Conventional Medicine:

Osteoarthritis (OA)

Osteoarthritis (OA) is a chronic joint disorder affecting millions, leading to pain, stiffness, swelling, and reduced mobility, particularly in the knees, hips, hands, and spine.

Osteoarthritis affects approximately 15% of the world’s population. It is three times more common in women than in men. This section of the website explores the underlying factors contributing to the development of OA and the pain associated with it, including diet and obesity. Conventional approaches to treating OA are reviewed as well as in-depth discussions of underlying neurologic processes that maintain the pain.

Because the conventional treatment options may be inadequate or unacceptable, people often turn to alternative, supplemental nutraceuticals for relief. For a review of these alternative treatment options, See:  Osteoarthritis (CAM) Treatment).

 

Other links:

 

Assessing Pain in OA

The intensity of pain in OA, especially in knees, correlates poorly with measures of tissue destruction as evidenced by xrays and other imaging studies. For example, 30% – 50% of individuals with moderate-to-severe x-ray changes of OA have no pain, while 10% – 20% of individuals with moderate-to-severe knee pain have normal findings on radiography. Thus one cannot measure or predict the extent of pain simply by obtaining x-rays.

Early research suggests that there may be measurable biomarkers, levels of pain-related chemicals, that can predict to some extent the degree of sensitization and indirectly the levels of pain. These findings require further research for their accuracy and predictive effectiveness before they can be used clinically.

Osteoarthritis (OA) – Conventional Treatment

Traditional western medicine (allopathic medicine) has limited answers to those with chronic pain due to osteoarthritis (OA).  Currently, there are no evidence-based treatment options can suppress, arrest or reverse the anatomic changes associated with OA. As such, treatment of OA is limited to pain control for the most part. 

It should be understood that OA is in fact a degenerative disease, not in its core an inflammatory disease like Rhematoid Arthritis, Psoriatic Arthritis and arthritis associated with Lupus.  A degenerative disease is one that is essentially a wear-and-tear process associated with use.

That being said, OA does have inflammatory components as well as neuropathic components with each of these conditions contributing more, or less, to the various stages of the degenerative process. As such, the pain of OA may respond to anti-inflammatory medications such as NSAIDs (ibuprofen, naproxen, meloxicam etc.) and steroids (cortisone, etc.) and/or they may respond to neuropathic medications (gabapentin and pregabalin (Lyrica).  Both of these classes of medications can be engaged as trials to control OA pain and some individuals will respond best to one, the other or a combination of the two.

When these two classes are inadequate to control OA pain, duloxetine (Cymbalta) may offer additional benefit and when the pain is severe, opioids are often engaged. Further exploration of these classes of medications can be found on other pages on this web site, see below for links.

In some cases, interventional treatments including injections into an affected joint of a lubricant-like medication (hyaluronic acid, Synvisc) can provide relief. Nerve blocks can also offer benefit in some cases. Consultation with an interventional pain specialist or orthopedist may be warranted to explore these treatment options.

 

Anti-inflammatories (NSAIDs)

The medical field unfortunately has nothing to offer in the way of a cure for OA. Surgery has little to offer for most people with arthritis and is generally not recommended in the absence of severe and debilitating cases.

The mainstay of traditional OA treatment has been the use of anti-inflammatories including cortisone (steroids) for severe, acute flair-ups and non-steroid anti-inflammaatory drugs (NSAIDs) such as ibuprofen, naproxen and a handful of prescription NSAIDs. Unfortunately, NSAIDs do nothing to slow the progression of OA or reverse the damages associated with OA. Worse, they have significant safety issues of their own, especially the steroids.

 

Neuromodulators

Neuromodulators are drugs that modify the function of nerves. Neuromodulator medications such as gabapentin (Neurontin), pregabalin (Lyrica), topiramate (Topamax), duloxetine (Cymbalta) and others  may be effective in OA pain by reducing the nerve pain component of OA pain. The neuromodulaters may also be effective in reducing pain associated with central sensitization.

 

Knee braces, knee sleeves, shoe inserts

Potential benefit may come from use of knee braces, knee sleeves, foot pads, and biomechanical training programs. To learn more about your potential benefits from these options, please talk with our physical therapist or physician. At Accurate Clinic we offer the free services of an orthotics technician to provide assessments of orthotic devices that may fit your needs.

 

Hyaluronic Acid Injections

  • Mechanism: HA, a key component of synovial fluid, lubricates joints and may reduce inflammation by modulating nociceptive signaling. In acute pain, HA injections could theoretically limit peripheral sensitization by stabilizing joint mechanics and reducing inflammatory mediators. In chronic pain, it may mitigate cartilage degradation, indirectly reducing central sensitization triggers.
  • Effectiveness:
    • Acute Pain (<90 days): Primarily used in knee osteoarthritis (OA) flare-ups. A 2020 study in Journal of Orthopaedic Research showed HA injections reduce pain within 1–4 weeks in acute knee OA exacerbations, potentially limiting early sensitization. Limited data for other joints or non-OA acute pain.
    • Chronic Pain: Modest pain relief and functional improvement in knee OA (6–12 months), per a 2016 meta-analysis in Clinical Orthopaedics and Related Research. Less evidence for hip, ankle, or shoulder OA. Oral HA shows weaker effects (2017 Nutrients review).
    • Sensitization: May reduce peripheral sensitization by decreasing joint inflammation and mechanical stress, but no direct evidence on central sensitization.

  • Joints

    • Knee OA: Studies, including a 2016 meta-analysis in Clinical Orthopaedics and Related Research, show HA injections reduce pain and improve function in mild to moderate knee OA compared to placebo, with effects lasting 6–12 months. Benefits are modest, and response varies by patient. The American Academy of Orthopaedic Surgeons (AAOS) gives a limited recommendation due to inconsistent trial results.
    • Hip OA: Limited evidence supports HA for hip OA. A 2017 study in Journal of Hip Preservation Surgery found pain relief in early-stage hip OA, but data is sparse, and it’s not routinely recommended.
    • Other Joints (e.g., Ankle, Shoulder): Research is minimal. Small studies suggest potential pain relief for ankle OA, but no strong guidelines exist.
    • Oral HA: Evidence is weaker. A 2017 review in Nutrients noted mild pain reduction in knee OA, but studies are small and lack long-term data.
  • Indications:
    • Acute Management : Consider HA injections for acute knee OA flares to reduce pain and inflammation, potentially preventing sensitization in high-risk patients (e.g., post-injury).
    • Chronic Management: Use as adjunctive therapy for knee OA to maintain function and reduce reliance on analgesics.
  • Patient Selection: Best for mild to moderate knee OA in patients avoiding surgery. Less clear for other joints or advanced OA.

  • Effectiveness

    • Knee OA: Studies, including a 2016 meta-analysis in Clinical Orthopaedics and Related Research, show HA injections reduce pain and improve function in mild to moderate knee OA compared to placebo, with effects lasting 6–12 months. Benefits are modest, and response varies by patient. The American Academy of Orthopaedic Surgeons (AAOS) gives a limited recommendation due to inconsistent trial results.
    • Hip OA: Limited evidence supports HA for hip OA. A 2017 study in Journal of Hip Preservation Surgery found pain relief in early-stage hip OA, but data is sparse, and it’s not routinely recommended.
    • Other Joints (e.g., Ankle, Shoulder): Research is minimal. Small studies suggest potential pain relief for ankle OA, but no strong guidelines exist.
    • Oral HA: Evidence is weaker. A 2017 review in Nutrients noted mild pain reduction in knee OA, but studies are small and lack long-term data.
  • Safety: Injections are safe with minor risks (swelling, pain at site). Oral HA has negligible side effects.
  • Cost: Injections are costly; oral supplements are affordable but less effective.  Injections: $500–2,000/course. Oral: $20–50/month.

 

Surgery – Joint Replacements

In addition to the reduction of pain associated with damaged joints when they are replaced with artificial joints, there is evidence that central pain can be reversed after joint replacement as well.

 

Understanding the Pain of OA – The Science

Osteoarthritis is characterized by the progressive destruction of the cartilage on the joint surfaces which results in impaired joint function, swelling, pain, and disability. In addition to the destruction of cartilage, OA involves damage to bone and nerves as well as inflammation. While osteoarthritis commonly affects the knees, hips, hands and shoulders it is also a major contributor to neck and back pain.

Conventional treatment of OA as noted above is generally focused on reducing the current symptoms, particularly pain. However, as OA pain becomes chronic, over time there are changes that occur in the nervous system that contribute as driving forces to maintain that pain, conditions including Peripheral and Central Pain Sensitization. 

Understanding these process and intervening on them to suppress that increasing pain severity that they generate represents an alternative approach that deserves further exploration, as reviewed below.

 

Peripheral and Central Pain Sensitization

The pain is a result of all of these conditions and pain severity is largely determined by the forces associated with compressing the arthritic joint. During the last decade there has been greater understanding not only of the inflammatory aspects of OA, including contributions from various inflammatory chemicals like interleukins, cytokines and nerve growth factor, but there is also a growing appreciation of the role of peripheral and central pain sensitization in OA. Manifestations of sensitization include the spread of perceived pain beyond areas of disease, including referred and radiating pain. This role of central sensitization in OA suggests the potential benefits of treatment directed at reducing existing sensitization and taking efforts at suppressing further develepment of sensitization.

 

A contributing mechanism of central sensitization is the dysregulation of nerve pathways that descend from the brain into the spinal cord to interact with ascending pain pathways. These descending pathways normally function to reduce pain signalling from the nerves in the dorsal horns of the spinal cord that contribute to pain perception. The control of the descending pathways to inhibit pain is referred to as Conditioned Pain Modulation (CPM). Reduced CPM has been shown in OA patients, strongly indicating dysregulated top‐down modulation develops as the pain state progresses. Treatments directed at restoring pain inhibition in these pathways are potentially effective in managing OA pain. These treatments include behavioral mind-based treatments as well as prescription medications such as duloxetine (Cymbalta) and tapentadol (Nucynta).

See: Central Sensitization

 

Neuroinflammation

 A growing body of evidence now points to inflammation, locally and more systemically, as a promoter of damage to joints and bones, as well as joint-related functional problems. The disease process underlying joint diseases is currently believed to involve communication between cartilage and the subchondral bone beneath the cartilage in the joint—and a loss of balance between these two structures. Research over the last 5-10 years indicates that chronic pain is largely due to a process called neuroinflammation, a condition characterized by activation of a number of inflammatory cells within the peripheral and central nervous systems.

 

Neuroinflammation is characterized by migration of immune cells into an area of injury which release inflammatory chemical products that lead to activation and maintenance of chronic pain. These inflammatory cells, mast cells and glial cells, are now targets for development of new medications for treating chronic pain. Evidence indicates that suppression of the activation of these cells may limit or abolish the evolution of acute to chronic pain and may also act to reduce chronic pain.

 

Dysregulation of the mast cells in joint structures is associated with damage to these structures (cartilage, bone, synovia, matrix, nerve endings, and blood vessels). This process includes neuroinflammation which in turn contributes to the chronic pain associated with arthritis.

 

Communication between the spinal cord and the joint can cause further neuroinflammatory changes at the spinal level involving the central nervous system and brain. A central sensitization process has also been observed in patients with arthritis, where pain thresholds to pressure and prick stimuli are lower than in healthy subjects,making the person experience pain more easily and severely. This central sensitivity to pain does not correlate with radiological findings, suggesting that central sensitization is the factor that contributes most to arthritis pain.

 

Unfortunately, current conventional treatment strategies for arthritis are directed only at relieving symptoms and do little to limit progression of the disease process itself.

 

OA and Obesity

Since the pain of arthritis is associated with compressing the joint, weight-bearing joints such as the knees and hips are most severely affected but so are the joints in the spine. The hallmark of treatment therefore is to lose excess weight. Studies have shown that obese individuals without significant knee arthritis who lose 10 lbs will reduce their risk of developing symptoms of knee arthritis by 50%. For those with knee arthritis, a weight loss of only 5-10% of body weight provides significant, easily noticeable improvement in pain and function. So it is not necessary to reach your ideal weight before benefitting from weight loss.

 

Obesity also contributes to arthritis beyond just placing mechanical stress on your joints. Obesity is associated with an increase in a number of hormones, peptides and other bioactive chemicals manufactured by fat cells that promote inflammation and pain. Because of this it is all the more important to lose excessive weight for those with arthritis.

 

See Accurate Clinic’s Weight Loss Program, offered at a substantial discount to those patients enrolled in our pain management programs.

 

OA and Diet

Diet can play a significant role in arthritis and inflammation. Aside from adjusting calories to maintain ideal body weight, it is important to include nutrients that may protect against further joint damage. These nutrients include anti-inflammatories, antioxidants and NRF2 activators which are commonly found in high concentrations in grapes, berries, cherries, pomegranates and peanuts as well as ginger and green tea. Fish and chia seeds are high in omega-3 fatty acids which are powerful anti-inflammatories.

 

Foods high in fat and sugar are known to promote systemic oxidation and inflammation and should be avoided in those with arthritis.

 

To learn more about the role of diet and OA, see Accurate Clinic’s Medical Nutrition Services, offered free to those patients enrolled in our pain management programs.

 

 

Exercise

Exercise is also very important and most people – though not everyone – will improve their pain and function with modest exercise just a few times a week. Our physical therapist and personal trainer can guide you in a home exercise tailored to your specific needs.

 

References

Osteoarthritis – Overview

  1. Osteoarthritis  – Diet & CAM Summary

Osteoarthritis – Central Sensitization

  1. What Fibromyalgia Teaches Us About Chronic Pain – 2013

 

Osteoarthritis Treatment (Tx)

For information about effective CAM treatment for Osteoarthritis: CAM – Osteoarthritis

 

Osteoarthritis Tx – Overview

  1. Osteoarthritis  – Diet & CAM Summary
  2. Non-Steroid Anti-Inflammatory Drugs (NSAIDs)

Emphasis on Education

 

Accurate Clinic promotes patient education as the foundation of it’s medical care. In Dr. Ehlenberger’s integrative approach to patient care, including conventional and complementary and alternative medical (CAM) treatments, he may encourage or provide advice about the use of supplements. However, the specifics of choice of supplement, dosing and duration of treatment should be individualized through discussion with Dr. Ehlenberger. The following information and reference articles are presented to provide the reader with some of the latest research to facilitate evidence-based, informed decisions regarding the use of conventional as well as CAM treatments.

 

For medical-legal reasons, access to these links is limited to patients enrolled in an Accurate Clinic medical program.

 

Should you wish more information regarding any of the subjects listed – or not listed –  here, please contact Dr. Ehlenberger. He has literally thousands of published articles to share on hundreds of topics associated with pain management, weight loss, nutrition, addiction recovery and emergency medicine. It would take years for you to read them, as it did him.

 

For more information, please contact Accurate Clinic.

 

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