Access to the PPM Journal and newsletters is FREE for clinicians.
12 Articles in Volume 12, Issue #4
Causes of Postoperative Pain Following Inguinal Hernia Repair: What the Literature Shows
Persistent Postsurgical Pain
Managing Adverse Drug Effects in Pain: Focus on Triptans and NSAIDs
Nonsurgical Treatments for Ankle Arthritis
Opioid Disposal: Dos and Don’ts
Survey Shows More Education About Fibromyalgia Needed Among Healthcare Providers
Anxiety in a Headache Patient: Case Challenge
“Centralized Pain”: A New Consensus Phrase
Tooth Loss in the Chronic Pain Population
When Prescribed Opioids Go Unused
May 2012 Pain Research Updates
May 2012 Letters to the Editor

Nonsurgical Treatments for Ankle Arthritis

Since so many pathologies result in ankle pain, an accurate diagnosis is the key to determining the most effective treatment.

Degenerative arthritis is a common condition in the general population and in many cases can be attributed to some antecedent injury earlier in life. Such injuries may include ankle sprain or more severe trauma, like ankle fracture, and has been demonstrated in female ballet dancers.1 However, development of degenerative arthritis is considered an ordinary disease of life, and when occurring at the level of the ankle joint complex can often be associated with changes in the normal function of the foot. Muehleman et al showed in 1,060 adult cadaveric specimens greater propensity for knee degeneration than ankle; however, they observed no cases of ankle degeneration that did not have more severe degeneration, or degeneration at all, of the ipsilateral knee joint.2 Because of ankle joint mechanics and pressure distribution, degenerative joint disease of the ankle is relatively minimal compared to the knee.3 It has also been suggested that cartilage degeneration can result from aberrations in the metabolism of the extra-cellular matrix.4

Patients who present with general ankle pain need to be closely worked up for accurate diagnosis because “ankle” as a term is a relatively unspecific anatomical term, and to the patient can mean virtually anything in the region of the joint including the subtalar joint, peroneal tendon complex, and/or Achilles insertion—whereas to the practitioner it usually denotes pathology of the talo tibiofibular articulation.

For those providers who routinely deal with lower extremity pathology, “ankle pain” is at best a nebulous complaint, and gives them only an area to start the examination. It is more common than not to have simultaneously more than one pain generator in play, which can result in more complex treatment decision-making. Sadly, patients with degenerative changes presenting on x-ray are often only given a diagnosis of “arthritis,” when in fact that may or may not contribute to the overall “joint” pain or any of it.

Diagnosis Misconceptions
As we can see in Table 1, there are myriad conditions frequently described by patients as “ankle pain.” Too many times we evaluate patients who have been diagnosed with degenerative joint disease of the ankle, based solely on a radiographic examination, and are currently being treated with a non-steroidal anti-inflammatory drug (NSAID), when in fact they have subtalar joint dysfunction, sinus tarsi syndrome, or frequently, stenosing tenosynovitis of the peroneal tendons. Accurate diagnosis is essential to eliminate these other possible generators, as many patients aged 50 to 70 years will have some radiographic evidence of degeneration, and their treatment is considered unsuccessful because they have been given the usual treatment regimen for “arthritis,” when in fact their real etiology of pain still lies unrecognized.

Ankle Injury
Most ankle sprains are of an inversion type, with the primary injury to the lateral collateral ligaments, and contribute to a significant amount of emergency room visits, previously estimated at an incidence of 2.15 per 1,000 person-years between 2002 and 2006.5 Most often, these sprains or strains are mild, with injury involving partial or complete rupture of the anterior talofibular ligament (ATFL), and the injured patient will heal in 6 to 8 weeks without sequelae. In one study evaluating 113 patients who had suffered 133 sprained ankles, 6.5% ended up with damage to the cartilage of the talus resulting in an osteochondral lesion.These types of lesions do not show up radiographically at the time of injury, most often present with symptoms greater than 3 months after the time of injury, and then can rarely be seen with plain film radiography. Computed tomography scans or magnetic resonance imaging (MRI) are definitive, objective tests to rule out this injury.

Because there are so many different tissues that can be injured at the time of an ankle sprain, it is imperative that the provider be aware of them, and understands that rarely is there an isolated pathology with a severe injury.

Figure 1. In this x-ray, a well-maintained joint space is consistent from medial to lateral in the AP view, with no incongruity of the joint surfaces. AP, anteroposterior


Figure 2. From the lateral view of the same ankle seen in Figure 1, there is no evidence of arthritis, and there is a normal joint space from posterior to anterior. There is no evidence of anterior talotibial impingement.


Figure 3. This example represents a severe degenerative ankle joint with joint space only noted on a small aspect of the medial gutter. This ankle requires fusion or total joint replacement and will not respond to adjuvant treatments.

Clinical Evaluation
To simplify the clinical evaluation of the painful ankle, it is recommended to divide the ankle joint into medial and lateral, and anterior and posterior, in addition to intra-capsular and extra-capsular (Figures 1-3). You can then, based on your anatomic knowledge, get an initial idea of the pathology so that appropriate evaluation can be done. Table 2 shows a categorization of possible pathology based on this simple concept, and will give the practitioner a good idea of what additional testing may be useful.

The patient who presents with the complaint, “my ankle hurts everywhere,” provides a conundrum for the practitioner (and more clinical evaluation is required for a truly accurate diagnosis), in contradistinction to the patient who can quickly and precisely pinpoint where their ankle hurts. It is helpful during the history of current illness to delineate not only a description of the type and level of the pain, but what type of physical or exercise activity exacerbates it, whether it starts to hurt after a certain period of time (this gives the physician a “baseline” to refer back to after treatment), and what type of shoes the patient wears most often.

Initially, the clinical evaluation should involve the amount and type of range of motion of the ankle both with the knee extended and flexed, as this will determine whether there is any limitation to the excursion of the ankle joint, which is defined as equinus. By definition, there should be at least 10 degrees of dorsiflexion available from neutral with the knee fully extended. If not, then what is the amount of dorsiflexion with the knee flexed? If it is greater than 10 degrees, you now know that the patient suffers from a gastrocnemius equinus, and this could be contributing to the ankle pain. Is their range of motion smooth, or is there grating when the practitioner moves the patient’s joint through the range of motion, which indicates cartilage wearing and degeneration? Is there only pain with forced inversion? This is probably indicative of pathology associated with the ATFL. Is there pain with palpation just inferior to the lateral malleolus, and if so, is there pain along the course of the peroneal tendons? This would indicate tendinopathy, which would require additional diagnostic testing such as MRI or high-resolution diagnostic ultrasound to determine the extent of the injury. Pain in the posterior aspect of the ankle joint would likely indicate something simple such as Achilles tendinopathy or a painful os trigonum. Another clinical test to rule out whether there is an os trigonum, and whether it is a source of the pain, is to force the hallux into dorsiflexion. The tendon of the flexor hallucis longus runs adjacent to this bony structure, and pain with this test indicates there may have been a disruption of the synchondrosis, and this is the source of the pain.

Pain on the medial aspect of the ankle joint could indicate a problem with the deltoid ligament, occult fracture of the medial malleolus, or if the pain is with palpation distal to the medial malleolus, potentially a problem with the posterior tibial tendon, which is very common in middle-aged women.

In those patients with pain on the anterior aspect of the ankle, there may be an anterior impingement between the talus and anterior aspect of the tibia (Figures 4 and 5). Radiographs will greatly aid in this diagnosis.

Figure 4. This is the same ankle seen in Figure 3, and there is no evidence of any joint space. Osteophytes are clearly seen posteriorly, with anterior impingement.

Figure 5. This mortise view shows moderate degeneration with loss of joint space in both the medial and lateral gutters, but there is normal space with relatively good congruity between the talus and the tibial plafond.

Nerve entrapments of the common and superficial peroneal nerves are very common, but frequently never diagnosed, and can occur from a simple ankle sprain. Evaluate the common peroneal nerve proximally at the level of the fibular neck to see if there is a provocation sign, or Tinel’s sign. What is the strength of dorsiflexion of the hallux compared to the other side? This could indicate that the patient’s “ankle” pain is in fact referred pain from an entrapment of the common peroneal nerve.

The superficial peroneal nerve entrapment is also frequently unrecognized, but the clinician must remember that where the nerve courses from the deep compartment to the superficial subdermal space there is a foramen, which in some patients is very small and can lead to entrapment after a simple ankle sprain. The location for this is usually 12 to 15 cm proximal to the lateral malleolus midway between the tibial crest and fibula.

Finally, the sinus tarsi must be evaluated. Because of its location just distal to the ankle joint, practitioners must be careful that they do not confuse these close, but anatomically distinct, areas during evaluation. While there is not any real imaging study that aids in the diagnosis of sinus tarsi syndrome, a simple local anesthetic block into the area is highly confirmatory if there is a significant relief of pain after the block. See Table 3 for other possible diagnoses of ankle pain.

In those situations of “generalized” ankle pain, one simple and reliable method to aid in the clinical diagnosis is to determine whether the symptoms coming from the ankle joint are due to degeneration of the cartilage, or other internal derangement, versus an extracapsular source (for example, peroneal tendinopathy), by locally anesthetizing the joint with lidocaine. Provided that the physician does not infiltrate any of the agent subcutaneously prior to being intra-articular, relief of pain for the patient confirms their symptoms are most likely solely due to a problem within the joint itself, and not something external such as sinus tarsi syndrome. Usually, 3 to 6 mLs of lidocaine are all that is necessary to perform such a block, and it is recommended the patient wait about 10 minutes prior to evaluation and testing it with ambulation.

Conservative nonsurgical treatment of degenerative arthritis of the ankle involves many different approaches ranging from bracing and simple corticosteroid injections to viscosupplementation, use of autologous platelet concentrates such as platelet-rich plasma (PRP), and the emerging technology of autologous stem cell therapy using bone marrow aspirate concentrate (BMAC) (Table 4, page 56). Hyaline cartilage, regardless of which joint is discussed, is a complex tissue with a complex biochemistry, interesting viscoelastic properties, and has the propensity to regenerate with use of PRP and BMAC.

Dietary Supplements
Chondroitin, glucosamine, and avocado-soy unsaponifiables have demonstrated some reduction in pain associated with symptoms of osteoarthritis. They are thought to modulate inflammatory and degradative enzyme pathways. It should be noted there are other pathways of biochemical significance that have been identified and studied. There is some suggestion that in animal testing, use of these types of supplements after chondral injury has some ability to delay the course of osteoarthritis. This has not yet been demonstrated in humans. Controversial results stemmed from the National Institutes of Health–funded Glucosamine/Chondroitin Arthritis Intervention Trial.7 Combinations and single administrations of chondroitin and glucosamine were found to be better than placebo, but not to a level of statistical significance. Compared with placebo, patient response to glucosamine was 3.9% higher (P=0.30), patient response to chondroitin was 5.3% higher (P=0.17), and the response to combined treatment was 6.5% higher (P=0.09). There was some evidence for clinical improvement, in fact highly statistically significant, in patients with moderate to severe degenerative arthritis on combined therapy when compared to placebo (79.2% vs 54.3%, P=0.002).7

Viscosupplementation, accomplished by a simple injection, is a common modality of treatment for the knee, and increasingly for the ankle and other joints.8 Synovial fluid is known to be a shock absorber, provide vital nourishment to hyaline cartilage, and is essential in the promotion of chondrocyte proliferation. Synovial fluid has also been shown, in degenerative arthritis, to be decreased volumetrically.9

Endogenous hyaluronic acid is produced by the synoviocyte and fibroblasts found within the joint. Supplementation via exogenous hyaluronic acid has been shown to be chondroprotective via downregulation of enzymatic pathways associated with osteoarthritis, and inhibit nociceptors. Interestingly, it has also been shown to increase or stimulate the production of endogenous hyaluronic acid, and aid in the tissue repair process of cartilage.9

Platelet-rich plasma (PRP) has been extensively studied for more than two decades with the first application in cardiovascular surgery, but with much more work done in the area of bone healing acceleration in maxillofacial surgery by Marx.10-12 Efficacy in repair of full-thickness chondral defects has been demonstrated clinically.13,14 To be defined as a platelet-rich product, there must be an increase in viable platelets over the normal baseline of 200,000 to some level above the native yield, usually 5x. It is important to note that there is variability between different types of processors. It is believed that a 4-6x level is most advantageous, and that levels above 6x may in fact be inhibitory.

Treatment with PRP is simple, safe, and can be processed easily for injection. As an autologous platelet concentrate, it has been referred to as “supraphysiologic,” which delivers high levels of growth factors to the level of injury, and has been found to prevent development of osteoarthritis in the rabbit model.15,16 The platelet contains within its alpha granule a plethora of both identified and yet to be identified growth factors, hemostatic proteins, adhesion proteins, and cytokines. It is imperative to understand that in addition to significant differences in platelet yield from manufacturer to manufacturer, there are also huge differences in technique, which can affect the efficacy of treatment with PRP in any musculoskeletal tissue.9 This would include not allowing the platelets to become activated prior to accurate tissue placement, and tissue placement itself. Platelets will become activated with either a mixture of thrombin, or when they come in contact with collagen. Another advantage of using PRP is that it is bacteriocidal, especially for Staphylococcus aureus and Escherichia coli bacteria. The chance of infection from an autologous PRP injection is remote, somewhere in the range of a 1:50,000 occurrence. Interestingly, a recent study by Batista et al showed better bone-healing outcomes with PRP compared to bone marrow aspirate.17

While some may consider the use of BMAC as a surgical procedure for the treatment of degenerative arthritis based on the fact that there must be some harvest from the iliac crest or other bone marrow source, the technique of obtaining the marrow is done percutaneously with a small-gauge aspiration and little trauma for the patient. The procedure can be comfortably done in the office setting with simple local anesthesia.

Bone marrow is the main source of mesenchymal stem cells in the human body—and even in bone marrow aspirate, they are quite rare. Bone marrow also contains hematopoietic stem cells. These pluripotent cells can be concentrated in a sterile, clinical setting, without having to be sent out to a laboratory to culture them, but can be effectively processed in about 15 minutes. The cells can then be injected into the degenerative joint, or any tissue type for that matter. BMAC has been shown to improve full-thickness cartilage repair.18 Additionally, autologous hematopoietic stem cells remain outside any controversy or discussion, which is frequently brought up when dealing with cells derived from fetal cord blood.

Orthotic Devices
While there are few peer-reviewed papers that deal with the efficacy of treatment for any foot condition with custom-made orthotic devices,19 it can be said empirically, for example, that a patient who has severe flatfoot deformity (pes valgo planus) can benefit greatly simply by being provided with better mechanical alignment for their foot. With severe pronation, as seen in flatfoot, there is an inversion, plantarflexion, and adduction of the talus within the mortise of the ankle joint complex, which can cause a significant mechanical shearing of the cartilage, with subsequent development of a degenerative ankle.

Figure 6. In this x-ray, there is severe talar tilt from a failed surgical correction, and this illustrates how important it is when surgically repairing a severe ankle fracture that an anatomical reduction is obtained. This ankle will require fusion.

Ankle joint pain is common, and more often than not it is multifactorial in presentation. Simply diagnosing a patient with “degenerative arthritis” of the ankle joint does not provide the treating physician with any real clue as to why it developed in the first place, and whether in fact that is the true source of the patient’s pain. If there is a concomitant pathomechanical condition such as severe pes valgo planus or extreme derangement (Figure 6), it does no good to simply treat the ankle joint with any of the above-mentioned modalities without simultaneously addressing the aberrant mechanics that have lead to the degeneration. There are so many different pathologies that can be classified as “ankle pain,” it is imperative to rule out conditions such as peroneal tendinopathy, sinus tarsi syndrome, anterior talotibial impingement syndrome, syndesmotic injury, etc, so the patient with pain can be effectively treated.


Last updated on: June 19, 2012
close X