Acute-Onset Achilles Tendon Pain and Swelling Treated with an Amniotic Fluid-Derived Allograft: A Case Study.

BACKGROUND: Tendinopathies are common musculoskeletal disorders that often develop because of chronic loading and failed healing. Tendinopathy related to systemic inflammation has been less extensively examined. Furthermore, although the use of biological agents to treat tendinopathies continues to gain popularity, the use of amniotic fluid-derived allografts in outpatient settings to resolve tendinopathies requires further evaluation. METHODS: The focus of this case report is a 25-year-old man who presented for a second opinion, having been diagnosed with Haglund deformity and Achilles tendinopathy. At the time of presentation, he complained of 10 of 10 pain to the right Achilles tendon. He was treating the injury conservatively with intermittent use of a controlled ankle motion boot and working with physiotherapy for approximately 5 months before presentation. Diagnostic ultrasound along with magnetic resonance imaging indicated distal thickening of the Achilles tendon, substantial fluid and edema in the Kager fat pad, and retrocalcaneal erosions with bursitis. Conservative management did not resolve the symptoms. As an alternative to surgery, the patient elected to undergo an Achilles tendon injection of an amniotic fluid-derived allograft. Before and after the initial injection, a microdialysis catheter was inserted into the Achilles peritendinous space to sample local levels of extracellular matrix enzymes and growth factors important for tendon remodeling. The patient received considerable relief with the initial injection, but did not return to full strength. Over the subsequent 8 weeks, the patient was followed closely and was able to return to daily activities with minimal pain. He was not able to return to a more active lifestyle without further Achilles pain, so a second amniotic fluid-derived allograft injection was performed 8 weeks after the initial injection. RESULTS: Injection of the initial allograft resulted in significant improvement, but not complete resolution of pain and swelling. Microdialysis findings suggested a reduction in peritendinous levels of the cytokine interlukin-6 in addition to changes in extracellular matrix regulatory enzymes. After 8 weeks of additional conservative therapy and a second injection, no further improvement in pain was noted. CONCLUSIONS: Based on the clinical improvement of symptoms in this individual and the changes seen with microdialysis methodology, the authors find the use of amniotic fluid-derived allograft injection for treatment of Achilles pain in this patient to be a viable treatment. Additional comorbidities of systemic inflammatory polyarthritis and possible seronegative disease were addressed after rheumatology consultation with a variety of medications that provided the patient additional relief of his symptoms. The patient ultimately moved and was lost to further follow-up.

The Impact of Genistein Supplementation on Tendon Functional Properties and Gene Expression in Estrogen-Deficient Rats.

Tendinopathy risk increases with menopause. The phytoestrogen genistein prevents collagen loss during estrogen deficiency (ovariectomy [OVX]). The influence of genistein on tendon function and extracellular matrix (ECM) regulation is not well known. We determined the impact of genistein on tendon function and the expression of several genes important for the regulation of tendon ECM. Eight-week-old rats (n = 42) were divided into three groups: intact, OVX, or OVX-genistein (6 mg/kg/day) for 6 weeks. Tail fascicles were assessed with a Deben tensile stage. Achilles tendon mRNA expression was determined with digital droplet polymerase chain reaction. Compared to intact, fascicle stress tended to be lower in untreated OVX rats (P = .022). Furthermore, fascicle modulus and energy density were greater in genistein-treated rats (P < .05) compared to intact. Neither OVX nor genistein altered expression of Col1a1, Col3a1, Casp3, Casp8, Mmp1a, Mmp2, or Mmp9 (P > .05). Compared to intact, Tnmd and Esr1 expression were greater and Pcna and Timp1 expression were lower in OVX rats (P < .05). Genistein treatment returned Tnmd, Pcna, and Timp1 to levels of intact-vehicle (P < .05), but did not alter Scx or Esr1 (P > .05). Several ß-catenin/Wnt signaling-related molecules were not altered by OVX or genistein (P > .05). Our findings demonstrate that genistein improves tendon function in estrogen-deficient rats. The effect of genistein in vivo was predominately on genes related to cell proliferation rather than collagen remodeling.