Osteoarthritis (OA) is the most prevalent form of arthritis, with an associated risk of mobility disability for those with affected being greater than that due to any other medical condition in people aged 65.

OA is a multifactorial process in which changes in structure and function of the whole joint occur, with involvement of articular cartilage, subchondral bone, menisci, ligaments, periarticular muscle, joint capsule and synovium. The result is pain, limitation of motion, deformity, and progressive disability. Symptoms of OA include morning stiffness, stiffness after inactivity for more than 15 minutes or stiffness related to weather, instability of weight bearing joints, crackling, crepitus joint sounds, enlarged bone growth causing deformities, and localized joint pain.

OA is caused by aberrant local mechanical factors acting within the context of systemic susceptibility.

Local mechanical factors that increase the likelihood of developing OA and facilitate progression of the disease are malalignment, muscle weakness, chronic inflammation, alterations in the structural integrity of the joint environment, previous trauma, and obesity. The underlying trigger for the majority of these risk factors which promote an environment for OA development is inflammation. Previous injury is the major cause of OA in young adults, increasing the risk more than four times. The association between obesity and OA has long been recognized. Patients with obesity develop OA earlier and present with more severe symptoms, higher risk for infection and more technical difficulties for total joint replacement surgery. In addition to increased biomechanical loading on the joints, obesity is thought to contribute to low-grade systemic inflammation through secretion of adipose tissue-derived cytokines, or inflammatory mediators. These inflammatory factors trigger a pathway to stimulate articular chrondrocyte breakdown processes and lead to extracellular matrix degradation.

Systemic factors that increase the vulnerability of a joint to OA include increasing age, female sex, and nutrient deficiencies. Changes in the American diet in this century have resulted in a dramatic imbalance in fatty acids, malnutrition and a shift in production toward more pro-inflammatory hormones. While some of these risk factors for OA are not modifiable, others can be prevented to reduce the possibility of developing OA.

Typical treatment of OA in Western Medicine entails use of NSAIDs, corticosteroids, or opioid analgesics to suppress the immune system and stop the inflammatory process. There are many disadvantages of routinely using these drugs, including potential toxicity and increased gastrointestinal complications with NSAID use.

Surgery may be indicated when symptoms cannot be managed with drugs, failure of conservative treatment, and if the person experiences debilitating pain and major limitations of functions to sleep or perform daily activities. Furthermore, although these medications can be successful in decreasing symptoms and in some cases prevent further joint destruction, they don’t solve the problem of why you developed the condition in the first place.

The functional medicine approach will dig deeper into what is contributing to your condition and give your the tools you need to heal naturally without drugs or invasive procedures.


“Hunter, David. Felson, David. “Osteoarthritis.” The BMJ. March 2006. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1403209/.

Chen, Di. Shen, Jie. “Osteoarthritis: Toward a Comprehensive Understanding of Pathological Mechanism.” Bone Research. 2017. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5240031/.

Grisani, Ronald. “Prevent and Treat Arthritis Pain with Nutritional Medicine” Sequoia Education Systems. 2004. https://www.functionalmedicineuniversity.com/ArthritisBookUpdated-1.pdf.