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Expert Insights On Therapies For Plantar Fat Pad Atrophy

Joseph Vella, DPM, and Stephen Schleicher, MD
June 2015

Given the potential of plantar fat pad atrophy to cause significant pain and adverse effects on function, particularly in patients with diabetes, these authors discuss keys to making an accurate diagnosis and outline current treatment options.

Our feet endure a lifetime of use and, at times, abuse. In 75 years, the human foot traverses over 100,000 miles.1 One consequence of this excess “mileage” is atrophy of the plantar fat pad, a common complaint that can cause significant pain and disability. Yi and colleagues documented that fat pad atrophy is the second most common cause of heel pain following plantar fasciitis.2 Associated with various conditions such as diabetes, rheumatoid arthritis, trauma, chronic steroid use and old age, fat pad atrophy results from atrophy of adipose tissue along with degeneration of the collagenous septae that impart resiliency.

Despite fat pad atrophy being a common complaint within the podiatric population, treatment is often difficult and may result in pain and limitation.

Treatment for the most part has concentrated on offloading the involved area via padding, inserts, corrective osteotomies and resections. For this article, we will take a closer look at augmentation of the fat pad via liquid silicone injections, autolipotransplantation and other supplemental graft materials.

The main function of the plantar fat pad is to protect the underlying structures (neurovascular tissues, sensitive periosteum, ligaments and tendons) from undue pressure and shocks. Various authors have studied and described the specialized anatomy of the plantar fat pad, a “honeycomb” structure with fat globules completely enclosed by fibroelastic septae.3-7 These septae connect to the skin, superficial fascia and underlying periosteum, and help prevent deformation, compression and displacement of the fat globules in the compartments. They do not normally allow fluid or fat leaks, keeping the shock absorbing fat globules in place over the sensitive structures beneath.

Pertinent Insights On The Pathophysiology And Etiology Of Plantar Fat Pad Atrophy

How does the plantar fat pad fail? The general consensus is that atrophy of the fat cells combined with degeneration of the septae cause loss of overall volume and displacement, thus exposing the sensitive underlying structures to increased stress.2-5,8-10 This process is associated with multiple factors including increasing age, diabetes, neuropathy, rheumatoid arthritis, vascular disease, collagen disorders, corticosteroid use, trauma and orthopedic deformities such as hammertoes.2,4-8,10-14 Clinicians have reported cases of plantar fat pad atrophy secondary to steroid injections for a neuroma.15

One of the most significant associations of fat pad atrophy is increasing age. Commenting on fat pad atrophy in the aging foot, Hsu and colleagues stated that “the most obvious abnormality in the senescent heel is the presence of more numerous, thicker and considerably fragmented elastic fibers.”8 They also noted “a gradual loss of collagen, a decrease in the elastic fibrous tissue and a decrease in water content occur in aging pads.”8 Their study compared the heel pads of younger (age 18-36) to older (age 62-78) patients with ultrasound in regard to unloaded heel pad thickness (UHPT), compressibility, stiffness and shock absorbency. While unloaded heel pad thickness was significantly increased in the elderly — a result they attributed to greater BMI in the older population — the senescent fat pad was less compressible with decreased shock absorbency. The stiffness was also increased in elderly fat pads, albeit insignificantly.8

The association of diabetes with fat pad atrophy is controversial. The literature is equivocal with some articles claiming no link and others demonstrating a clear association.10,14,16-18 Regardless of whether diabetes itself is a contributing factor to fat pad atrophy, the condition can lead to serious consequences (such as ulceration and resulting infection)in a patient with diabetes. Indeed, Gooding and coworkers found via sonography that patients with diabetic ulceration (or a history of ulceration) had significantly thinner heel pads than patients with diabetes without ulceration.19 Avoiding or treating fat pad atrophy in patients with diabetes may decrease the risk of ulceration and other untoward consequences.

Essential Diagnostic Tips

The diagnosis of fat pad atrophy is usually a clinical one with thinning of the fat pad and resulting underlying prominences easily palpated. Yi and coworkers discussed the clinical diagnosis of plantar heel fat pad atrophy and how to differentiate it from other causes of heel pain, such as plantar fasciitis. They found that people with plantar heel fat pad atrophy presented with bilateral centralized heel pain (as opposed to unilateral medial tubercle pain) that occurred after prolonged standing or walking, and at rest. Plantar fasciitis, on the other hand, was more associated with unilateral medial calcaneal tubercle pain and post-static dyskinesia.2

Even though fat pad atrophy is mostly a clinical diagnosis, imaging can at times be useful. Yi and colleagues discussed the clinical aspects of fat pad atrophy diagnosis and were able to diagnose it by ultrasound if the fat pad was less than 3 millimeters, a factor which helped in differentiating fat pad atrophy from other causes of heel pain.2 Turgut and coworkers utilized plain radiography and the “visual compressibility index” to diagnose fat pad atrophy. They compared loaded heel pad thickness to unloaded heel pad thickness and found that in the normal patient, the former is approximately half of the latter.7 For the diagnosis of fat pad atrophy, clinicians have used other imaging modalities as well, including computed tomography, magnetic resonance imaging and even ambulatory pressure pads.3

Current And Emerging Treatment Concepts

Currently, the treatment for fat pad atrophy consists mainly of offloading and cushioning via padding, shoe inserts and modifications. These are particularly important in neuropathic patients. However, frequently patients only get minimal relief or experience recurrent ulceration. One may attempt additional offloading surgically via osteotomies or resections. Alternative options are available should fat pad atrophy persist and for candidates unsuited for osteotomies or resections although the evidence supporting these treatment modalities is limited.

An obvious response to loss of fat in the plantar fat pad is to replace it. Fortunately, extra adipose tissue is usually not difficult to obtain. Chairman retrospectively interviewed 50 patients in whom he had augmented the plantar fat pad via “autolipotransplantation,” a procedure involving harvested adipose tissue from the calf, ankle or abdomen of the same patient.20 This procedure was done concurrently with other pedal procedures such as bunionectomies, neuroma excisions, and metatarsal osteotomies. All 50 patients reported less or no callus formation, 48 felt more padding on the foot, and only one patient required a second transplantation postoperatively. No one experienced pain at the host site postoperatively and only one person had pain for 48 hours at the donor site. Two years after surgery, 96 percent of patients had relief and retention of the plantar fat pad.

Others have used similar tactics but with different graft materials. For example, Rocchio reported on a procedure called the “parachute technique,” in which he augmented the fat pad with a regenerative dermal tissue matrix after performing concurrent procedures such as metatarsal osteotomies or condylectomies in 25 patients.13 Overall, there was a 95.8 percent satisfaction rate with most patients reporting 80 to 100 percent pain relief at their final postoperative visit. All patients with an ulceration at the time of surgery healed with no recurrence. Although only a few patients had an ultrasound in the past six months, those that did retained 90 percent of the thickness of the graft.

One of the most interesting (and controversial) methods of treating fat pad atrophy is via liquid silicone injections. Much of the literature on this subject comes from a single institution but the results seem promising. Balkin reported on 1,585 patients that had received 25,000 silicone injections over 40 years.1,21-22 He noted that 60 to 80 percent of patients experienced moderate to complete pain relief and elimination of calluses. He had the most success with digital corns and calluses although a significant percentage of plantar calluses responded as well. Balkin also noted that 79 percent of plantar ulcers and 100 percent of digital ulcers did not return after patients resumed normal shoe gear wear. He documented minimal complications that consisted mostly of asymptomatic fluid migration in earlier patients but he attributed this to inexperience with the amount injected in earlier patients.

Others have also had success with silicone injections, particularly in the treatment and prevention of plantar foot ulcerations. Van Schie and coworkers published two studies measuring plantar tissue thickness and peak plantar pressures in people with diabetes and pre-ulcerative calluses after injecting small amounts of liquid silicone.23,24 They found a significant increase in plantar tissue thickness and a significant decrease in peak plantar pressures with an insignificant trend in callus reduction that persisted for months to years without significant complications.

However, not all have had success with liquid silicone injections. Tollafield and colleagues injected 45 lesions in 31 patients with either liquid silicone or saline, and found no significant difference in pain between the two.25 Additionally, the safety of silicone injections is somewhat questionable and well documented complications include inflammatory responses, foreign body reactions, host rejection, migration locally or to lymph nodes, and potential for carcinogenesis.26 These complications have mostly occurred with silicone breast implants and many have attributed their occurrence to larger amounts used and impurities in the silicone.1,21,26-27

Despite adverse events associated with silicone breast implants, multiple studies have demonstrated the safety of injecting small amounts of silicone.1,21-25,27-29 Balkin, Wallace and colleagues performed a histology on 148 silicone injected specimens — some having been injected as long as 38 years prior — and found no substantial host response other than stable fibrous tissue formation.29 Fifteen percent of lymph nodes were positive for a small amount of silicone but there was no associated lymphadenopathy. Zappi and coworkers confirmed the safety of small amounts of injectable silicone and stated that “LIS (liquid injectable silicone) remains in the target areas in 100 percent of the cases years after its administration without eliciting any significant adverse reactions. ... LIS, if used appropriately, is a precise and valuable filler for tissue augmentation … “28 Clearly, further research in this area is needed but such therapy is promising.

The future will probably bring new and improved treatments for fat pad atrophy as well. For instance, some dermal fillers used to reduce facial wrinkles and defects stimulate collagen production as part of their therapeutic effect.30 These fillers have the potential to rebuild fragmented collagen in the plantar fat pad, thus providing increased volume for shock absorption and decreased pain. Studies utilizing these agents are ongoing in the United States.

In Conclusion

Plantar fat pad atrophy is a significant cause of pain and limitation of function, particularly in the elderly. In the patient with diabetic neuropathy, it can have catastrophic consequences. While the diagnosis is usually straightforward, treatment can be difficult. Several therapeutic modalities have demonstrated varying degrees of efficacy. Other potential treatments are in clinical trials and will hopefully add to our therapeutic options.

Dr. Vella is a Podiatric Dermatology Fellow with St. Luke’s University Health Network in Allentown, PA.

Dr. Schleicher is an Associate Professor of Medicine at the Commonwealth Medical College, an Adjunct Assistant Professor of Dermatology at the University of Pennsylvania Medical College, and a Clinical Instructor of Dermatology at King's College. Dr. Schleicher founded the DermDOX Center for Teledermatology and is on the staff of Reading Dermatology Associates. He currently supervises the only podiatry-dermatology fellowship in the United States under the aegis of the American Podiatric Medical Association and St. Luke's University Health Network.

References

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19. Gooding GA, Stess RM, Graf PM, et al. Sonography of the sole of the foot: evidence for loss of fat pad thickness in diabetics and its relationship to ulceration of the foot. Invest Radiol. 1996;21(1):45-48.

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29. Wallace WD, Balkin SW, Kaplan L, Nelson S. The histologic host response to liquid silicone injections for prevention of pressure-related ulcers of the foot. J Am Podiatr Med Assoc. 2004;94(6):550-557.

30. Yutskovskaya Y, Kogan E, Leshunov E. A randomized, split-face, histomorphologic study comparing a volumetric calcium hydroxylapatite and a hyaluronic acid-based dermal filler. J Drugs Dermatol. 2014;13(9):1047-1052.

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