Compared with plantar fasciosis, heel fat pad syndrome has received relatively little research attention. For many years, it was considered an uncommon cause of heel pain and was often overlooked in favour of more familiar diagnoses such as plantar fasciitis. However, more recent research has shown that heel fat pad syndrome is probably underdiagnosed rather than uncommon and should be considered whenever patients present with pain beneath the centre of the heel.
One of the strongest findings in the literature is that heel fat pad syndrome has a distinct clinical presentation. Studies consistently report that patients describe pain directly beneath the central heel, worsening symptoms on hard surfaces and discomfort during prolonged standing. This differs from plantar fasciosis, where pain is usually localised to the medial plantar aspect of the heel and is characterised by marked pain during the first few steps after rest.
Research has also improved our understanding of the anatomy of the heel fat pad. Rather than acting as a simple cushion, the fat pad consists of highly organised chambers of fat enclosed by strong collagenous septae. This specialised structure enables the heel to absorb and redistribute forces generated during walking and running. Damage to this architecture, whether through ageing, repetitive overload or trauma, reduces the fat pad's ability to dissipate impact forces and contributes to chronic heel pain.
Diagnostic ultrasound has become an increasingly valuable investigation. Several studies have demonstrated that ultrasound can assess heel fat pad thickness, evaluate the internal architecture of the fat chambers and identify disruption of the fibrous septae. Importantly, ultrasound also allows simultaneous assessment of the plantar fascia, enabling clinicians to distinguish heel fat pad syndrome from plantar fasciosis or identify when both conditions are present.
Research has shown that heel fat pad thickness alone does not determine whether a patient has heel fat pad syndrome. Some individuals naturally have relatively thin heel fat pads without pain, while others experience significant symptoms despite measurements that fall within the normal range. This reinforces the importance of combining imaging findings with the patient's history and physical examination rather than relying on measurements alone.
The evidence supporting individual treatments remains relatively limited. High-quality randomised controlled trials are scarce, and many recommendations are based on biomechanical principles rather than large clinical studies. Nevertheless, there is broad agreement that reducing repetitive impact through the heel is central to successful management.
Studies examining footwear consistently demonstrate that cushioned footwear reduces plantar pressures beneath the heel compared with barefoot walking or minimalist shoes. Although these studies often involve healthy volunteers rather than patients with heel fat pad syndrome, the findings support the clinical recommendation to maximise shock absorption during everyday activities.
Similarly, heel cups and silicone heel cushions have been shown to reduce peak plantar pressures beneath the calcaneus. While the quality of evidence varies, many clinicians recommend these devices because they are inexpensive, low risk and biomechanically logical. Individual responses vary, and selecting the most appropriate device often requires trial and adjustment.
Evidence supporting orthotic therapy is less direct. Orthoses are unlikely to restore the structure of the fat pad itself but may improve abnormal foot mechanics and redistribute pressure away from painful areas. Their benefit therefore depends on whether biomechanical abnormalities are contributing to the patient's symptoms rather than the diagnosis alone.
One area where evidence remains particularly limited is regenerative medicine. At present, there is insufficient high-quality research to support routine use of platelet-rich plasma, prolotherapy or other injectable regenerative treatments specifically for isolated heel fat pad syndrome. Likewise, there is little evidence supporting shockwave therapy as a primary treatment for fat pad pathology in the absence of coexisting plantar fasciosis.
Perhaps the most important message emerging from the research is that heel pain is frequently multifactorial. Many patients have heel fat pad syndrome together with plantar fasciosis, calcaneal bone marrow oedema or Baxter's nerve entrapment. The best outcomes are therefore achieved when clinicians identify every clinically significant pain generator and develop an individualised treatment programme rather than assuming a single diagnosis explains all symptoms.
Although further research is needed, current evidence supports a practical approach based on accurate diagnosis, mechanical protection of the heel, appropriate footwear, rehabilitation and management of contributing biomechanical factors. This approach remains more strongly supported than relying on any isolated procedure or intervention.