Coblation Therapy: Can It Have An Impact For Plantar Fasciosis?
Given the emerging recognition of plantar fasciosis as a degenerative condition, this author surveys the literature, questions the use of therapy for short-term relief, suggests a fresh perspective on diagnostic protocols and offers insights on the roles of relatively new modalities to treat this condition.
The paradigm is changing as scientific evidence challenges traditional heel pain treatment. Despite anecdotal evidence of how cortisone injections help the pain of plantar fasciitis, we also know it does not work for all patients all the time. We need to step back and look at how we have come up with this treatment protocol of injections, taping, night splints and orthotics. Who made up this treatment protocol and what was it based on?
One of the most pivotal points is the fact that plantar fasciitis is not inflammatory but is actually a well documented degenerative condition.1 To clarify, after tendon or fascial injury has occurred, there is a brief period (approximately two weeks) when there is an inflammatory component. 2
What does the literature say? Most of the basic clinical science has focused on tendons and we can extrapolate that data to fascia since the cell types are essentially the same.
Macroscopic evaluation of plantar fascia reveals disorganized tissue that shows evidence of myxoid degeneration. Microscopic histopathology of the tissue reveals degenerative changes to the collagen with fibrosis. Inflammatory mediators are not present. There appears to be decreased vascular infiltration (ectasia) within the tissue. 1
In several studies by Almekinders from 1998 through 2002, he demonstrates clearly that there is minimal inflammatory response within tendon and fascia after direct tissue injury, and no inflammatory response in tissue that has suffered repetitive motion type injuries. 3-5 Khan, et al., used a rat model to produce acute tendinopathy by exposing the tissue to proinflammatory cytokines. They demonstrated no inflammatory response but did show derangement and degradation of the collagen fibers. 6
Aside from pathology evaluation, there are diagnostic modalities that provide additional evidence. In a Doppler ultrasound study in 2007, Karabay evaluated 23 patients with heel pain and 23 control patients. The symptomatic patients exhibited increased thickness of the plantar fascia with reduced echogenity. 7 A 2005 study by Sabir had similar findings. 8 Magnetic resonance imaging (MRI) studies also reveal thickening of the plantar fascia without concomitant fluid accumulation in the fascia. The MRI studies do reveal significant bone marrow edema in the calcaneus. 9
Injections And NSAIDs: Do They Alter The Disease Process?
Why have we been using anti-inflammatory modalities to treat a process that has no inflammatory components? The fact is that nonsteroidal anti-inflammatory drugs (NSAIDs) and steroid injections do provide a short-term decrease in pain, much in the same way analgesic medications provide pain relief. These medications do not alter the natural history of the disease process. 10
A study by Altay, et al., demonstrated no clinical improvement in efficacy for a corticosteroid injection versus lidocaine injection in the treatment of lateral epicondylitis. These authors theorized that the actual patient benefit resulted not from the injected agents but rather from making multiple passes through the tendon with the needle. 11 The mechanical disruption of injured tendon is theorized to be similar to debridement. This tissue irritation promotes an inflammatory response, which is a necessary phase in the wound healing cascade.
In Frater’s study of 20 feet responding to injection, 14 had focal hyperemia on blood-pool images and six had minimal extension into the proximal third of the plantar soft tissues. No patient with diffuse hyperemia in the plantar fascia had a response (five of 12 feet). The response to injection was of a short duration. 12
It is clear that the answer to treating heel pain is not that simple. Many studies clearly demonstrate that heel pain localized to the plantar fascia does not have an inflammatory response. It appears clear that in order to treat tendinopathies and fasciopathies, we need to stop the collagen damage and injury pattern. We also need to stimulate collagen repair by increasing vascularity and increasing the levels of growth factors in the injured tissue. Then the tissue will respond.
What The Research Reveals About Emerging Modalities And Pain Relief
Several studies by Medlock and Tasto provide evidence to support the aforementioned statements. They published three studies documenting abnormalities in alpha V integrin levels and vascular endothelial growth factor (VEGF) levels in injured tendon. They also demonstrate a method to increase those levels to repair the tissue yet minimize the damage to the treated tissue. There are other studies but Medlock and Tasto state and demonstrate the evidence clearly.
In their first study, an in vivo study, they tested tissue from six normal and eight injured rotator cuffs.
They measured for the expression of the two angiogenic markers alpha V integrin and VEGF. Both were significantly lower in the injured tissue in comparison to the uninjured normal subjects. 13
The second in vitro study using a rat model measured the same angiogenic markers after Coblation therapy (Arthrocare). At nine days, researchers noted a significant increase in both alpha V integrin and VEGF mRNA levels. 14
In a third in vivo study utilizing radiofrequency Coblation of rotator cuff injury, Medlock and Tasto reported a significant decrease in post-treatment pain as well as a rapid return to function of the treated shoulders. 15
Medlock, et al., further studied the effect of coblation versus needling in aged rabbit tendons. 16 Researchers chose this model because the changes rabbit tendon undergoes as it ages are similar to that of a tendon with tendinosis.
They treated three rabbit tendons with needling and three with radiofrequency Coblation. The tendons that underwent needling had no changes to them and remained hypovascular. They also had minimal crimping and the collagen bundles were loose and disorganized. However, the tendons treated with Coblation demonstrated collagen remodeling, increased crimping and increased cellularity with dense collagen bundles. 16
Additionally, Takahashi, et al., studied the rapid relief of pain. This group found a significant antinociceptor response with a significant reduction in the quantity of epidermal nociceptors. 17
If we also consider the results of a multitude of studies utilizing extracorporeal shockwave therapy, the aforementioned studies suggest that there is a non-inflammatory etiology to heel pain. 18 They demonstrate a method of stimulating the tissue to release growth factors by exposing the tissue to rapid intense stimulation from the shockwave, whether physicians use high-energy or low-energy shockwave therapy.
Another approach is injecting platelet rich plasma into injured tissue. Again, the concept is to increase the presence of growth factors within the injured tissue to stimulate a healing response. These studies show high rates of resolution of patients’ pain and discomfort, and the ultrasound studies confirm definitive changes to the tissue with decreased thickness of the plantar fascia. 2
Rethinking Our Diagnostic Protocol
We have evidence that clearly and unequivocally shows that heel pain is not an inflammatory process for the majority of cases. We also know that NSAIDs and corticosteroid injections are not long-term answers.
How should we change our approach in light of the presented evidence? The first step is in our workup of heel pain. No longer should we assume that the diagnosis is plantar fasciitis and write off all of the other differential diagnoses (see “A Guide To Differential Diagnoses For Heel Pain” on page 38). We also need to alter our treatment regimen and reorient it based on the findings of each individual patient.
Consider the multitude of studies that demonstrate the effectiveness of utilizing diagnostic ultrasound in evaluating the plantar fascia for thickness, changes in vascularity and the presence or absence of soft tissue masses. Also consider the studies that demonstrate fairly equal diagnostic capabilities of ultrasound versus MRI. It seems
appropriate to use ultrasound as a routine diagnostic modality in working up painful heel syndrome. Of course, plain radiographs are equally as important to rule out fractures and arthritic changes.
Clinical examination is just as important as using diagnostic tools. A thorough neurological, vascular and biomechanical workup is essential in developing the correct diagnosis.
Since the focus of this article is on fasciosis, I will leave the alternative diagnoses to other authors and discuss the treatment of fasciosis.
What Should The New Treatment Algorithm Entail For Plantar Fasciosis?
DiGiovanni concludes that a program of non-weightbearing stretching exercises specific to the plantar fascia is superior to the standard program of weightbearing Achilles tendon-stretching exercises for the treatment of symptoms of proximal plantar fasciitis.19 Several articles of related study types do show improvement with stretching of the fascia and posterior muscle group. A study by Pfeffer in 1999 demonstrated that the most effective conservative treatment was the use of orthoses and stretching. 20
What is missing from all of this literature and research is a definitive treatment algorithm. The Cochrane
Review found limited evidence that conservative modalities alter the natural history of the heel pain syndrome. 21
Yet we do have evidence that treating the tissue with modalities that increase the presence of growth factors modulates and changes the quality of the tissue, and resolves the patients’ pain. We have strong evidence that radiofrequency Coblation stimulates the presence of alpha V integrin and VEGF. We have evidence that injecting platelet rich plasma into the injured tissue increases a wide spectrum of the patient’s own growth factors. The evidence suggests that extracorporeal shockwave therapy stimulates the release of growth factors in the treated area.
Certainly, we cannot expect a radical change in how we approach the treatment of heel pain syndrome. However, we need to reconsider our present approach and consider that what has been accepted as a community standard does not have the evidence to support its continued use.
If the clinical examination suggests involvement of the plantar fascia, one should pursue a diagnostic ultrasound. It is of low cost and is highly specific. If there is marked thickening of the plantar fascia and your tried and true conservative modalities have failed to provide your patient with relief, do not keep injecting and do not make another pair of orthotics. Offer your patient a treatment that has evidence and science behind it.
Radiofrequency Coblation is minimally invasive and has a minimal learning curve. It has an extremely low complication rate yet is highly effective in resolving
tendinosis and fasciosis injuries. There is an 85 percent resolution rate of heel pain at 12 weeks and pain typically reduces with the first several days of treatment. 22 The risks and complications are markedly less than that of a medial and central band plantar fascial release.
One can utilize radiofrequency Coblation wands percutaneously to avoid the typical portal pain associated with the endoscopic approach. The same can be said for injections of platelet rich plasma and extracorporeal shockwave therapy.
The typical drawback with these modalities has been financial and not due to a lack of success or evidence in the literature. We still need specific studies on each of these modalities to provide more guidance on when to use these therapies and to give us more direction on appropriate patient selection.
It is clear, however, that increasing the body’s own ability to heal itself by stretching, changing the biomechanics and generating growth factors will ultimately lead to resolution of a very painful entity.
Dr. Werber is a Fellow and Past President of the American College of Foot and Ankle Surgeons. He is board-certified in reconstructive foot and ankle surgery by the American Board of Podiatric Surgery. Dr. Werber is also board-certified by the American Board of Podiatric Orthopedics and Primary Care. He is also a Fellow of the American Academy of Podiatric Sports Medicine.
References:
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