Achilles tendon pain – A rare aetiology

A 51-year-old woman presented with insidious pain and limited range of motion in her right ankle. Medical background reveals a history of undergoing bilateral surgery for clubfoot during childhood, with no post-intervention pain complications. Clinically, the patient had restricted movement on dorsiflexion.

An ultrasound was performed during the physiatry appointment, demonstrating a large area of marked echogenicity with no through-transmission (Figure 1).

The lateral ankle X-ray (Figure 2) confirmed the ossification of the right Achilles tendon with no evidence of fracture within the ossification.

Magnetic Resonance Imaging (MRI) (Figures 3a, 3b, 3c and 3d) was performed to evaluate the Achilles tendon’s integrity and confirmed an extensive ossification within the substance of the tendon. The remaining tendon appears thinned with loss of fibrillar texture, showing significant substance loss indicative of chronic (non-acute) rupture. There was no significant oedema in the subcutaneous adipose tissue surrounding the ankle, the peritendinous tissue, ankle effusion, or evidence of the ossified mass fracture.

The diagnosis of Achilles tendon ossification (ATO) was made based on the imaging findings corroborated by the clinical (insidious pain and restricted range of motion) and medical history (past surgery for clubfoot decades before).

ATO is a rare, acquired condition characterised by ossified masses within the body of the Achilles tendon, occurring more frequently in males with no age predilection [1–4]. It is occasionally asymptomatic and typically manifests as insidious discomfort, restriction of motion, and heel pain [3,4]. Ossification fracture or Achilles tendon rupture produces acute symptoms with a painful mass [2–4].

ATO is believed to have a multifactorial aetiology, with previous trauma (such as tendon rupture or micro-trauma) or surgery (often decades before) being common predisposing factors [1–5]. However, in literature, clubfoot surgical release, as seen in our patient, is considered a rare cause of ATO [3]. Metabolic conditions like diabetes, Wilson’s disease, and vascular insufficiency are also implicated in its development [2–4,6]. The exact pathogenesis remains unclear, but it is thought to involve a process of decreased oxygen tension leading to fibrocartilage transformation and subsequent calcium deposition within the tendon [3,4,6].

When the diagnosis of ATO is suspected, a plain radiograph should be obtained as it confirms the calcified masses within the tendon and assesses the ossification extent and location, in which classification is based, with three main types described [2–4]. Type 1 lesions occur at the tendinous insertion, type 2 lesions are located 1–3 cm from the insertion, and type 3 lesions extend up to 12 cm [2–4,6]. Additionally, lesions can be categorised based on the degree of ossification, ranging from partial to complete tendon involvement [2,3]. Extensive ossification involving greater than 50% of the tendon bulk is highly unusual [2–4]. Furthermore, radiographs better depict fractures [4].

On the other hand, the diagnosis can be further delineated with an ultrasound that reveals a hyperechoic mass [4,6] Although MRI is not required for the diagnosis, it can be used to assess the integrity of the tendon, providing more detail regarding the composition and location of the ossification and the extent of soft tissue damage [4].

ATO treatment approaches vary depending on the symptoms’ severity and the fractures’ presence [2,4]. Conservative management, including rest, physical therapy, and orthotics, is often the first line of treatment, especially in cases without fractures [4]. Surgical intervention may be required for severe pain or fractures, with techniques such as excision of ossified masses and tendon repair utilised to preserve function [2,4,6].

ATO is a rare condition commonly associated with previous trauma or surgery. Diagnosis supported by imaging studies is essential for effective management and prevention of long-term complications.

All patient data have been completely anonymised throughout the entire manuscript and related files.