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Is it merely a curiosity that fat pads are found adjacent to the area of tendon affected by tendinopathy? We propose that fat pads share an anatomical and functional relationship with their adjacent tendons and may therefore contribute to the pathogenesis of tendinopathy. Fat pads and tendons have a shared blood supply,1 and cytokines produced in the fat pad have only a short distance to travel in order to affect the tendon.2 Fat pads lubricate, insulate, protect and provide structural support for tendons. However, the functional significance of the fat pad is often overlooked. In an early study of fat pad function, the distal tip of Kager's fat pad migrated into the retrocalcaneal bursa during ankle movement in healthy individuals, but not in an individual with a hindfoot disorder.3 This ‘variable plunger’ mechanism minimises pressure changes within the bursa during ankle movement. …

Background 12 weeks of eccentric exercise has been shown to be a useful therapy for Achilles tendinopathy, but little is known of the time-course of recovery, or the nature of any structural changes during therapy. Objectives To assess the time-course and pattern of Achilles tendon symptoms, thickness, stiffness, and ultrasound (US) signs during 12 weeks of eccentric exercise (EE). Methods Five subjects of age range (mean) 38–52 (46) years with main-body AT were included. For each subject, serial measurements of VISA-A score, the presence of neovascularisation and grey-scale US signs within the tendon, and the thickness of the Achilles tendon at 3 points were recorded for the first three weeks of a twelve week EE programme. Results Median VISA-A score increased from 48.5 to 54.5 (p=0.116). Median mid-tendon thickness decreased from 0.834 cm to 0.790 cm (p=0.107). A trend towards a decrease in tendon thickness was noted directly superior to the retrocalcaneal bursa and at the soleus myotendinous junction. Neovascularisation, paratenon blurring and hypoechoic areas improved in 1/3, 1/3 and 2/5 tendons respectively. No significant change occurred in median tendon stiffness. Conclusion 3 weeks of EE do not produce significant changes in AT symptoms and tendon thickness or stiffness, but improve US signs and neovascularisation in some subjects. The non-significance of findings may be a type II error and further work with larger sample sizes is planned.

We aspirated the retrocalcaneal bursa in cadavers to determine the characteristics of bursal fluid. A small amount of clear, viscous fluid was constantly present in the bursa. Leucocyte count was low, and the mucin clot test was good. With the same technique we aspirated the retrocalcaneal bursae of 4 patients. Three had Reiter's syndrome; the bursal fluid was inflammatory, and symptoms promptly resolved after local corticosteroid injection. The fourth patient presented with heel pain; intracellular, positively birefringent crystals were present in the aspirate, consistent with the diagnosis of pseudogout.