Myths In Podiatric Dermatology

Multiple times per week, a practitioner will encounter a patient who asks questions regarding how onychomycosis developed in their nails and/or discusses a home remedy found on the internet that is supposed to clear onychomycosis. Any nail specialist, whether dermatologist or podiatric physician, can name a litany of the possibly logical and illogical “cures” that one will find displayed with a simple internet search. When faced with a patient who tried these home remedies did not see the result that they wanted, it is best not to judge or make light of the treatment, but instead, give them the facts as to the possible source of the fungal infection and why common household remedies have or have not worked.

Likewise, several myths have passed down in the podiatric profession from attending to resident. I attempt to break these patterns with my own students at Temple University School of Podiatric Medicine; however, when they begin their residency, they soon acclimate to the myths that perpetuate the podiatric profession in terms of podiatric dermatology. I hope to dispel some of these handed-down thoughts that, have no evidence in the literature, or in my experience, are just false.

Myth #1: Home Remedies And Over-The-Counter Products Treat Onychomycosis

In the podiatric profession, I’ve noticed there are doctors who recommend one or more of the following products, and there are patients who present to the office after trying the following “cures” for onychomycosis: Listerine^® (Johnson & Johnson); Vicks^® VapoRub^™ (Procter & Gamble); oil of oregano; apple cider vinegar; bleach; and tea tree oil. In my experience, patients are inundated with various remedies in the foot care aisle in their local pharmacy, promising a clear nail in a small amount of time. This isn’t possible from a physiological standpoint, and there is a lack of evidence to support any of these remedies.

Analyzing The Use Of Apple Cider Vinegar For Onychomycosis

Apple cider vinegar (ACV) is touted as a cure-all tonic for many ailments and has websites dedicated to its properties. It is generally inexpensive and easy to obtain. I’ve observed such websites with faceless, picture-less, “my toenails look better!” testimonials, claiming that the anonymous person’s nail disease resolved. What is in apple cider vinegar? Maleic acid, acetic acid, pectin, beta carotene, acetoin, methanol, alanine, ethanol, ethyl acetate, lactic acid, methanol, glycerol, tartaric acid, in addition to mineral salts, phosphorus, potassium, chloride, sodium, and other minerals.^1,2 The maleic acid that purportedly has both bactericidal and fungicidal properties.^3,4 Some theorize that acetate can inhibit lanosterol demethylase, which would impact ergosterol production in a fungal cell; others feel that acetic acid is permeable to the cell membrane and its presence is toxic to the cell.^3,4

There have been no clinical trials showing that apple cider vinegar creates a mycological or clinical cure for onychomycosis. The closest study to dissect its antifungal properties was in the Journal of Prosthodontics where the authors studied apple cider vinegar for denture stomatitis, usually caused by Candida albicans.¹ This study showed the MIC (minimum inhibitory concentration) of apple cider vinegar versus the common antifungal for Candida, nystatin, but more importantly, it showed the microbial death curve. The microbial death curve is a more dynamic measure, as it allows “quantitative analysis of the fungicidal activity and of the time required until microbial death,”¹ ultimately showing the behavior of antifungal agents in the presence of the organism. In this study, the kinetics of antifungal activity of apple cider vinegar varied at all concentrations and time intervals from nystatin and control. All groups (apple cider vinegar and nystatin) showed fungistatic activity when tested at MIC and MICx2, between zero and 180 minutes. When tested at MICx4, apple cider vinegar exhibited fungistatic activity only between zero and 30 minutes; however, after 30 minutes, it began to exhibit fungicidal activity. So, ultimately, for Candida albicans, apple cider vinegar concentration and time exposed to the organism will affect whether it acts as a fungistatic or fungicidal agent.¹

When translating this to clinical practice, there are no available MIC data or microbial death curves on apple cider vinegar’s effect on T. rubrum or T. mentagrophytes, the most common dermatophytes seen in toenail onychomycosis. Although it seems that apple cider vinegar does exhibit antifungal behavior in vitro, we cannot make that direct connection in vivo to onychomycosis, or determine the concentration/time exposed needed to have a fungicidal effect. More studies are necessary to determine its true effect on fungal toenails. At this stage, it remains a folk remedy with widely varying results.

What Does The Evidence Reveal About Mentholated Ointment?

Another folk remedy readily found on the internet and recommended by physicians is Vicks VapoRub, an over-the-counter mentholated ointment, which has descriptions as a treatment for onychomycosis.⁵ I’ve noted that many physicians feel there is a cost-benefit of using an easily attainable product with no side effects, but are unaware of the research on this product. The components of Vicks VapoRub are thymol, menthol, camphor, and oil of eucalyptus, which seem to be broad-spectrum anti-infectives that show activity in vitro against Candida, Aspergillus, and some dermatophytes.⁵ There is some data generated about its use for toenail onychomycosis in vivo.

The first clinical trial completed using Vicks VapoRub on mycotic nails is a pilot study performed by a family medicine group.⁵ Eighteen subjects who had nail disease completed the 48-week study. This study has some positive aspects, but it did not follow all of the protocols that typically take place for topical antifungal studies for onychomycosis. Unlike Phase 3 clinical trials for toenail onychomycosis, this study did not exclusively enroll patients who cultured dermatophytes like T. rubrum or T. mentagrophytes and did not limit the percent of affected nail to 50 or 60 percent. Instead, they allowed patients whom cultured organisms like “fungal elements,” Cryptococcus, Candida, Penicillium, and Fusarium, and allowed up to 100 percent visual involvement of the nail. Of the 18 patients, only nine subjects cultured either T. rubrum or T. mentagrophytes.⁵

Their results included the following findings: five of the 18 (27.8 percent) had a mycological and clinical cure, and 10 (55.6 percent) had “partial clearance.”⁵ However, let us dissect this further: if we were to look at the nine subjects who cultured the most common dermatophytes causing onychomycosis, those who had T. rubrum fared the worst. Five had partial clearance (at times, only a 10 percent change in the nail appearing clearer at week 48), and one had no change at all. T. mentagrophytes-infected toenails did the best with all three subjects going onto a complete cure, but “complete cure” was not zero percent surface area affected. These patients still had five percent or more of the nail visually affected at 48 weeks. Of the other organisms involved, both subjects who had Candida parapsilosis went onto a complete cure, but Penicillium species and Candida albicans (one subject each) had no change.⁵ 

Ten of the 18 subjects had greater than 60 percent affected nail at the beginning of the study, with some having 89 or 100 percent affected nails.⁵ This is highly unusual for a toenail clinical trial, and one can indeed argue that a 48-week treatment period is not long enough to manage a totally dystrophic nail. Adding a modality such as nail debridement could be synergistic for a topical study that enrolls nails as involved as these.

While this study is a positive start in supporting or shattering the use of a mentholated ointment for mycotic nails, it does not convince one to recommend it to patients in the office. A study that controls percent nail involvement, nail thickness, nail debridement, organisms cultured, and product use (some patients used it daily; some only three-to-five times per week) while having a vehicle arm and a larger sample size, would create a more convincing evidence-based protocol. Time will tell if this ointment truly can eradicate fungus, or by virtue of its ointment properties, simply create a more hydrated nail unit that gives the appearance of a healthier nail.

Is There Any Merit To The Use Of Tea Tree Oil?

Another readily available over-the-counter product, tea tree oil (TTO), is an essential oil derived from the leaves of Melaleuca alternifolia described as anti-inflammatory, antibacterial, and antifungal.⁶ However, it also has the potential to cause skin irritation and allergic contact dermatitis.⁶

When creating a topical antifungal product, one must consider the size of the particle being engineered to go through the pores of the nail plate, along with the lipophilic and hydrophilic properties of the molecule. One study placed tea tree oil in either a nanoemulsion or nanocapsule formulation that, in theory, could better penetrate the nail unit. This controlled in vitro study combined a culture of T. rubrum, nail powder (from healthy nails), and either formulation of the tea tree oil. Given that nail hydration improves penetration through the nail plate of poorly water-soluble drugs, an aqueous solution would hydrate the nail keratin and possibly cause the pores to increase in size.^7,8 Ultimately, the nanocapsule tea tree oil had the most antifungal activity, possibly due to it being an aqueous suspension with a small particle size.⁶

The previous study took place in a lab and did not use human subjects. In a double-blind, randomized, controlled study comparing topical use of clotrimazole 1% solution and tea tree oil 100%, subjects used either product twice daily for six months.⁹ Researchers enrolled 116 patients with distal subungual onychomycosis who either tested culture-positive for T. rubrum or T. mentagrophytes. After six months, they reported on “culture cure” (clotrimazole=10 percent, tea tree oil=18 percent). Via clinical assessment, they noted partial or complete cure with clotrimazole in 61 percent, and tea tree oil in 60 percent. Adverse events, including erythema and irritation, occurred more in the tea tree oil group than in the clotrimazole group.⁹ Compared to Phase 3 clinical trials for onychomycosis, this is a short study that used clotrimazole as a “control.” Clotrimazole solution is not an FDA-approved topical for onychomycosis and proved mildly beneficial in limited studies on nails. A more convincing protocol design would incorporate a vehicle arm compared with the tea tree oil solution for 48 weeks. Again, these are interesting and mildly positive results but not enough evidence to create a paradigm shift in practice.

The remaining products that a patient would find in the pharmacy foot care aisle or their physician’s office include topicals that take their FDA approval for dermatophyte infections to the limit. Many of them show a fungally infected nail on the package, but if one reads the fine print, one will note that the product is indicated for the “skin around the nail” and is FDA approved for “fungal infections” or “tinea pedis.” None of the products are specifically FDA-approved for the treatment of mycotic toenails. These include formulations containing undecylenic acid, clotrimazole, tolnaftate, and various antiseptics like polyhexamethylene biguanide (PHMB). In conclusion, even though the price may be reasonable and the packaging convincing, buyers should be aware that these products may utilize creative wordsmithing, visual graphic packaging, and small data sets.

Myth #2: Removing A Toenail Will Cure Onychomycosis

For a singularly painful or thickened nail, some patients may opt for total nail removal of the nail plate. Simple total avulsion of the nail itself is not curative for a mycotic nail, as the procedure has not addressed the basis of infection, which originates in the nail bed, not in the nail plate. Combining nail avulsion and topical antifungals has been a treatment of choice for some physicians and patients. However, this practice has little evidence to support it and may result in potentially long-term issues of the nail unit from a cosmetic and functional standpoint. In a study, total nail avulsion with a topical azole cream applied twice daily to the exposed nail bed resulted in a high dropout rate.¹⁰ All patients with total dystrophic onychomycosis failed, and only 56 percent of patients (15/27) experienced a cure with this approach,¹⁰ highly suggesting that one should not recommend this procedure for the treatment of onychomycosis.

A potential sequela of totally avulsing the nail plate is the development of a disappearing nail bed. Disappearing nail bed is the physiologic change of the nail bed to distal skin due to onycholysis of the nail unit.¹¹ It is unknown how long onycholysis must be present for this to occur, but once epithelialization of the nail bed happens, it is irreversible. Not only will the nail bed physiologically change, but the nail plate will become shortened and narrowed, which is cosmetically displeasing to the patient.¹²

Myth #3: Oral Antifungals Will “Wreck” My Liver

A common misconception among general practitioners, some specialists, and patients is that oral antifungals cause liver disease immediately upon ingestion and warrant categorical avoidance. These agents, oral terbinafine, itraconazole, and fluconazole, are the subject of many studies to determine safety and efficacy. Of these, terbinafine and itraconazole are FDA-approved for the treatment of toenail onychomycosis. Before placing a patient on one of these medications, it is imperative to determine whether the nail disease is indeed a fungal infection and not one of the many differential diagnoses. Second, a thorough history and physical with pertinent blood work evaluation is prudent before taking the first dose. As is true with any medication, patient selection is key.

Finally, a meta-analysis elegantly dissected the safety of these medications, looking at 122 studies that enrolled 20,000 patients.¹³ The analysis cited pooled risks of treatment discontinuation resulting from adverse reactions for continuous therapy of terbinafine (250 mg/day, 3.44 percent), itraconazole (100 mg/day, 4.21 percent), pulsed terbinafine (2.09 percent), pulsed itraconazole (2.58 percent), and intermittent fluconazole (150 mg/week, 1.98 percent). The risk of liver injury requiring medication termination ranged from 0.11 (continuous itraconazole) to 1.22 percent (continuous fluconazole). The risk of liver function values elevating asymptomatically and not requiring treatment or discontinuation of antifungal therapy was less than two percent for all regimens evaluated.¹³ Therefore, in an immunocompetent population, the risk of adverse events when taking these oral antifungal medications is low. Of course, oral antifungal medications are not for every patient, but the sustaining myth that liver damage is imminent in a healthy population should be re-examined by those who have perpetuated that belief for years.

Myth #4: Toenail Fungus Cannot Be Cured. Topical And Oral Antifungals Do Not Work.

“Cure” is a challenging word, as it denotes absolute finality. Treating mycotic nails is not like treating a superficial bacterial skin infection with an antibiotic. As anyone who has treated or themselves developed mycotic toenails understands, it has the potential to recur for various reasons. One must be diligent about not only managing this clinical entity pharmacologically, but also manage the environment. This can include considerations related to socks, shoes, and shared shower spaces. The clinician must also educate the patient that their predisposition (genetic or medical condition) may cause them to revisit this diagnosis in the future.¹⁴ Concomitant tinea pedis warrants treatment along with the nail. Patients would benefit from education on seeking treatment upon the first signs of either nail disease or skin involvement.

The effectiveness of both oral and topical antifungal medications in the treatment of this infection is well-documented.¹⁴ Again, these agents will assist the nails to achieve a mycological and visual cure, but one must also consider and manage the environment to obtain a longer state of clear nail (and skin) for the patient.

Patient expectations are also a pertinent undertaking. Often, the mycotic nails are of a many-year duration, which can cause permanent dystrophic changes such as onychorrhexis and Beau’s lines. Once achieving mycological cure, the nails may always have some degree of dystrophy, which visually will appear disappointing to the patient and practitioner. Also, if patient biomechanics impact the nails (ie a hammertoe on a lesser digit), the nails may always appear onychauxic due to chronic repetitive trauma. Patient education is key regarding that nails are subject to the environment and forces around them, which are often in flux.

Myth #5: A Porokeratosis Is A Callus On The Plantar Foot And Is A Blocked Sweat Gland

One of the most frustrating statements that I encounter from fellow practitioners is the use of the term, “porokeratosis” to describe any crater-like and/or punctate hyperkeratotic lesion on the plantar surface of the foot. There is a distinct difference between the term porokeratosis in the dermatology world versus the term porokeratosis plantaris discreta used in the podiatric world. I urge our profession to discontinue casually using this term, just as Yanklowitz and Harkless emphatically stated in their article.¹⁵

A true porokeratosis (PK) is a disorder of keratinization and is a rare entity.¹⁶ All forms of porokeratosis (porokeratosis of Mibelli, disseminated superficial actinic porokeratosis, punctate porokeratosis, and linear porokeratosis) may undergo a malignant transformation to become a squamous cell carcinoma. All of the subtypes have a characteristic histologic phenomenon called the cornoid lamella, which is one can observe in the lesion’s edge on biopsied specimens.¹⁶

The lesion traditionally described in podiatric medicine (porokeratosis plantaris discreta) is not a true porokeratosis. It does not have a cornoid lamella and has not been known to undergo malignant transformation. Why? The original paper by Taub and Steinberg in 1970 described a “plug” in the center of the punctate hyperkeratotic lesion that was “comparable” to the cornoid lamella in a true porokeratosis lesion.¹⁷ Twenty years later, a study of eighteen lesions from six patients with porokeratosis plantaris discreta had none of the previously described characteristics.¹⁵ This central plug observed over the years is not the result of a “blocked sweat gland.” It is a compact hyperkeratotic plug of cells that is not histologically a cornoid lamella.¹⁸

A true blocked sweat gland is known as hidradenitis suppurativa and can be a painful, disabling, and chronic entity that can occur in the groin, axilla, or under the breasts. I urge our profession to stop saying that porokeratosis plantaris discreta are blocked sweat glands, as this does not occur in these punctate lesions and is false information.

From a medicolegal standpoint and also as a communication issue between medical professions, I recommend discontinuing the use of the term “porokeratosis” to describe these hyperkeratotic lesions on the plantar foot and instead to call them “punctate keratodermas” or “plantar keratoderma discreta” to distinguish from the potential malignant path that at true porokeratosis can undergo.¹⁸

Final Thoughts

One should carefully consider the above podiatric dermatology myths the next time you have a conversation with a patient or a podiatric resident. As medicine evolves from an observational studies paradigm to an evidence-based medical approach, it is time we dissect such handed-down information and determine what is veracity within previously told medical fables.

Dr. Vlahovic is a Clinical Professor in the Department of Podiatric Medicine at the Temple University School of Podiatric Medicine in Philadelphia.

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