Osteoarthritis Treatment

Lifestyle Modifications: Weight management and low-impact exercise can reduce joint stress and improve mobility.

Physical Therapy: Exercises to strengthen muscles around the joint and improve range of motion.

Analgesics (e.g., acetaminophen) and NSAIDs (e.g., ibuprofen) for pain relief.

Topical Agents: Creams containing capsaicin or NSAIDs applied to the skin.

Injections:

Corticosteroids: Injections to reduce inflammation and pain.

Hyaluronic Acid: To improve joint lubrication (though the effectiveness is debated).

Spinal osteoarthritis surgical treatment.

- Maintain Healthy Weight: Reducing body weight decreases joint load, particularly in weight-bearing joints.

- Regular Exercise: Activities like swimming and cycling can strengthen joint-supporting muscles without adding joint stress.

- Joint Protection: Using supportive braces or altering activities to prevent joint strain.

The development of valid and feasible quality indicators (QIs) is needed to track quality initiatives for osteoarthritis pain management in primary care settings.

A literature search identified published guidelines that were reviewed for QI extraction. A panel of 14 experts was assembled, including primary care physicians, rheumatologists, orthopedic surgeons, pain specialists, and outcomes research pharmacists. A screening survey excluded QIs that cannot be reliably extracted from the electronic health record or that are irrelevant for osteoarthritis in primary care settings. A validity screening survey used a 9-point Likert scale to rate the validity of each QI based on predefined criteria. During the expert panel, discussions, stakeholders revised QI wording, added new QIs, and voted to include or exclude each QI. A priority survey used a 9-point Likert scale to prioritize the included QIs.

A literature search identified 520 references published from January 2015 to March 2021 and 4 additional guidelines from professional/governmental websites. The study included 41 guidelines. The extraction of 741 recommendations yielded 115 candidate QIs. Feasibility screening excluded 28 QIs. Validity screening and expert panel discussion excluded 73 QIs and added 1 QI. The final set of 15 prioritized QIs focused on pain management safety, education, weight management, psychological well-being, optimizing first-line medications, referral, and imaging.

This multi-disciplinary expert panel established consensus on QIs for osteoarthritis pain management in primary care settings by combining scientific evidence with expert opinion. The resulting list of 15 prioritized, valid, and feasible QIs can be used to track quality initiatives for osteoarthritis pain management ¹⁾.

Anti-Inflammatory Effects: Studies suggest that KD may reduce inflammation by inhibiting the NLRP3 inflammasome, a component involved in inflammatory responses. In a rat model of OA, KD significantly decreased joint inflammation and cartilage degradation.

Weight Management: Obesity is a known risk factor for OA. KD has been effective in promoting weight loss, which can alleviate stress on weight-bearing joints and potentially reduce OA symptoms. MDPI

Pain Reduction: By decreasing systemic inflammation and body weight, KD may contribute to reduced joint pain and improved function in individuals with OA.

Considerations and Risks

Nutrient Deficiency: Strict adherence to KD may lead to deficiencies in essential nutrients, including vitamins and minerals vital for bone health.

Hepatic Steatosis: Long-term KD has been associated with the development of fatty liver in animal studies. Modifications, such as intermittent KD or supplementation with vitamin D, have been proposed to mitigate this risk.

Conclusion

While preliminary studies indicate that KD may offer benefits in managing OA through anti-inflammatory effects and weight reduction, further research is necessary to fully understand its efficacy and safety in humans. Individuals considering KD for OA treatment should consult healthcare professionals to ensure a balanced approach that addresses potential risks and nutritional needs.

The ketogenic diet (KD) has demonstrated efficacy in ameliorating inflammation in rats with osteoarthritis (OA). However, the long-term safety of the KD and the underlying mechanism by which it delays OA remain unclear. Cai et al. found that while long-term KD could ameliorate OA, it induced severe hepatic steatosis in mice. Consequently, they developed two versions of ketogenic-based diets: KD supplemented with vitamin D and intermittent KD. Both KD supplemented with vitamin D and intermittent KD effectively alleviated OA by significantly reducing the levels of inflammatory cytokines, cartilage loss, sensory nerve sprouting, and knee hyperalgesia without inducing hepatic steatosis. Furthermore, β-hydroxybutyrate (β-HB), a convenient energy carrier produced by adipocytes, could ameliorate OA without causing liver lesions. Mechanistically, β-HB enhanced chondrocyte autophagy and reduced apoptosis through the activation of the Erb-B2 receptor tyrosine kinase 3 (ERBB3) signaling pathway; a pathway which was down-regulated in the articular chondrocytes from both OA patients and mice. Collectively, the findings highlighted the potential therapeutic value of β-HB and KD supplemented with vitamin D and intermittent KD approaches for managing OA ²⁾.