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A Closer Look At Soft Tissue Augmentation With Dermal Fillers

Could dermal fillers have an impact on the plantar surface of the foot? With this in mind, this author discusses potential complications with loss or atrophy of the plantar fat pad, and reviews the properties and potential of dermal filler products.

Soft tissue filler treatments have revolutionized the practice of aesthetic medicine. Physicians performed over 2.3 million filler procedures (mostly facial) in the United States in 2014.1 For these procedures, 78 percent used hyaluronic acid (HA)-based injections, 11 percent used calcium hydroxyapatite/carboxymethyl cellulose (CaHA/CMC) fillers and the remaining 11 percent used other materials (e.g., poly-L-lactic acid).1  

Usually aesthetics deals with how you look and not how you feel. However, in the podiatric world, painful feet can affect your happiness, ability to work at a job, shoe selection, job performance, financial status, quality of life, ability to walk, stability, fall probability and weight loss results.

In some patients with insensate feet, such as patients with diabetes, the loss of soft tissue padding on the plantar aspect of the feet can have more dire consequences with the development of ulceration that may lead to amputation. While it is necessary for these patients to wear shoes with proper inserts to help recreate the needed padding, we also know patients do not always wear the special shoes and are sometimes unable to get the shoes due to cost or insurance. Coupled with a loss of sensation are mechanical abnormalities such as flat feet and cavus feet, which may increase the pressure in different areas.

What You Should Know About The Plantar Fat Pad

The plantar fat pad is a specific tissue made up of adipose chambers enveloped by fibrous septa. Aging, pathology or trauma may affect the plantar fat pad’s histomorphological configuration and mechanical response.2 Hsu and colleagues have called these adipose chambers of the heel the superficial microchamber and the deep macrochamber of adipose tissue.3 The deep macrochamber layer responds to loading with large deformation and the microchamber layer has a high degree of tissue stiffness. Decreased microchamber stiffness may cause diminished cushioning capacities in the heels of patients with diabetes and older people.4 The main function of the fat pad is to protect the underlying structures from pressure and shock.5

Disruption of the body’s plantar fat pad can occur due to fat pad atrophy secondary to age, abnormal biomechanics, sports, steroid use, diabetes, rheumatoid issues or collagen vascular disease.

In addition to the actual anatomy of the fat pad, the foot type may determine the area of pain. In pes cavus, we know the medial longitudinal arch elevation reduces the contact surface area and increases the corresponding plantar pressure measurements. This poor distribution of loads may produce associated pathology and pain in the area under the metatarsal heads.6

Much of the research on the plantar fat pad anatomy focuses on patients with diabetes in order to understand the causes of foot ulcers. One study showed a substantial decrease in intrinsic foot muscles and plantar tissue thickness under the metatarsals in patients with type 2 diabetes in comparison to people without diabetes.7 The authors also showed that structural changes appear in the foot before peripheral neuropathy develops so trauma to the fat pad may give rise to neuropathy. The prior speculation was that neuropathy leads to trauma.

Just like the face with its different anatomical features, the heel fat pad is different from the metatarsal fat pad. Heel fat pad atrophy in patients with diabetes in theory results in an irregular arrangement of collagen fibrils within the septal walls as well as diminishing adipocyte size due to thickened septal walls while distal fat pad migration from under the metatarsal heads renders the metatarsal heads vulnerable to increased pressure.8

Cheung and colleagues state that magnetic resonance elastography (MRE) can image the intrinsic elastic properties of tissues.9 The authors have found plantar fat pads in patients with diabetes “feel” different on palpation than those of healthy people and it is due to changes in the elastic properties of fat pads. An MRE may have the potential to document early changes in the mechanical environment of the diabetic foot and provide a noninvasive means to monitor the progression of diabetic foot disease.

Another disease in which there is a loss of fat padding is rheumatoid arthritis. In one study, the heels of patients with rheumatoid arthritis demonstrated a significant change in the composition of saturated fatty acids in comparison with the heels of people without rheumatoid arthritis.10 This composition reflects an increased fat viscosity, which decreases the ability of the heel to absorb and dissipate the energy. This could cause degeneration of the heel septal system with resulting fat pad atrophy as well as forefoot pad atrophy. Researchers believe the cause of the metatarsal pain is increased joint loading.11 Biomechanical evidence indicates that foot orthotics and specialized footwear may change muscle activation and gait patterns to reduce joint loading, and therefore increase the padding of the foot (with fillers). This is similar to wearing a better shoe or an orthotic for an effective aesthetic/non-surgical intervention.

A New Approach To Utilizing Filler Products

Treatment for pain or lesions such as intractable plantar keratoses on the plantar aspect of the feet is usually with skin debridement, offloading with metatarsal pads or with the use of functional or accommodative orthotics. Presently it is not uncommon to do foot surgery consisting of lesser metatarsal surgery, metatarsal head resections or reconstructive foot surgery on patients with pre-ulcerous lesions or with ulcers in order to prevent or heal the ulcers. One must now consider soft tissue augmentation as a possible treatment.

Silicone was the first injectable material podiatric clinicians used for painful corns and calluses. Researchers noted that the fluid induces a relatively stable soft tissue prosthesis between skin and bone to resolve pain and lesions.12 In an incredible 41-year retrospective study, Balkin reported on 1,585 patients (more than 25,000 injections).12 He found painful corns resolved 60 to 80 percent of the time with silicone and long-term follow-up showed no evidence of adverse side effects as long as physicians used medical fluid silicone.

Balkin introduced this modality into the podiatric world and showed that physicians could easily inject silicone with a 25-gauge needle and a standard syringe.12 Bret Ribotsky, DPM, further advanced the interest in augmentation of pedal soft tissue. He came up with the pedal soft tissue temporary augmentation (PSTTA) technique for pain under the heel as well as metatarsal heads and between the toes. In his lecture on this topic, he cites the work of Balkin as the father of pedal soft tissue augmentation.

Most of us would rather have a noninvasive treatment for a medical condition. We always thought of bone surgery as the top tier treatment for plantar intractable plantar keratoses but now we know that the down time and complications with lesser metatarsal surgery are problematic. We all work and play and do not want any extended down time. Fillers bridge the gap.

How Facial Aesthetics And Fillers Evolved Into A Functional Treatment

Most of the research on fillers is on facial soft tissue augmentation. Clinicians may employ different fillers to successfully address signs of aging by filling soft tissue defects caused by age, scar formation or disease. When utilizing dermal fillers, clinicians aim to achieve the same goal: long-lasting soft tissue augmentation without side effects. Each dermal filler preparation available for patient use has unique compositions and characteristics that impact its proper handling, therapeutic results, potential complications and, ultimately, its ideal use.13

In regard to dermal fillers, physicians originally only used them in the dermis of the skin. But now with the wide array of injectables, physicians often use them in the dermis and below the dermis in the subcutaneous layer as well as the fatty layer.

In the foot there are no lines, wrinkles, folds or furrows as one would see in the face. We just get pain from bones that push on the ground, and bone on bone irritation when there is friction between toes.

A Pertinent Overview Of The Classifications Of Dermal Fillers

Soft tissue fillers can be classified by their duration of effect as temporary, semi-permanent and permanent.
Hyaluronic acid fillers. These are temporary fillers that form a fibrous capsule and induce limited collagen production.

Poly-L-lactic acid and calcium hydroxyapatite. These semi-permanent fillers increase tissue volume by stimulating fibroblasts to make collagen and elastic fibers.

Polymethyl methacrylate. Encapsulation holds this permanent filler in place and provides a scaffold upon which the dermis can recover to its original thickness.

Fillers can also be classified by their immune status and risk of reactions:

Autologous products. These products carry no risk of immune-mediated adverse reactions. However, autologous products require a harvesting procedure followed by processing. This affects convenience and cost.

Allogenic products. These products are readily available but carry the risk of allergic/immune and infectious reactions.

Xenogenic products. These have similar allergic/immune and infectious issues with higher hypersensitivity.

Synthetic agents. These may be mass produced with consistent formulation and have the potential for permanent implantation. At the same time, their permanent foreign body nature can lead to long-term challenges.

Jordan and Stoica also categorize fillers based on the ability of enzymes to metabolize these products.14 Biodegradable fillers include: hyaluronic acid, collagen (bovine, human), poly-L-lactic acid and calcium hydroxyapatite. Non-biodegradable fillers include autologous fat, silicone and polymethyl methacrylate.

A Closer Look At The Rheological Properties Of Dermal Fillers

The physiochemical properties of fillers predict how fillers will perform clinically.15 Viscoelasticity is a property of a filler that exhibits both viscous and elastic behavior when undergoing shear deformation. Purely elastic materials like rubber bands deform up to a certain point under shear stress and recover when the stress is removed. Purely viscous materials like honey keep deforming as long as shear stress is maintained but do not recover afterward.16

There are four main rheological parameters that describe viscoelastic properties: G* (measures overall viscoelastic properties or “hardness”), G’ (measures elastic properties), G” (measures viscous properties), and tan (δ) (measures the ratio between viscous and elastic properties).16

Historically, G’ predicts and describes the lift capacity of a filler, which is essentially the strength of the filler.15 A purely elastic filler would be almost impossible to inject through a needle as it would require an immense force on the plunger to inject it in a nonreversible manner. Similarly, a purely viscous filler would irreversibly deform on stress and would not retain its shape for a significant amount of time even when the stress is removed. For example, when one injects a saline solution (i.e., a material with low viscosity and low elastic property), the correction is short lived because water lacks elasticity.16

Gel hardness (G*) is proportional to the level of cross-linking. Cohesivity characterizes how the filler behaves as a gel after implantation. It mainly relates to the degree of attraction between cross-linked hyaluronic acid units.16
Viscosity is a measure of a filler’s resistance to flow when shear stress is applied. As higher amounts of stress are applied, the viscosity of a filler decreases.

What You Should Know About Allogenic Fillers

Collagen. Collagen is the structural foundation of skin. Collagen-based dermal fillers developed as a logical replacement for this dermal component lost through aging. Collagen products will always have a role in soft tissue augmentation given the strong correlation between high type I collagen levels and youthful skin. Collagen remains the standard against which clinicians measure all other dermal implants. As the saline is absorbed, a network of collagen forms to restore skin contour. Over a period of months, host connective tissue cells grow into the network, giving it the texture and appearance of normal host tissues. The injected collagen material is eventually detected as a foreign substance and degraded by collagenases and inflammatory cells.

Bovine collagen. Bovine collagen was the original non-autologous injectable filler. Zyderm and Zyplast soon followed, but have since been discontinued as newer fillers such as hyaluronic acids were available and offered a more natural, non-animal alternative with no requirement for pre-testing (allergy).

Human collagen. The Food and Drug Administration (FDA) approved CosmoDerm and CosmoPlast but these have since been discontinued due to the availability of newer dermal fillers, which have fewer immune reactions. Human collagen was initially used for the restoration of the lip border and correction of facial wrinkles, acne scars and other soft tissue contour deformities. These products contained purified collagen from human fibroblast cell culture lines.  

Hyaluronic acid. Hyaluronic acid is a major component of the connective tissue matrix in the dermis. It forms the elastoviscous fluid matrix in which collagen and elastin fibers are embedded. Unlike collagen, the chemical structure of hyaluronic acid is uniform throughout living species, thereby decreasing its immunogenicity. The hydrophilic nature of hyaluronic acid attracts and maintains water within the extracellular space, which affects dermal volume and compressibility. Older skin has lower levels of hyaluronic acid than younger skin with a resultant loss of tissue hydration.

Use of hyaluronic acid as a tissue filler lasts only one or two days in its natural state. To increase longevity, a cross-linking process can stabilize native hyaluronic acids. A cross-linked or modified hyaluronan (also called a hylan, Hylans or hyaluronic acid gel) is swollen with water (95 percent of the weight) and has the unique attribute of dynamic viscosity. Under the pressure of injection (high shear rate), the gel can pass through a small gauge needle.17 Upon removal of the shearing force, viscosity increases and a thick gel that is unlikely to migrate develops at the site of tissue implantation.

Four hyaluronan formulations have received FDA approval and are commercially available in the United States. No allergy testing is required.

Restylane (Galderma Laboratories) received FDA approval in December 2003 for moderate to severe facial wrinkles. Restylane is produced from cultures of Streptococcus equine bacterium. The resulting hyaluronic acid chains are chemically stabilized through permanent cross-linking with epoxides.18

Hylaform (Allergan) was FDA approved in April 2004 for facial tissue correction of mild to moderate facial wrinkles and folds. It uses hyaluronic acid derived from the dermis of rooster combs that is chemically cross-linked to increase its viscoelasticity and longevity. It breaks down over a period of months.

Juvederm (Allergan) was introduced for the correction of moderate to severe facial wrinkles and folds and for lip augmentation in adults over the age of 21. This bacterially derived product differs from the other hyaluronic acid products in that it is a homogeneous gel, rather than gel particles, with the potential for increased biocompatibility and duration.

Utilizing Dermal Fillers With Autogenous/Autologous Fat

Autogenous fat is the original filler material. The method involves two steps, fat harvesting and fat injections. Fat harvesting, generally from the abdomen or upper thighs, is an invasive procedure with a potential risk of infection, bruising and scarring.19 In the podiatric world, many of the papers on this subject have been authored by Gusenoff and Gusenoff, who have found that autologous fat grafting (fat transfer) in patients with diabetes and fat pad atrophy lessens pain and improves quality of life.20

In a case study that looked at heel pain due to fat pad atrophy, Gusenoff and Gusenoff injected 12 cc of the patient’s own fat into the microchamber of the heel and this resulted in resolution of pain at the six-month follow-up.21  

Pedal fat atrophy affects 30 percent of patients over the age of 60 and impacts foot function, pain and appearance. Researchers have found that fat grafting for pedal fat pad atrophy in the metatarsal head region had a minimal effect on the thickness of the dermis at one year out.22 However, fat grafting did have a significant impact on pain and function.

Luu and coworkers have used fat grafting to prevent reulceration of diabetic foot ulcers after healing.23 The term “lipofilling” describes the regional fat augmentation process. In one case, researchers injected autologous fat at the level of the styloid process that had residual fat pad atrophy after a previous ulcer had healed. It worked to prevent re-breakdown of the ulcer.23

Others have used autologous lipotransfer (fat grafting, lipofilling) to heal chronic diabetic foot wounds. In another study by Stasch and coworkers, autologous lipotransfer healed 88 percent of chronic wounds.24  

Assessing Other Dermal Filler Options

Allograft adipose matrix. Renuva (MTF Biologics) is comprised of dehydrated adipose tissue and is intended for the replacement of damaged or inadequate integumental adipose tissue matrix. It is known as a small volume fat transfer, which is currently in use for facial, breast and hand atrophy. Shahin and colleagues detail the use of this material for resolution of chronic diabetic foot ulcers.25 Whether one can use this product for fat pad atrophy/healing of foot wounds is unknown at this point. It is available for purchase to all clinicians including podiatrists as I have inquired about this but for now it appears as if it is for off-label use.

Poly-L-lactic acid. Sculptra (Galderma Laboratories) is injectable poly-L-lactic acid. It was FDA approved for correction of the signs of facial lipoatrophy associated with HIV infection. Physicians use it off-label in the U.S. for cosmetic soft tissue augmentation. Poly-L-lactic acid is a synthetic polymer of the alpha-hydroxy acid family. Products derived from this family of polymers have been in use for over 20 years and include absorbable sutures (Vicryl). The poly-L-lactic acid in Sculptra is of synthetic, non-animal origin so allergy testing is not required. Sculptra is available as 150 mg of injectable poly-L-lactic acid, which is supplied as a lyophilized powder that one can reconstitute with 3–5 mL of sterile water for injection. Clinicians can add lidocaine during reconstitution to decrease the pain of injection.

Calcium hydroxyapatite. Radiesse (Merz Aesthetics), formerly known as Radiance or Radiance FN, is FDA approved for oral/maxillofacial defects, vocal cord insufficiency, and to smooth moderate-to-severe facial wrinkles and folds, such as nasolabial folds and to correct volume loss in the back of the hands. Its primary component is calcium hydroxyapatite. Hydroxyapatite is the mineral component of bone so its biocompatibility is excellent and no allergy testing is required.

Since Radiesse has calcium in it, it may be visible on X-ray as well as on ultrasound. Not only can one see the material after placing it, the physician can use these imaging tools to monitor the soft tissue thickness over time. For every positive effect, there is a negative effect. The radiological impact of the use of calcium hydroxyapatite dermal fillers is the potential cause of false positives when doing a study in the injected area.26

The product is highly viscous but one can inject it with a 27-guage needle. However, if one anesthetizes the area prior to injection, one can use a 22-gauge needle and the product flows more easily. Many clinicians inject without prior anesthesia. With its high level of viscoelasticity, calcium hydroxyapatite is well suited for supraperiosteal, subdermal and deep dermal placement. The in situ addition of lidocaine results in significant pain reduction without compromising aesthetic improvement.27

Digital massage to contour the product after injection is also important. Over a period of many months to years, the hydroxyapatite particles will ultimately degrade to calcium and phosphate ions. Radiographic evidence of implant material persists for at least six years with no evidence of calcification or bone formation.

Injectable liquid silicone. Silicone is FDA-approved for use in ophthalmology, but is used in an “off-label” manner for soft tissue augmentation and the correction of scars. Silicone can exist as solids (elastomers), gels, foams and liquids, depending on the degree of polymerization. Medical-grade silicone is an inert, clear, oily liquid derived from silica and composed of polydimethylsiloxane polymer. Pure liquid silicone has been in use for soft tissue augmentation worldwide for at least 50 years. Researchers have found injected silicone fluid to be safe and effective as a facial dermal filler as well as a soft tissue substitute.12

Avoiding Filler Migration And Other Complications

We can think of soft tissue fillers as foreign bodies and they therefore have the potential for a host of complications, both immediately and months and years later. In the face (again there is no data for use in plantar fat pad), the reactions may include: nodules and lumps from uneven distribution of the injection, needle marks, erythema, swelling, inflammation, pain, itching, bruising, bluish discoloration, herpetic outbreaks, and localized infection.14 There have been accounts of allergic skin reactions, anaphylaxis, migration, scarring, skin necrosis, retinal artery occlusion and paralysis of the upper lip, face and forehead.14

The majority of the late-onset adverse effects are inflammatory and immune-mediated in nature. Edema, granulomas, sarcoid-like disorders and panniculitis are the most common findings.28

Filler injection is essentially a blind procedure in which we cannot see exactly where we are placing the material unless one is using calcium hydroxyapatite under guided ultrasound.

Let us review the pathogenesis of filler migration to be aware of the many different ways a filler can travel to another site:

1. Poor injection technique
2. High volume of filler injected
3. Filler injected under pressure
4. Overzealous massage after injection
5. Pressure-induced displacement
6. Lymphatic spread
7. Intravascular injection

Injection necrosis is one of the most severe complications of dermal fillers and is related to vascular disruption due to intravascular injection or compression of vessels in the area. In cases of intravascular injection, immediate blanching and severe pain occur. Studies have reported rare cases of intra-arterial embolization.29   

Key Considerations With Patient Selection

Soft tissue augmentation is an elective procedure and not all those seeking treatment may be suitable candidates on medical grounds. In a 2015 consensus paper, DeBoulle and Heydenrych reviewed a list of preexisting conditions that may pose problems with using dermal fillers.30 I should state that most all of the papers on dermal fillers in regard to complications, prevention, assessment and treatment are focused on the facial area. A smaller subset of articles on dermal fillers focus on the hand and no papers at this time reference the foot.

DeBoulle and Heydenrych divide complications into: skin related factors and systemic factors.30 Do not use fillers for patients with multiple or severe allergies and those with a history of anaphylaxis. The authors note that infections in and adjacent to the region to be treated can be exacerbated, and lead to complications since the infecting organism may populate the site of the filler use. These conditions include the following: viral conditions such as herpes simplex virus (HSV) and human papilloma virus (HPV), molluscum contagiosum, bacterial infections such as staphylococci and streptococci, impetigo, and fungal or yeast infections.

While dermatitis may not be present on the plantar aspect of the skin, the clinician would want to make note if the patient has active inflammatory dermatitis if he or she is injecting corns on toes or injecting the dorsum of the foot for foot atrophy.

Dermal filler treatment may aggravate general skin conditions such as prominent scars, hypertrophic scarring and keloids. Fillers may also aggravate bullous disease, pyoderma, systemic lupus erythematosus, Marfan syndrome, Ehlers-Danlos syndrome, mixed connective tissue disease, lichen planus and psoriasis.

There is no established association between the use of fillers and autoimmune conditions. Thus, one may use fillers for patients with HIV, rheumatoid arthritis, diabetes, or scleroderma.

Case by case evaluation is necessary when considering patients with tuberculosis, transplant patients or those with inflammatory bowel disease, food intolerance, repetitive urinary infections, or impaired renal, thyroid, or hepatic function.31

Patients with disorders of hemostasis including coagulopathies, protein C deficiency, hemophilia and hemoglobin disorders need a careful assessment.

Advise patients to stop anti-inflammatory and anti-platelet agents one week prior to treatment with a dermal filler. Patients with cardiovascular stents or those taking anticoagulants for the long term need to understand the risks.

In Conclusion

The use of dermal fillers in the podiatric practice is becoming more popular as patients and doctors seek out less invasive treatments for foot pain, intractable plantar keratoses and ulcer prevention. This article provides basis for the practitioner to understand the properties of the fillers, used off-label in order to achieve positive results.

Dr. Morse is the scientific coordinator for the Dermfoot Seminar. He is board-certified by the American Board of Podiatric Orthopedics and Primary Podiatric Medicine as well as the American Board of Podiatric Surgery.

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2.     Fontanella CG, Nalesso F, Carniel EL, Natali AN. Biomechanical behavior of plantar fat pad in healthy and degenerative foot conditions. Med Biol Engin Computing. 2016; 54(4):653-61.
3.     Hsu CC, Tsai WC, Wang CL, et al. Microchambers and macrochambers in heel pads: are they functionally different? J Appl Physiol. 2007; 102(6):2227-31.
4.     Hsu CC, Tsai WC, Hsiao TY, et al. Diabetic effects on microchambers and macrochambers tissue properties in human heel pads. Clinical Biomechanics. 2009; 24(8):682-6.
5.     Vella J, Schleicher S. Expert insights on therapies for plantar fat pad atrophy. Podiatry Today. Available at . Published June 2015.
6.     Fernandez-Seguin LM, Diaz Mancha JA, Sanchez Rodriguez R, et al. Comparison of plantar pressures and contact area between normal and cavus foot. Gait Posture. 2014; 39(2):789-92.
7.     Kumar CG, Rajagopal KV, Hande HM, Maiya AG, Mayya SS. Intrinsic foot muscle and plantar tissue changes in type 2 diabetes mellitus. J Diabetes. 2015; 7(6):850-7.
8.     Dalal S, Widgerow AD, Evans GR. The plantar fat pad and the diabetic foot--a review. Int Wound J. 2015; 12(6):636-40.
9.     Cheung YY, Doyley M, Miller TB, et al. Magnetic resonance elastography of the plantar fat pads: Preliminary study in diabetic patients and asymptomatic volunteers. J Computer Assisted Tomography. 2006; 30(2):321-6.
10.     Resnick RB, Hudgins LC, Buschmann WR, et al. Analysis of the heel pad fat in rheumatoid arthritis. Foot Ankle Int. 1999; 20(8):481-4.
11.     Riskowski J, Dufour AB, Hannan MT. Arthritis, foot pain and shoe wear: current musculoskeletal research on feet. Curr Opin Rheumatol. 2011; 23(2):148-55.
12.     Balkin SW. Injectable silicone and the foot: a 41-year clinical and histologic history. Dermatol Surg. 2005; 31(11 Pt2):1555–9.
13.     Johl SS, Burgett RA. Dermal filler agents: a practical review. Curr Opin Ophthalmol. 2006; 17(5):471-9.
14.     Jordan DR, Stoica B. Filler migration: a number of mechanisms to consider. Ophthal Plast Reconstr Surg. 2015; 31(4):257–62.
15.     Hee CK, Shumate GT, Narurkar V, et al. Rheological properties and in vivo performance characteristics of soft tissue fillers. Dermatol Surg. 2015; 41(Suppl 1):S373-81.
16.     Pierre S, Liew S, Bernardin A. Basics of dermal filler rheology. Dermatol Surg. 2015; 41(Suppl 1):S120-6.
17.     Fallacara A, Manfredini S, Durini E, Vertuani S. Hyaluronic acid fillers in soft tissue regeneration. Facial Plastic Surgery. 2017; 33(1):87-96.
18.     Carruthers J, Carruthers A, Humphrey S. Introduction to fillers. Plast Reconstr Surg. 2015; 136(5 Suppl):120S-131S.
19.     Kühne U, Imhof M. Treatment of the ageing hand with dermal fillers. J Cutan Aesthet Surg. 2012; 5(3):163–9.
20.     Gusenoff BF, Gusenoff J. Can autologous fat grafting help address fat pad atrophy in patients with diabetes? Podiatry Today. 2016; 29(5):16-22.
21.     Gusenoff BF, Gusenoff J. Key insights on fat grafting for heel fat pad atrophy. Podiatry Today. Available at .
22.     Dreifuss SE, Minteer D, Gesenoff J. Foot rejuvenation with pedal fat grafting: a randomized cross-over clinical trial. Plast Reconstr Surg Glob Open. 2017; 5(4 Suppl):21-22.
23.     Luu CL, Larson E, Rankin TM, et al. Plantar fat grafting and tendon balancing for the diabetic foot ulcer in remission. Plast Reconstr Surg Glob Open. 2016; 4(7):e810.
24.     Stasch T, Hoehne J, Huynh T, et al. Debridement and autologous lipotransfer for chronic ulceration of the diabetic foot and lower limb improves wound healing. Plastic Reconstr Surg. 2015; 136(6):1357-66.
25.     Shahin TB, Vaishnav KV, Watchman M, et al. Tissue augmentation with allograft adipose matrix for the diabetic foot in remission. Plast Reconstr Surg. 2017; 5(10):e1555.
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27.     Rho NK, Chang YY, Chao YY, et al. Consensus recommendations for optimal augmentation of the Asian face with hyaluronic acid and calcium hydroxylapatite fillers. Plast Reconstr Surg. 2015; 136(5):940-56.
28.     Alijotas-Reig J, Fernandez-Figueras MT, Puig L. Inflammatory, immune-mediated adverse reactions related to soft tissue dermal fillers. Semin Arthritis Rheumatism. 2013; 43(2):241-58.
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By Joel Morse, DPM
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