The development of arthritis involves complex interactions between genetic susceptibility and environmental causes, which modify individual risk. Although there is still uncertainty about the relative contribution of genetics and environmental factors, the findings presented here provide an overview of the contribution of environmental triggers.
Arthrosis is a chronic inflammation in the joint, in which inflammatory molecules and cytokines (e.g., cytokine-dependent recruitment to inflammatory sites, increased turnover, tissue destruction and increased numbers of chondrocytes and mesenchymal stem cells) are generated and perpetuate the inflammation.
Arthrosis of the hip and knee affects less than 1% of adults. Given the fact that the incidence rate of arthrosis increases with age, a substantial proportion of older people with hip and knee arthrosis in the United States (especially younger men) are expected to be undiagnosed and untreated. Improved recognition of arthrosis in the United States will provide an opportunity for the implementation of effective strategies designed to prevent and delay the onset of disease.
There is no evidence that joint arthrosis can be cured and there is strong evidence of morbidity and death associated with arthroplasty procedures. Nevertheless, arthrosis is common. It is not clear, therefore, whether arthrosis is a chronic problem or whether it is just a symptom and not a disease in itself. If not an insidious disease, it is a sign of progressive and disabling loss of quality of life.
Most patients with hand arthrosis require nonoperative management, such as splinting, joint irrigation, and hand and wrist physiotherapy. If conservative measures are unsuccessful, or where it cannot be determined with diagnostic accuracy or patient comfort, an arthrodesis can be considered as a treatment option.
Symptoms of arthrosis are similar to joint dysfunctions. This may result in long duration and difficulty with activities of daily living as well as in the workforce.
The first diagnosis of arthrosis is usually by age 30, and the average age after the initial diagnosis is 42.2 years. However, the average age of the third diagnosis is much earlier than that, being age 41.9 years old. The reasons in this case seem to be medical and psychological, possibly because people want to postpone the moment when they may have to undergo a replacement of the joint surface. In order to help people live longer, we ought to increase awareness of arthrosis and try to help people get over this disease as soon as possible.
There is not enough evidence to conclude whether a new medication is efficacious for treating arthrosis. Current therapies can help alleviate the symptoms associated with this disease.
Arthrosis has a major role in adult life. However, the seriousness of the condition of the arthrosis itself is dependent on several factors and the condition may in turn affect the quality of life of the patient. Arthrosis can be treated through surgical methods such as osteotomy, fusion and arthroplasty, of which it may also be a predisposing factor.
Low-intensity transcranial electrical stimulation/active transcranial ultrasound may be used alone or combined with other treatment modalities, depending on the patient. The use of active low-intensity transcranial electrical stimulation/active transcranial ultrasound alone may lead to a favorable change of the functional status, as well as clinical improvement with no additional side effects that may be associated with combined treatment.
Active low-intensity tTES/aRTUS is more effective than a placebo for the treatment of the signs and symptoms of subacromial impingement syndrome, thus demonstrating a clinically significant benefit of this kind of intervention. Further studies are needed to define the effects of active low-intensity tTES/aRTUS on functional recovery and to evaluate the long-term clinical efficacy of tTES/aRTUS.
Recent findings add to the accumulating evidence for the familial transmission of AAO. Recent findings adds further evidence to the emerging belief that the susceptibility gene for AAO does not reside within the genes for HAO. Whether other susceptibility genes exist for both AAO and HAO is yet to be determined with greater epidemiologic studies.