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The Academy of Minimally Invasive Foot and Ankle Surgery Cadaver Seminar

Mar 4 2022 09:18:29 PM

The Academy of Minimally Invasive Foot and Ankle Surgery Cadaver Seminar in Orlando Florida was a huge success this past weekend February 24-26th. Practical examinations were provided for many who strive for MIFAS Board Certification. The ABMSP booth supported the Academy and was well attended, with certification information provided by Association Manager Jenna Ayala, Dr. Neal Vichinsky and Dr Beth Pearce.

Dr TJ Ahn, Dr Rich Cowen and Dr Larry Kales all MIFAS Certified participated as faculty.

Over 85 doctors, exhibitors and world renown faculty from across the globe participated. Many doctors were new to the skill set, while others seasoned with years of experience shared pearls of wisdom and technique.

Among the field of national experts was Dr. TJ Ahn (Chicago) who lectured on shortening the learning curve of MIS Bunion technique, and Dr. Orlando Nunez (Coeur d’alene) who lectured on the Leventen formula for metatarsalgia resolution.

International experts Dr. Carmen Narranjo Ruiz from Spain, taught the decision cascade of hammertoe corrections while orthopedic surgeon Dr. Fernando Sancho Barroso from Mexico City offered insights on Hallux Various correction. The Canadian faculty included both Dr. Sheldon Nadal and Hartley Milchin both sharing their succesful bunionectomy techniques.

An honoring of the late Dr. Earl “Boots” Horowitz with a history of technique was showcased by Dr. Larry Kales (Hudson Tampa).

Dr. Michael Warshaw coding/billing expert, and Larry Koback DPM, Esq rounded out the field to provide legal recommendations for charting.

The power of MIFAS technique with value of board certification in the field was evident throughout the event.

The Academy of Minimally Invasive Foot and Ankle Surgery Cadaver Seminar
Dr. Neal Vichinsky, Dr Beth Pearce and Association Manager Jenna Ayala

Chicago 2021 MIFAS Event

Jul 29 2021 05:08:54 AM


TJ Ahn’s 2021 International MIFAS Cadaver Lab Workshop was yet again, a very impressive event held at the Orthopedic Learning Center in Rosemont, Illinois. Dr. Ahn (MIFAS diplomate # 001) successfully doubled the size of his learning group to nearly 70 participants, and 2 dozen faculty for this event despite the challenges of COVID over the past 18 months. His staff organized a seamless and incredibly successful event.

The legendary Dr. Steve Isham brought his expertise and support to this meeting. Canadian expert and speaker Dr. Hartley Miltchin was able to get a special waiver to attend, while other international speakers, Dr. Naranjo-Ruiz, Dr. Juanto, Dr. Benavides, Dr. Carbone, were “Zoomed” in for their presentations. We are proud that our MIFAS Board certified Diplomates Dr. Timothy Shea and Dr. Larry Kales participated as both speakers and lab faculty.

About two dozen candidates took the MIS practical exam in anticipation of board certification. Both novice and experienced minimally invasive foot and ankle surgeons from the US and around the globe participated to share knowledge, improve skills, and enhance business strategies. Dr. Ahn showcased his Mastermind strategies for doctors to remain financially viable in the rough seas of today’s medical economics.

ABMSP booth of the MIS..
ABMSP booth of the MIS “royalty” that gathered (Center Dr. Beth Pearce).(From left to right) Doctors TJ Ahn, Oscar Benavides (Past President of the Academy), Steve Isham and Borys Markewych.
Outstanding facility
Outstanding facility
International MIFAS CADAVER LAB Workshop, July 16-17, 2021
Dr. Steve Isham
Dr. Steve Isham
Distinguished Authors Series
The opinions expressed here are those of the authors and do not necessarily reflect the positions of the American Board of Multiple Specialties in Podiatry or its Directors.

Concise Review: Cellular Senescence, Receptor Dysfunction, Faulty Wound Healing


Dr. Matthew Regulski, DPM

Chronic wounds are associated with very unique intracellular and extracellular/ ECM interactions both in cellular senescence and in growth factor deficiency but also with receptor dysfunction.
Integrins are the main cellular receptors that mediate cell-ECM interaction and cell-cell mediated interactions. They anchor cells to their surrounding environment and transduce a variety of signals that influence cell behavior. In chronic wounds integrins can be up regulated or down regulated by chronic inflammation in the form of excessive ROS that leads to oxidative stress. There is a deficiency of α5-β1 integrin which is necessary to adhere keratinocytes to fibronectin to stimulate and enhance their migration and proliferation. Also,we see the up-regulation of αV-β6 integrin, which leads to premature and excessive secretion of TGFbeta causing premature senescence of fibroblasts and myofibroblasts. Significant production CCN1 binding to α6-β1 integrin leads to the production of excessive ROS, DNA damage and activation of the cyclin dependent kinase inhibitor p53, the master regulator of senescence. This causes irreversible growth arrest and the senescent phenotype ensues. This receptor dysfunction results in increased senescent cells including fibroblasts, myofibroblasts, and keratinocytes- this will produce an ECM that is corrupt and a wound bed that is inflamed, corrosive and un-responsive. By understanding this process of cellular senescence and thus growth arrest, we should intervene earlier, when the biofilm has been reduced and thus chronic inflammation extinguished, with cell based therapies that will re-capitulate the proliferative phase in order to repair and regenerate before chronicity becomes terminal.

What Factors Can Affect Wound Healing?

In hostile environments that are rife with microbial invaders, human respond to wounding and tissue injury with a vigorous inflammatory response coupled to the rapid synthesis and deposition of the extra cellular matrix, thereby maintaining tissue integrity and providing defense against microbes while the wounded tissue is being repaired and remodeled.

In virtually all organ systems, wound healing occurs similarly in three overlapping but distinct phases; inflammation, ECM deposition and tissue formation, and tissue remodeling (2,3,4). Each of these steps must be tightly regulated for optimal wound healing.

However, excessive ECM deposition may occur in wound repair, particularly in association with chronic injury and inflammation (4,5,6). When excessive non-functional ECM replaces functioning parenchyma, the resulting fibrosis, scarring, and loss of tissue function may lead to severe consequences. Examples being fibrotic scarring in the liver due to viral infections, in the lung from obstructive pulmonary disease, and in the heart following myocardial infarction which can lead to organ failure and death (2).

These types of exaggerated, dysregulated wound healing adversely affect a large number of people worldwide and this can be a tremendous burden on public health.

The vast majority of chronic wounds that fail to heal in a timely fashion fall into one of three categories: pressure ulcers, diabetic ulcers, and venous ulcers (2,7). Although these wounds all have different etiologies, chronic wound development is most often associated with a background pathophysiologic sequence of an ischemia-reperfusion injury with resultant prothrombotic and procoagulant phenotype, biofilm formation which results in a prolonged inflammatory response (8,9,10).

In many cases, healing does not occur despite adequate standard of care (7,10). Failure to re-epithelialize can be a consequence of a number of factors, including prolonged inflammation, an imbalance of regulatory growth factors and cytokines, defective extracellular matrix that fails to support keratinocyte migration, modified fibroblast function, and defective capillary function leading to inadequate tissue oxygenation (11). The ECM of these wounds has been referred to as corrupt or corrosive (11,12), characterized by chronic wound fibroblasts that are unresponsive to growth factors, cytokines, and other signals (13), containing high levels of matrix metalloproteinases (MMPs), neutrophil elastase, serine proteases, cathepsins and lacking of receptors such as integrins which are quite necessary for fibronectin binding and keratinocyte migration (14).

There is vast evidence that has shown chronic wound healing may be related to increased or reduced integrin receptors, production of senescent cells that are unresponsive to growth factors and cytokines, and with changes relating to cell signal or receptor dysfunction (7,11,13-21). Integrins coordinate and translate these effector signals that control cell signaling, proliferation, ECM maturation, and cellular spreading. This is quite germane to the chronic wound state where specific changes in integrin type and receptor sensitivity may trigger the changes in cellular phenotype that contribute to this chronicity (2).

Integrins provide a mechanical connection between matrix components and the cytoskeleton and transduce an astonishing variety of signals, either alone or in collaboration with growth factor receptors or other protein signals (2, 22-26).

They were originally discovered as receptors that anchor cells to their surroundings by concomitantly binding to the cytoskeleton and the ECM. Also, integrins were shown to activate cellular signalling pathways and, in this way, to contribute to the decisions of both cell behavior and fate (22,27). Direct binding to growth factors and regulation of endocytosis and trafficking of growth factors makes integrins even more multifunctional than previously appreciated (17,22).

How Does Senescence Corrode Wound Healing

Traditionally senescent in culture is associated with telomere shorting during repeated cell divisions eventually leading to cell cycle arrest, which is known as replicative senescence (28). In the chronic wound, cellular senescence to a degree is associated with telomere length, but rather this phenotypic cell change is initiated by oxidative stress, ER stress, carbonyl and nitrosative stress, activated oncogenes, repressor proteins, and cyclin-dependent kinase inhibitors (20). In the chronic wound environment, ROS attack DNA, (causing an accumulation of lipofuscin), which is un-degradable by the cell, thus stimulating the DNA Damage Response (DDR) and then DNA damage-induced cell cycle arrest (29).

Fibroblast senescence in chronic wounds is also related to chronic inflammation and molecular dysfunctions(20). When exposed to chronic wound fluid, normal fibroblasts in culture appear to switch to a senescent mode, showing changes in morphology and increase in pro-inflammatory protein synthesis, which is consistent with senescent associated secretory phenotype (SASP) (20). Chronic wound fluid rapidly degrades integrin receptors, exogenous growth factors, decreases the production of cyclin, D1, phosphorylated retinoblastoma protein RB, and increases p21 (30).

The main cell type that contributes to the synthesis and deposition of ECM in healing wounds is the myofibroblast, which expresses alpha smooth muscle actin and promotes wound contraction (6). Myofibroblast can be sourced from a variety of cell lines including differentiation of activated resident fibroblast and recruited fibrocytes, and epithelial and endothelial-mesenchymal transitions of epithelial and endothelial cells respectively (6,7).

Activated myofibroblast will proliferate and initially promote wound repair by producing ECM components, fibrosis may result when wound healing becomes chronic or if the ECM producing activity of myofibroblast continues unchecked.The conversion of fibroblast to myofibroblast plays a significant role in the stimulation of wound contraction and healing by producing ECM constituents to form granulation tissue. Therefore, this system is kept in balance by myofibroblast being driven into senescence at later stages of wound healing, thereby converting these ECM-producing cells into ECM-degrading cells, thus balancing and limiting fibrosis of the wound (28).

Triggering of Myofibroblast Senescence is a Necessary Step in the Genesis of Chronicity

In skin wound healing, myofibroblast senescence is triggered by the dynamically expressed matricellular protein CCN1 (also known as CYR61) through integrin signalling (28). CCN1 is an angiogenic matrix cellular protein of the CCN family. CCN is the acronym of the first three members: CYR61, CTGF, and Nov. CCN1 is normally expressed at a low level in most tissues but becomes highly expressed because of bacterial, viral infections (28,31) or in tissue repair (28,32,33).

The physiology of CCN1 will induce fibroblast senescence through its direct binding to the integrin alpha 6 beta1 and cell-surface heparin sulfate proteoglycans (HSPG) (28). This triggers formation and accumulation of ROS, DNA damage, and p53 activation resulting in these cells being driven into senescence and thus the production of inflammatory proteins that will stimulate the degradation of the ECM.

Through integrin signaling, myofibroblast senescence brings about increased expression of a multitude of pro-inflammatory cytokines/chemokines (e.g. IL-1, IL-6, IL-8, MCP-2, MCP-4, MIP-1a, MIP-3a,) and ECM-degrading enzymes MMPs, which will down regulate expression of certain ECM components (e.g. collagen) (28). Therefore, senescent myofibroblast will accumulate as part of this normal process of tissue repair and function to limit the extent of fibrogenesis associated with wound healing (28, 34).

Also, premature cellular senescence is stimulated by events often present in the evolution of a chronic wound (infection particularly biofilm, corrosive CWF). This results in CCN1 binding to integrin alpha 6- beta 1, ROS stimulation, fibroblast, and then myofibroblast senescence, increased inflammation, and degradation of the ECM.

Therefore, during skin wound healing, recruited fibroblast and differentiated myofibroblasts proliferate and deposit ECM to form the granulation tissue. Myofibroblast will then be driven into senescence at later stages of wound healing, where they cease to proliferate and up regulate the expression of matrix degrading enzymes (MMP2, MMP3, MMP9), concomitant with down regulation of collagen and TGF-beta, thereby exerting anti-fibrotic effects (35).

At this point you can see that the control of fibrogenesis during wound healing is efficient and balanced – the very cells that synthesize ECM in wound healing, the myofibroblasts, are themselves converted to matrix-degrading senescent cells to produce a self-limiting effect. These senescent cells may also promote tissue remodeling and clearance of the myofibroblast during wound maturation (35, 36).

In a clinical presentation, chronic wound bed changes have direct implications on healing. The length of venous leg ulcerations can have a direct correlation with ultimate healing (11). It is apparent that the longer a wound remains open and in the inflammatory phase, the more cellular defects arise and accumulate, therefore becoming less responsive to treatment. Premature senescence with the production of the SASP leads to ongoing ECM degradation. This has been shown to be a contributing factor to chronic wound prevalence (11, 20, 28). Accumulation of greater than 15 percent of senescent fibroblasts has been described as a threshold beyond which wounds become very hard to heal (11). Therefore evidence for this declares that there is a positive relationship between higher levels of fibroblasts with a senescent phenotype that have bee identified in VLU and DFU, will portend for a poor prognosis (11, 37).

While much attention has focused on fibroblast senescence in the chronic wound, other cells have been shown to be affected by cellular senescence formation. Many of the same reasons that cause abnormal changes in the fibroblast also affect keratinocytes and endothelial cells (20). Increases in proteolytic enzymes and chronic inflammation can lead to a gradual loss of endothelial cell function, mimicking replicative senescence in fibroblasts and keratinocytes (20).

Therefore, induction of fibroblast senescence may have a direct effect on the induction of senescence in endothelial cells and keratinocytes. This has been termed “the bystander effect”. This is due to the formation of the SASP that occurs in senescent cells. This phenomena is also found within the cells of our immune system . Macrophages also have been shown to produce significantly less vascular endothelial growth factor (VEGF) when isolated from chronic wound tissue with increased senescence compared to young controls (20).

CCN1, Contributor to Senescence and Chronic Wound Healing

CCN1 protein can directly induce fibroblast senescence, both as a cellular factor and as an immobilized cell adhesion substrate (35).

CCN1 induces fibroblast senescence through its direct binding to integrin alpha 6-beta 1, and cell surface heparin sulfate proteoglycans (HSPG), thereby activating RAC1 and the RAC1-dependent NADPH oxidase 1 to trigger a robust and sustained accumulation of reactive oxygen species (ROS).

Consequently, CCN1 induces a DNA damage response and p53 activation, and triggers the ROS-dependent activation of p38 MAPK, and ERK, which in turn activate p16 INK4A/pRb pathway to induce senescence (35).

Both p53 and p16 INK4A/pRb pathway also contributes to CCN1 induced senescence (38, 39). Cell adhesion to CCN1 induces a much higher and more sustained level of ROS than cell adhesion to other ECM proteins, such as collagen, fibronectin, and laminin, which do not induce senescence. The accumulation of substantial level of ROS sustained for at least 10 hours appears necessary for efficient induction of senescence in fibroblasts (35).

Apart from cellular senescence induction, CCN1 can up regulate plasminogen activator inhibitor-1 (PAI-1) possibly through the activation of p53 (20, 28, 40). Plasminogen activators activate plasminogen to produce plasmin. Plasmin participates in the breakdown of other glycoproteins in the ECM and the activation of MMP’s (28). Chronic wounds are associated with elevated levels of plasmin, collagenases, and other degradative enzymes. Overexpression of PAI-1 is sufficient to drive fibroblast into senescence (20, 28).

As you can see it would appear that there is a dichotomy occurring in the ECM of a chronic wound. Fibroblasts secrete factors that will stimulate matrix degradation, yet they also produce matrix-promoting factors (TGF-beta 1 and PAI-1). PAI-1 and CCN1 may then stimulate the senescent myofibroblast phenotype but will result in ratios of PAI-1 and TGF-beta1 to plasmin that will lead to a degraded and defective ECM (41).

The association between fibroblast senescence and ECM degradation appears to be supported by these changing ratios that will shift the balance towards degradation of the ECM as senescence is propagated (41).

The secretory function of fibroblasts may decrease with senescence, although Herrick et al (42) have shown that chronic wound fibroblast show no decrease in matrix secretion – thus the observed degradation of ECM appears to be possibly related to increases in matrix remodeling enzymes and their proteolytic activity.

Fibroblast Unresponsivness Can Lead to ECM Degradation, The How and Why?

Another reason for the continuance of ECM degradation is its unresponsiveness to the stimulatory action of a multitude of growth factors and cytokines, including TGF-beta, PDGF, and EGF, as well as bFGF (42). Research has shown that VLU fibroblasts have decreased TGF-beta type II receptor expression (13). This was accompanied by failure of ulcer fibroblasts to phosphorylate Smad2, Smad3, and p42/44 mitogen-activated protein kinase, and was associated with a slower proliferative rate in response to TGF-beta (13).

This continues to highlight the possibility that non-healing chronic wounds are associated and related to a decrease in receptor expression and a failure in specific signal transduction pathways (2). Much of the corrosive ECM that is associated with cellular senescence relates to the increased presence of MMPs. In acute wounds, there is a balance between protease activity and ECM deposition encouraged by tissue inhibitors of metalloproteases (TIMPs). The ratio of MMP-9/TIMP-1 in chronic wounds is an important healing measurement parameter (20, 43).

Chronic wound fibroblasts will have decreased capacity to react to a multitude of growth factors and other signaling proteins. This decreased response to bFGF, EGF and PDGF does not appear to be related to a decrease in receptor quantity, but rather a dysfunction in intracellular signalling (42).

The more reasonable approach to changing the degradative ECM wound milieu is wound bed preparation, including sharp debridement to stimulate vascularization and decrease bacterial burden thru reduction of the wound biofilm (9,10,11). Also by removing the senescent cell burden and their SASP this will contribute greatly to this change. Only then can exogenously applied growth factors, cytokines, various stimulatory proteins and biologics can then be expected to exert their stimulatory effect on the surrounding healthy tissue and promote proper and organized wound healing.

Proteolysis by MMPs exposes specific amino acid binding sites on ECM proteins, such as fibronectin, fibrogen, osteopontin, tenascin, and vitronectin. These specific sequences are referred to as the RGD sequence (arginine, glycine, aspartic acid). This is a very well studied and elucidated binding motif that is quite necessary and incredibly critical for facilitating cell surface integrin recognition and attachment of the cell to the ECM protein (44). This then will initiate growth factor and paracrine signaling (44). Chronic wounds are associated with increased inflammation, and copious corrosive wound exudate, with increased proteolysis and degradation of the ECM, which will result in an abnormal wound matrix that induces less growth factor action because of the diminished integrin binding (9, 10, 11, 15, 16, 17, 24, 25, 26, 45, 27, 46, 47).

Aside from increased protease activity, (particularly MMP’s, gelatinases, collagenases, stromelysins), chronic wound edge keratocytes also display growth factor – ECM receptor dysfunction, which fails to convert them into a migratory phenotype because their intregrin receptors which are necessary for their locomotion and therefore their movement, are degraded by the chronic inflammation (2, 48). In chronic wounds, VEGF wound fluid levels were also significantly higher in non-healing VLU ‘s than in normal wounds despite excessive degradation of VGEF by plasmin (48, 49).

However, the VGEF inhibitor, soluble VEGFR-1, was increased fourfold in wound fluids of chronic VLU’s compared with wound fluids from acute excisional wounds on the lower leg (48).

Thus, it is more than likely that abnormal ECM composition which fails to activate adhesion receptors on fibroblasts, thus preventing their binding to the ECM, which is a prerequisite for maximal growth factor stimulation, responsiveness, migration, and proliferation (48, 15, 18).


Wound chronicity is a timely process. The typical biochemical abnormalities described in this review occur over time and the resulting wound milieu often renders the wound non-responsive to most treatments. We must find a way to have early focus and target the Biofilm mass causing subsequent chronic inflammation that leads to cellular senescence and receptor dysfunction in the wound milieu so that we can change the course of this chronicity. This will be very relevant for patients that have chronic wounds with multiple co-morbidities that slow the healing process. Patients with diabetic, venous, or pressure ulcers often do not respond adequately to several weeks of standard care due to multiple pathogens, biochemical and molecular dysfunctions.

Because of the consequences of the biofilm mass, defective degraded ECM, cellular senescence with growth factor/cytokine/chemokine dysfunctional signalling, we must find strategies that aim to repair and regenerate the entire wound healing paradigm so that it will be beneficial to these high risk groups to reduce their morbidity and mortality.

As it has been noted previously, topically applied growth factors have been tested extensively in chronic wounds with very mixed results (50, 51, 52, 53). It has been postulated that topical application of these agents in the corrosive environment of the chronic wound bed are rapidly degraded by these destructive proteases (9, 54).

Therefore, a plausible explanation for the relative lack of success of growth factors in the treatment of chronic wounds may reside in the phenotypic abnormalities of wound cells and their relative unresponsiveness to stimulatory signals.

The keys to understanding the pathogenesis of chronic wounds in all age-related wound defects, as well as age-related diseases and tissue dysfunction, is identifying cellular receptors that mediate the responses of the epidermis to provisional wound matrix and determining how these changes in the receptors contribute to impaired wound healing through cellular senescence. Integrins are the major cell surface receptors for cell adhesion and migration (15, 16, 17), and many cell lines, including epidermal keratinocytes, fibroblasts, and endothelial cells express several integrins that bind ECM proteins in this provisional wound matrix (28, 29, 50).

As we can see, chronic wound healing is a complicated and fascinating series of molecular pertubations, which occur at the most basic of structural, biochemical, and molecular levels. Cellular senescence is a state of irreversible growth arrest but with metabolically active cells that secrete pro-inflammatory cytokines, proteases, chemokines growth factors, and many other proteins that can have a negative effect upon wound healing. This inflammatory repertoire is termed the senescence associated secretory phenotype (SASP). In this review, I have shown that cellular senescence can be triggered by receptor dysfunction, oxidative stress, chronic inflammation, DNA damage, as well as oncogene activation and telomere shortening. Cellular senescence underlies a vast majority of age-related chronic diseases including diabetes, chronic wound healing, and atherosclerosis. We encounter these pathologies every day in our wound patients.

Therefore, would it not make sense that in order to repair dysfunctional and degraded ECM, paracrine protein dysfunction, and non –proliferative cellular dysfunction, should we be looking at adding robust, young, healthy cell lines into this wound milieu to extinguish the chronic inflammation, and replace the senescent and thus non-proliferative cells? Applying young cellular constructs that are not fettered or molested by age, senescence or chronic inflammatory disease processes, might provide a better platform or scaffolding for enhanced proliferation and epithelialization. As physicians, clinicians, scientists, we must learn and understand these dysfunctions in order to avail ourselves of the proper therapies and paradigms to correct these abnormalities. I believe by adding robust cellular constructs that will coordinate the proper cell signalling pathways, secretory pathways, proper scaffolding arrangements and proper protein profiles, we will be able to change the chronic wound environment in order to re-establish a proliferative and proper wound healing trajectory.


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Author Biography

Dr. Matthew Regulski, DPM

Dr. Regulski is a Graduate of Temple University School of Medicine, where he graduated Summa Cum Laude. He performed his residency at the Main Line Health System in Philadelphia, PA, and is currently the Medical Director of the Wound Care Institute of Ocean County, LLC. Dr. Regulski is also Co-Director of The Center for Wound Healing & Hyperbaric Medicine at Community Medical Center and is involved at the Wound Care Center at the Kimball Institute. He has been the principal investigator for multiple clinical trials for wound healing, diabetic foot, and venous leg ulcers, and has authored several peer-reviewed articles for the treatment of chronic wound healing and limb-salvage surgery.

Dr. Regulski is currently on the Board of Directors of the Federation of International Podiatry and is the Scientific Chairman for the Federation of International Podiatry. He is also the Communications Director for the Foot Working Group of the American Diabetes Association. Dr. Regulski is a wound care certified physician and fellow of both the Academy of Physicians in Wound Healing and the American Professional Wound Care Association. He is also a National Delegate for the Association for the Advancement of Wound Care and is a member of the Wound Healing Society. An International and National lecturer of wound healing and limb-salvage surgery, Dr. Regulski has multiple certifications in wound healing, diabetic wounds, and limb-salvage surgery.

Dr. Matthew Regulski is a fellow faculty member at the Royal College of Physicians and Surgeons of Glasgow, Scotland.

Champions Blog

The Birth of Podiatric Sports Medicine: The Academy and Now Board Certification

A number of important figures present and past have made possible the new podiatric sports medicine certification.


The long-awaited board certification in podiatric sports medicine is now available to all doctors who want a valuable credential allowing them to declare that they are a qualified podiatric specialist in sports medicine. It has been a long and interesting journey involving two unique organizations and a host of talented individuals. Here is the full story… highlighting those whose contributions made it possible.

The 1970’s brought about the birth of podiatric sports medicine. The impetus for most of the interest in sports medicine by podiatrists back then arose out of the running boom and the development of the American Association of Podiatric Sports Medicine. Doctors George Sheehan, Robert Barnes, George Pagliano, Richard Gilbert and Steven Subotnik brought the role of the podiatrist in sports medicine to national attention.

The momentum they created has not stopped; and now the field is in full bloom where physicians such as Dr. Jeff Ross merges his expertise in diabetic foot medicine and surgery with biomechanics and sports medicine, culminating in an efficacious bridging of podiatry with collegiate and high-school sports. Dr. Ross served as team podiatric physician for the Baylor University football team and is a consultant for the University of Houston track team, while also playing an active role in high school sports. Adding to his credentials and fueled by his intense love for skiing, his in-depth research defined its biomechanics. His incredible passion was a driving force that propelled podiatric sports medicine to the pinnacle of recognition and the establishment of the highly anticipated board certification by the American Board of Multiple Specialties in Podiatry (ABMSP).

“Dr. Richard Gilbert, podiatrist to the San Diego Chargers, was a pioneer in the development of the AAPSM.”

The Trailblazers
The idea of a board certification in podiatric sports medicine was initially seeded by the esteemed Dr. Richard Gilbert (Figure 1), pioneer in the development of the American Academy of Podiatric Sports Medicine (AAPSM) and podiatrist to the San Diego Chargers. His powerful motivation was to unite the various avenues of podiatric medicine and surgery through an amalgamation of talents vital to forming a complete spectrum of podiatric sports medicine expertise, where trained DPMs could interchange ideas and knowledge with seasoned professionals.
Arguably, the first podiatric sports medicine celebrity was Dr. Steve Subotnik, an athlete himself who was featured in Runner’s World.

Figure 1: Richard Gilbert, DPM, The Father of Podiatric Sports Medicine

Magazine and author of The Running Foot Doctor (Figure 2). Because of his groundbreaking work in surgery, biomechanics and sports medicine, Dr. Subotnik was possibly the single most influential force in putting podiatry on the map. He cut his “sports medicine teeth” as a professor at the California College of Podiatric Medicine where he taught surgery and biomechanics. This period of his 50-plus year career was especially gratifying to him, particularly when established doctors, who were students of his in those fledgling years, came up to him at meetings and told him what an impact he had on their career.

Dr Subotnik’s sports medicine career rocketed when he became a marathon runner, and his intense involvement and resulting contributions brought the podiatry profession new recognition and acceptance. His notable cabal included health-related celebrities such as Dr. George Sheehan, a cardiologist who became the legendary philosopher of the recreational running movement in the 1970’s and 1980’s.

For years, Dr.Subotnik, one of the founding fathers of the American Academy of Podiatric Sports Medicine, felt that board certification in podiatric sports medicine would take this specialty to the next level, as it separates the spectators from the players. His commitment to board certification was key to the formation of the new certification by The ABMSP. Dr. Subotnik states: “Sports medicine helps define modern podiatry because biomechanics is the defining factor in podiatry and is also an integral part of sports medicine. The podiatric practice of sports medicine is so important, now more than ever, because it will continue to keep podiatry on the map; because through biomechanics we can make a real difference.” He goes on to say, “Once you’re an athlete who sustains a foot injury, and being active is part of your life, you will seek the help of a sports medicine podiatrist at any cost, regardless of any bureaucratic or insurance limitations.”
His driving philosophy summarizes the importance of the foot and its biomechanics: “Controlling the feet controls the rest of the body”, which is philosophically apropos coming from this champion podiatric sports physician.

“Arguably, the first podiatric sports medicine celebrity was Dr. Steve Subotnik, an athlete himself.”

The Protégés
From these trailblazers came their protégés who turned out to be the innovative architects of modern podiatric sports medicine. A key figure is Dr. Tim Dutra, who has advanced the traditional teachings as well as integrated this established doctrine with up-to-date sophisticated computerized gait and motion lab analysis of the athlete. His position as an assistant professor and clinical investigator at Samuel Merritt University allows him to parlay his knowledge of biomechanics and sports medicine into skillfully watermarked ideas and principles commendably driven into his students’ psyche. His uncompromising enthusiasm for improving the podiatric health of athletes is demonstrated through his tireless engagement in the Special Olympics, consulting for the Golden State Warriors basketball team as well as working with the University of California, Berkeley as a consultant for inter-collegiate sports. He has been active with the AAPSM since he started the student chapter while at the California College of Podiatric Medicine. What Dr. Dutra brings to sports medicine is merging the podiatry profession with the community; to memorialize the podiatrist’s vast training, knowledge and experience and to encourage the sporting community to take advantage of this valuable resource.

Figure 2: What started it all: Dr. Steve Subotnik and The Running Foot Doctor

Dr. Jeff Ross, president of the Texas Podiatric Medical Association and an associate professor of surgery in the division of vascular surgery and endovascular therapy, as well as a clinical associate professor in the department of medicine at Baylor College of Medicine, brings to sports medicine a whole new perspective. He not only served as president of the AAPSM but also co-chaired the Governor’s Council on Physical Fitness, served for 12 years as a member of the Texas Department of State Health Services Council and was an esteemed member of the Texas Diabetes Council. His credentials sanction him as a national and international expert in sports medicine, biomechanics, wound healing and limb preservation. Dr. Ross’s unique contribution, therefore, is being able to fuse the disciplines and surgical principles of diabetic foot medicine with sports medicine, as there are pathways common to both that are brought to light through his extensive lecturing and vast publications. Dr. Ross, inspiring to all, is a valued and motivated partner in the creation of the new certification.


This new board certification could not have happened without the genius of Stephen B. Permison, M.D., who serves as president of Standards Based Programs, Inc. (SBP Inc.), director of the ABMSP Standards Development Organization ( and a voting member of multiple professional boards. SBP Inc. has developed and is currently developing standards, credentialing and certification programs for private industry, medical professional boards and the U.S. Government. Professional credentials, such as the ABMSP certification in sports medicine for podiatrists, assures the public that certified professionals have the proper skills to practice their designated professions with consistent medical outcomes. These intensely scrutinized policies bestow a hand of trust, allowing the public to expect quality and consistency in both in the practice of podiatric sports medicine and any products or devices that support this discipline. Dr. Permison states that “the definition of professional is quality, consistency and integrity”, exactly what his expertise imprinted into the structure of the new board certification.

“Dr. Earl Horowitz’s focus on the geriatric patient contributed powerfully to the unique quality of this new board certification.”

Dr. Victor Quijano is Chief of Podiatric Medicine and Surgery at the Veterans Administration Medical Center in Portland, Oregon. His Ph.D. and his knowledge of molecular endocrinology boosts his pursuit of comprehensiveness in the practice of podiatric sports medicine beyond the treatment of the traditional athlete. He calls for more academic and clinical inclusiveness in the discipline of podiatric sports medicine to embrace those challenges that deal with diabetes and other metabolic disorders, as well as those conditions that affect our country’s veterans. His was a needed voice in the development of this quality certification.

Dr. Earl Horowitz (Figure 3) is the president of the ABMSP and most recently became one of the first podiatrists in the United States to become board certified in Geriatric Podiatry. Dr. Horowitz is a true visionary with a passion for the health of the senior population. Preventing the geriatric patient from developing unnecessary muscle weakness, inactivity and immobility, through sports, exercise and precaution is what fuels Dr. Horowitz’s zeal for the field of podiatric sports medicine. “Maintaining foot health, balance and strength as we age are essential considerations in preventing such things as falls, which often starts a downhill spiral that can even lead to death in an elderly person. This can all be prevented by seriously addressing this part of our practice.” His focus on the geriatric patient contributed powerfully to the unique quality of this new board certification.

Figure 3: Earl Horowitz DPM, A True Visionary, President of American Board of Multiple Specialties in Podiatry

Rita Yates, executive director of the American Academy of Podiatric Sports Medicine worked hand in hand with the Executive Director of the American Board of Multiple Specialties in Podiatry, Joan Campbell, to formulate a meaningful advancement from Fellow of AAPSM to Board Certification by ABMSP. This was done in collaboration with the formative team which, in addition to those already discussed, also included the following doctors whose contributions were invaluable: David Jenkins, D.P.M; Diane Mitchell-Prey, D.P.M; Doug Taylor, D.P.M; Richard Blake, D.P.M; and Steven Tager, D.P.M.

To summarize, world-class talent representing a wide range of expertise, each having intense passion for their individual niche, brought this board certification to fruition. The intended and expected outcome is to support the highest level of practice in sports medicine for the modern podiatrist; and to secure the optimum level of care for their patients. This bright light will undoubtedly ensure a brilliant future for the unabridged formidable field of podiatric medicine and surgery.

In conclusion, podiatric sports medicine defines the future of podiatry because it’s an area where committed athletes are committed to staying in the game no matter what; and there is no better place to get help for those with sports-related problems of the lower extremity than a podiatric physician and surgeon who is board certified in podiatric sports medicine.