Research has discovered that there is a connection between diabetes and osteoarthritis (OA). Each condition predisposes an individual for the other due to the large overlap between OA and diabetes. A number of similar risk factors, including obesity and age, can lead to the onset of both conditions. In addition, there are a number of overlapping mechanisms such as decline in cell function and mitochondrial dysfunction, or a dysregulation in lipid metabolism, which can lead to hyperlipidaemia – a risk factor for both OA and diabetes.
One of the main reasons is that with age comes a decline in cell function and decrease in telomere length. Aging is associated with diabetes because beta cells’ function found in the pancreas declines as we get older. Similarly, in OA, older chondrocytes are more likely than young chondrocytes to secrete inflammatory mediators. As a result, those inflammatory mediators such as IL-10 and IL-1b are directly related to cartilage degradation because of the oxidative stress produced. Obesity and age in conjugation lead to a higher load placed on joints which can add to the cartilage damage found in OA. Aging is directly due to a decline in mitochondrial health and that has been hypothesised to contribute to both diabetes and cartilage degradation and thus OA. The function of mitochondria is to generate ATP (adenosine triphosphate) and carry oxygen, both of which, play a vital role in diabetes and OA.
It has previously been established that diabetes is associated with hyperlipidaemia and alterations in lipid metabolism; surprisingly also a relationship with lipid metabolism and OA. There is emerging evidence that demonstrates a direct connection between alterations in lipid metabolism and hyperglycaemia with cartilage health and subchondral bone. This contributes to the development and progression of OA. Individuals with arthritis have a 61% higher risk of developing diabetes compared to those individuals without a joint disease. Hyperglycaemia can lead to negative impacts on subchondral bone which highlights the idea that diabetes itself is a risk factor for OA. Obesity and other metabolic syndromes such as diabetes have been described as independent risk factors for OA. One of the most important mechanisms associated with both conditions is the chronic inflammation and cellular dysfunction of specific interleukins such as IL-1b or IL-10. Pro-inflammatory cytokines including IL-1b and TNFa have been identified in increasing numbers among both conditions, especially in obese patients.
Patients who are suffering from atherosclerosis are found to have more inflammatory tissue as well. Since obesity rates have been increasing at such an alarming rate for the past few years, it is no surprise that more and more research is occurring in this area. Adipokines, which are cell signalling molecules produced by the adipose tissue in the body to regulate metabolic processes of the body, inflammation and obesity, have been a keen area of interest. As new therapeutic approaches are being made for OA and diabetes, those same approaches can be used for addressing obesity and a secondary approach after lifestyle methods. More research and associated funding should be put into identifying anti-inflammatory pathways that can be used for those millions suffering from OA, diabetes, and atherosclerosis. This information can be used to help correlate not only a better targeted treatment but also lead to future research into why obesity is one the biggest risk factors for both conditions. This might limit the amount of medication needed for treatment and as an added benefit, less side effects and negative drug interactions are likely.
With obesity rates rising due to increased availability of processed foods, decreased availability of fresh produce, and lack of proper exercise, our society might be moving towards more drug-based treatments for obesity which makes this interleukin therapy key. All in all, it is vital that we recognise the interrelation between OA and diabetes to better develop treatments in the future. This makes it of utmost importance to spread this information and prevalence not only in the medical community but to those suffering from either condition.
ReferencesCourties, A, Sellam, J (2016) Osteoarthritis and type 2 diabetes mellitus: what are the links? Diabetes research and clinical. doi.org/10.1016/j.diabres.2016.10.021
Ruscitti, Cipriani, Liakouli, et al, (2018) The emerging role of IL-1 inhibition in patients affected by rheumatoid arthritis and diabetes. ReviewsonRecentClinicalTrials. doi.org/10.2174/1574887113666180314102651
Herder, Dalmas, Böni-Schnetzler, et al, (2015) The IL-1 pathway in type 2 diabetes and cardiovascular complications. Trends in Endocrinology & Metabolism. doi.org/10.1016/j.tem.2015.08.001
Louati, Vidal, Berenbaum, et al, (2015) Association between diabetes mellitus and osteoarthritis: systematic literature review and meta-analysis. doi.org/10.1136/rmdopen-2015-000077