Conservative Care For Mid-Portion Achilles Tendinopathy
Given the common nature of mid-portion Achilles tendinopathy, this author reviews the literature and shares insights on a variety of conservative modalities ranging from eccentric loading exercises and activity modification to prolotherapy injections and shockwave therapy.
Achilles tendinopathy is a common cause of pain and disability in people with an active lifestyle, particularly middle-aged men.1-5 The mid-portion of the Achilles (2 to 6 cm distal to the insertion) is the most commonly affected region.6 It is one of the most common sports overuse injuries, which repetitively load the Achilles tendon.1-3,7
Achilles tendinopathy has a 24 to 52 percent lifetime incidence in former runners and a current prevalence of 6.5 to 18 percent among runners.8,9 Mid-portion Achilles tendinopathy can also affect the sedentary population, suggesting that physical activity may exacerbate symptoms rather than cause them.10,11
This article will focus on Achilles tendinosis, the term employed when ultrasound reveals structural changes in the Achilles tendon, as this is by far the most common form of Achilles tendinopathy.12 Ruptures, peritendinopathy and insertional tendinopathy are outside the scope of this article.
Key Insights On Tendon Pathophysiology
An understanding of tendon pathophysiology is essential when you are considering treatment options. A number of studies in the last 10 years have shown that Achilles tendinopathy is largely a non-inflammatory process.13-19 In 2002, Khan and colleagues alerted all medical practitioners dealing with tendon injuries with the slogan “time to abandon the ‘tendinitis’ myth.”12 The four main events that occur in tendinopathy are cellular activation and increase in cell numbers; increase in ground substance; collagen disarray; and neovascularization.20
In situ intratendinous microdialysis studies have revealed no difference in concentrations of prostaglandin E2 (PGE2) between healthy tendons and tendons with tendinosis (i.e., there is no chemically mediated inflammatory process). Higher concentrations of glutamate (a powerful pain modulator) and lactate are also present in tendons with tendinosis in comparison to normal tendons.13,15,19
Researchers have conducted studies on tendons with tendinosis using gene technology (using complementary DNA (cDNA) arrays and real-time polymerase chain reaction (PCR)).16,21 These studies have found a down-regulation of matrix metalloproteinase-3 (MMP-3) and an up-regulation of type I and type III collagen, MMP-2 (the enzyme involved in degrading processes), the fibronectin receptor involved in healing processes (FNRB) and vascular endothelial growth factor (VEGF). There is also no regulation of genes for a variety of cytokines known to be involved in the inflammatory process.22
Following tendon injury, nitric oxide synthase (NOS) induces nitric oxide (NO) in rats. Research has shown NOS activity to be up-regulated in rat Achilles tendinopathy while tendon healing increases with the addition of more NO.23,24
While there is no chemically mediated inflammatory process, immunohistochemical analyses of tendon biopsies have revealed that there may be some neurogenic inflammation.13,25-27 Biopsies of areas of tendinosis with accompanying neovascularization have shown nerve structures in close proximity to vessels.26 Substance P (the pain neurotransmitter that also increases vascular permeability and vasodilatation) and neurokinin-1 receptor (the endogenous receptor for substance P) were also present in the vascular wall.27 This neural pathway associated with the neovascularization of tendinosis may explain the pain associated with this problem.20