictograph B shows a sportsman. In this case, the extremely forced physical activity, wrong movement, and direct joint impact or torsional load, lead to an increased joint risk. This risk is mostly located in the joint of the shoulders, arms, hips and knees; (C) Pictograph C shows a person who leads a sedentary lifestyle. Here, little physical training is responsible for muscle weakening and, consequently, to wrong posture. The major risk is visible in the joints of the spinal column and shoulders. Furthermore, the use of smart phones and computers increases the risk of OA in the joints of hands and wrists; (D) Pictograph D shows an obese subject. Here, the increased body weight lies heavily on the joints of the spinal column and of the lower limbs, such as hips, knees and ankles; (E) Pictograph E shows a subject not consuming a proper diet. The loss of vital nutrients increases the risk of developing OA in most of the joints of the subject itself.

Figure 4

The OA-associated molecules, including IL-1β, TNF-α, RAGE, leptin, IGF-1, TGFβ1, iNOS, MMP13, laminin, fibronectin, integrin and collagen are involved in chondrocyte activation. These molecules contribute to the pathogenesis of OA by destroying the cartilage in the joints or serving as the substrates for extracellular matrix destruction (i.e., laminin, fibronectin and collagen type II).

Figure 5

Target genes involved in OA. Molecular graphics and analyses were performed with the UCSF Chimera package. Chimera is developed by the Resource for Biocomputing, Visualization, and Informatics at the University of California, San Francisco.