The paw pad is a specialized cutaneous structure designed for weight-bearing, capable of absorbing ground reaction forces through its distinctive micro-anatomy. This mechanical function explains both the considerable thickness of its cornified covering and the frequency of lameness when this covering is affected. Indeed, paw pad disorders are among the common causes of lameness in dogs. Let us review the many dermatoses affecting the paw pads in dogs.
The difficulty of the differential diagnosis of paw pad dermatoses lies in the fact that the elementary lesion of the paw pad, hyperkeratosis, has no orienting value in and of itself. Indeed, the same podal hyperkeratosis is encountered in hereditary, metabolic, infectious, dysimmune, or mechanical conditions, whose prognosis ranges from a mere cosmetic concern to a fatal outcome. Thus, the old term “hard pad disease,” which referred to paw pad thickening in canine distemper, was gradually abandoned, precisely because this presentation is also found in zinc-responsive dermatosis, hepatocutaneous syndrome, and pemphigus foliaceus (Gröne et al., 2004a). In this review, we will address the main paw pad dermatoses in dogs in order to establish the broadest possible differential diagnosis.
1 Anatomical and Functional Background
Understanding paw pad dermatoses requires first recalling what distinguishes this integument from haired skin. The paw pad consists of a thick stratified epithelium, endowed with an abundant stratum corneum, deep epidermal ridges, and tall dermal papillae that interdigitate extensively with the epidermis (Ninomiya et al., 2011). Its surface, smooth to the naked eye, is actually composed of multiple conical papillae approximately 200 to 300 micrometers in size (Ninomiya et al., 2011). Histologically, the canine paw pad resembles human palmoplantar skin, sharing its thick stratum corneum organized in columns; it differs, however, by particularly deep epidermal ridges (Bowden et al., 2009). This architecture sheds light on one point: the stratum corneum of the paw pad, capable of absorbing forces reaching up to six times body weight per limb, is also the most susceptible to fissuring whenever its thickness and hardness increase at the expense of its flexibility (Utzmann et al., 2025).
2 Diagnostic Approach to Paw Pad Lesions
Since no podal lesion is pathognomonic, systematic reasoning takes priority over visual recognition. The workup must therefore proceed in steps, first characterizing the elementary lesions, then placing them in their topographic and general context, before resorting to complementary tests. History-taking and a complete physical examination are never incidental: foot dermatoses are most often a component of a more generalized dermatosis or a concurrent systemic condition, such that an examination limited to the foot alone risks overlooking the underlying disease (Jackson, 1999).
2.1 Elementary Lesions and Semiology
Lesions encountered on the paw pads fall into a small number of types: fissures, erosions, ulcerations, crusts, margin hypertrophy, swelling, and depigmentation. Vertical fissures that form on a hyperkeratotic paw pad are often painful and precede secondary inflammation and infection (Utzmann et al., 2025). Thus, the same hyperkeratosis may remain simple corneal thickening or become complicated by deep cracks, and it is this progression, more than the hyperkeratosis itself, that motivates the consultation. From a pathophysiological standpoint, thickening of the stratum corneum is accompanied by a loss of plasticity: the stratum corneum, thicker but less hydrated, poorly tolerates the shear stresses of weight-bearing and cracks, opening the way for bacterial and yeast colonization of the fissures (Utzmann et al., 2025).
2.2 Orientation by Topography and Context
The most useful discriminating factor is determining whether the involvement is limited to the paw pads or is accompanied by lesions of the haired integument, mucocutaneous junctions, or systemic signs. Indeed, metabolic, infectious, and dysimmune dermatoses almost always produce lesions elsewhere than the paw pads, or are accompanied by poor general condition (Utzmann et al., 2025). However, two entities are exceptions: hereditary paw pad hyperkeratosis, which affects only the pads and begins at a young age, and idiopathic nasodigital hyperkeratosis, in which only the nasal planum is also affected (Utzmann et al., 2025). Strictly podal involvement in a young dog of a predisposed breed therefore immediately points toward a primary cornification disorder, whereas involvement of multiple feet associated with systemic signs warrants investigation for a metabolic, infectious, or immune cause. Whether the involvement is mono- or multifocal constitutes a second orienting axis: a lesion on a single paw pad suggests a corn, trauma, or tumor, whereas symmetric involvement of all four feet points toward an internal or hereditary cause (Hardy, 2017).
2.3 Role of Biopsy and Cytology
Histopathology occupies a central position. Indeed, parakeratotic hyperkeratosis, in which nuclei persist within the stratum corneum, points toward zinc-responsive dermatosis (White et al., 2001) or hepatocutaneous syndrome (Gross et al., 1993), whereas orthokeratotic hyperkeratosis is encountered more often in hereditary forms (Drögemüller et al., 2014) and in canine distemper (Koutinas et al., 2004). Cytology retains its value: the identification of acantholytic keratinocytes points toward pemphigus foliaceus, while the presence of amastigotes allows a diagnosis of leishmaniasis to be made. Two practical points must be noted. First, paw pad biopsy is technically demanding: the sample must target a representative, preferably non-ulcerated lesion, be deep enough to include the full thickness of the stratum corneum, and its healing, which is slow and painful in a weight-bearing zone, requires a protective bandage and relative rest (Jackson, 1999). Technically, a 6-mm punch biopsy is appropriate for most situations, but a wedge biopsy is preferable for deep, bullous, or ulcerative lesions, as it allows sampling of both the lesion margin and the adjacent epidermis while permitting careful closure (Hnilica and Patterson, 2017). Second, surface cytology, performed by impression smear or swabbing of fissures and interdigital spaces, characterizes the nature of secondary superinfection — cocci, bacilli, or Malassezia — upon which the choice of topical antimicrobial treatment depends (Ortalda et al., 2016). The workup is completed, depending on the clinical orientation, by bacteriological culture with susceptibility testing, fungal culture, Demodex detection by deep skin scraping or trichogram, serology or PCR for leishmaniasis, and biochemical and hepatic ultrasound evaluation when superficial necrolytic dermatitis is suspected (van den Broek and Horváth-Ungerböck, 2011; Burns DeMarle et al., 2021).
3 Primary Disorders of Keratinization
These conditions share a common characteristic: involvement is confined to the paw pads, possibly associated with the nasal planum, without systemic signs. They result from an intrinsic defect in cornification, often of genetic origin, and tend to manifest in young dogs.
3.1 Hereditary Footpad Hyperkeratosis
Hereditary footpad hyperkeratosis is transmitted in an autosomal recessive manner and was first reported in the Kromfohrländer and Irish Terrier (Drögemüller et al., 2014). It results from a variant in the FAM83G gene, leading to the replacement of an arginine by a proline at position 52 of the PAWS1 protein (Drögemüller et al., 2014). This finding was confirmed by whole-genome sequencing of a Kromfohrländer family trio, which identified the same variant as the sole candidate consistent with the phenotype (Sayyab et al., 2016). FAM83G mutations impair the interaction of PAWS1 with casein kinase 1 alpha and attenuate the Wnt signaling pathway, a mechanism shared with palmoplantar keratodermas in humans (Wu et al., 2019).
Clinically, the condition begins in young dogs within the first six months of life and affects all four feet, with all paw pads becoming covered by hard, dry, and cracked horn showing an orthokeratotic pattern on histological examination; the animal otherwise remains in good general health, but severe hyperkeratosis may be complicated by fissures, secondary infections, and lameness (Drögemüller et al., 2014; Hardy, 2017). The monogenic basis allows for genetic testing to advise breeders to exclude carrier breeding animals (Leeb et al., 2021). Related familial forms have also been described in the Dogue de Bordeaux and the Rottweiler (Utzmann et al., 2025; Leeb et al., 2021), and a variant in the GJB6 gene, encoding connexin 30, was recently reported in a Labrador Retriever with paw pad hyperkeratosis resembling human Clouston syndrome (Rietmann et al., 2026). These entities must be distinguished from the congenital “dry eye curly coat” syndrome of the Cavalier King Charles Spaniel, linked to a deletion in the FAM83H gene, in which paw pad hyperkeratosis is associated with keratoconjunctivitis sicca and nail dystrophy (Forman et al., 2012). The condition is not curable, and its management is purely symptomatic.
3.2 Idiopathic Nasodigital Hyperkeratosis
Idiopathic nasodigital hyperkeratosis corresponds to an alteration of cornification affecting the nasal planum and paw pads in dogs of various breeds; relatively common in older dogs, it is regarded as a senile change in desquamation (Utzmann et al., 2025; Hardy, 2017). In its uncomplicated form, it causes primarily a cosmetic concern; however, the prevention of fissures and secondary infections justifies management (Viaud et al., 2025). Hyperkeratosis is most noticeable at the edges of the paw pad, where the normal wear from weight-bearing is absent (Hardy, 2017). Treatment is based on topical application of emollients and keratolytics. Indeed, a randomized, placebo-controlled trial demonstrated, for idiopathic nasal hyperkeratosis, the efficacy of a balm based on essential oils and essential fatty acids applied daily (Catarino et al., 2018), and an open-label pilot study confirmed the good tolerability and clinical improvement achieved with an emollient balm (Viaud et al., 2025). These data concern the nasal planum, and their extrapolation to the paw pad remains empirical.
3.3 Split Paw Pad Dermatosis and Cohesion Abnormalities
Split paw pad dermatosis is characterized by horizontal fissuring and scaling of the paw pad stratum corneum, with frequent recurrence. The dominant signs are pain, lameness, pruritus, and licking, with all four feet most often involved over the course of the condition; large-breed dogs weighing more than twenty kilograms are overrepresented (eight of thirteen dogs in the reference series, mean weight 24.6 kilograms), the German Shepherd Dog is frequently mentioned, and seasonality as well as concurrent atopic dermatitis are noted in a subset of cases (Utzmann et al., 2025). No single causative factor has been identified, making it necessary to consider several mechanisms, including hypersensitivities, excessive shear forces, humidity, heat, and obesity; no single treatment prevents relapses, and only barrier-supportive measures provide partial benefit, with a small subset responding to anti-inflammatory treatment (Utzmann et al., 2025).
A genetic epidermal cohesion abnormality was identified in a family of German Shepherd Dogs presenting with intermittent podal lesions and lameness. An in-frame 18-base-pair deletion in the KRT5 gene was identified, associated with a cleavage plane within the stratum spinosum and stratum corneum, a finding likened to localized epidermolysis bullosa simplex in humans (Rietmann et al., 2024). This observation illustrates the fact that a structural defect in a keratin filament can manifest as fragility of the paw pad stratum corneum.
4 Metabolic and Nutritional Dermatoses
Unlike primary cornification disorders, these dermatoses are the consequence of a systemic, hepatic, pancreatic, or nutritional derangement. Podal involvement is therefore rarely isolated, and its recognition is important in that it opens the workup to the underlying condition.
4.1 Superficial Necrolytic Dermatitis (formerly Hepatocutaneous Syndrome)
Superficial necrolytic dermatitis, also called hepatocutaneous syndrome or metabolic epidermal necrosis, is a rare and grave condition affecting middle-aged to older dogs, with no established breed or sex predisposition (Cellio and Dennis, 2005). It manifests as an erosive, crusting, and scaly dermatosis with symmetric distribution involving the face, extremities, inguinal region, mucocutaneous junctions, and pressure points; paw pad involvement, consisting of hyperkeratosis, fissuring, and ulceration, is nearly constant and was present in twenty-one of the twenty-two dogs in a landmark series (Gross et al., 1993). The history commonly includes lethargy, anorexia, weight loss, and a painful gait (Cellio and Dennis, 2005).
Severe form of superficial necrolytic dermatitis
From a pathophysiological standpoint, the condition is most often associated with severe vacuolar hepatopathy, and less commonly with a pancreatic neuroendocrine tumor or glucagonoma (Gross et al., 1990; Papadogiannakis et al., 2009). Prolonged administration of phenobarbital or phenytoin has also been cited among triggering contexts (Papadogiannakis et al., 2009; van den Broek and Horváth-Ungerböck, 2011), as has copper-associated hepatitis (Talbot et al., 2022). Cutaneous histology is highly suggestive: parakeratosis, intercellular and intracellular edema of the upper half of the epidermis, and hyperplasia of the basal layers compose the classically described stratified appearance (Gross et al., 1993). Given the non-specific nature of the clinical signs, diagnosis relies on targeted investigations: marked plasma hypoaminoacidemia was present in all cases in a large review, and abdominal ultrasound showed a honeycomb-patterned liver in nearly all affected dogs, allowing a minimally invasive diagnostic approach based on amino acid profiling combined with imaging (Burns DeMarle et al., 2021).
Treatment remains disappointing and essentially palliative: amino acid supplementation by intravenous or oral route, high-quality protein intake, and, when copper-associated hepatitis is confirmed, copper chelation (Talbot et al., 2022). Zinc and essential fatty acid supplementation, along with topical antiseptic and keratolytic care of paw pad lesions, complement the animal’s comfort (van den Broek and Horváth-Ungerböck, 2011). However, the prognosis remains poor, with most dogs dying or being euthanized within months of the onset of signs (Cellio and Dennis, 2005).
4.2 Zinc-Responsive Dermatoses
Zinc-responsive dermatoses fall into two forms. The first is a familial form in northern breeds, most notably the Siberian Husky and the Alaskan Malamute, in which a defect in zinc absorption or metabolism is implicated; the second affects growing puppies fed a zinc-deficient or unbalanced diet (Colombini, 1999). Periocular crusting is the most frequent sign, and parakeratosis is found on biopsy in all dogs in a series of forty-one cases dominated by the Siberian Husky (White et al., 2001). Paw pad and pressure point involvement is possible, with lesions often beginning unilaterally before becoming symmetric, and with a seasonal component (Colombini et al., 1997).
Treatment is based on oral zinc supplementation. An initial dose of 2 to 3 mg/kg per day of elemental zinc is recommended in the series by White et al. (2001), while Colombini et al. (1997) suggest starting at 1 mg/kg per day and increasing progressively in the absence of response. The familial form requires lifelong supplementation, and relapses tend to occur when a dose is missed or the dosage is reduced (Colombini et al., 1997). Furthermore, localized parakeratotic hyperkeratoses resembling zinc-responsive dermatosis have recently been described on the pinnae of Boston Terriers and French Bulldogs, with partial response to supplementation, without any difference in tissue zinc concentrations compared to controls (Lee et al., 2016; Dubin et al., 2025).
4.3 Lethal Acrodermatitis of Bull Terriers
Lethal acrodermatitis is an autosomal recessive genodermatosis of the Bull Terrier and Miniature Bull Terrier, linked to a variant in the MKLN1 gene (Bauer et al., 2018). The clinical picture combines growth retardation, splaying of the digits, dermatosis of the face and feet, and immune deficiency; in older animals, paronychia, nail abnormalities, and paw pad hyperkeratosis appear, the latter being more severe as the puppy exceeds six months of age (McEwan et al., 2000; Jezyk et al., 1986). Histology reveals parakeratotic hyperkeratosis resembling zinc deficiency, but, unlike zinc-responsive dermatoses, the condition does not respond to zinc supplementation and results in a median survival of approximately seven months (Jezyk et al., 1986). Genetic testing now allows identification of carriers and prevention of the production of affected puppies (Bauer et al., 2018).
4.4 Other Nutritional Deficiencies and Imbalances
Beyond zinc-responsive dermatoses, podal cornification may be affected by broader nutritional imbalances, particularly with poorly balanced home-prepared diets or atypical feeding regimens. The old concept of “generic dog food dermatosis,” reported in puppies fed low-quality, deficient foods, represents the archetypal example and is partly linked to a deficiency in zinc intake or bioavailability (Utzmann et al., 2025). Essential fatty acid deficiency also impairs barrier function and stratum corneum quality; their supplementation is moreover proposed in the long-term management of several podal dermatoses, including symmetric lupoid onychodystrophy (van den Broek and Horváth-Ungerböck, 2011). These considerations justify including a dietary inquiry in the workup of podal hyperkeratosis in a young dog before concluding that a hereditary form is present.
5 Infectious and Parasitic Dermatoses
The infectious aspect of podal involvement falls into two categories. On one hand, two conditions dominate by their consistent expression on the paw pad itself: canine distemper, whose paw pad thickening long gave rise to its common name, and leishmaniasis, in which nasodigital hyperkeratosis accompanies onychogryphosis; in both cases, podal involvement is part of a systemic picture that leads to their suspicion.
5.1 Canine Distemper
Hyperkeratosis of the paw pads and nasal planum, referred to as “hard pad disease,” constitutes a late and uncommon sequela of canine distemper virus infection (Koutinas et al., 2004; Gröne et al., 2004a). Histologically, it produces orthokeratotic hyperkeratosis associated with acanthosis and thickening of the epidermal ridges; viral antigen localizes preferentially to the stratum spinosum and stratum granulosum as well as to eccrine sweat gland cells (Koutinas et al., 2004; Gröne et al., 2004a), and is accompanied by a disturbance in keratinocyte differentiation, evidenced by altered cytokeratin expression (Gröne et al., 2004b). Inclusion bodies and ballooning degeneration, once considered characteristic, are in fact inconsistent in naturally infected paw pads (Koutinas et al., 2004). Beyond the nasodigital regions, hyperkeratosis may involve other sites, such as the nasal planum, the periocular region, or the ventral abdomen (Areco et al., 2022).
Podal involvement fits within the broader clinical picture of canine distemper, with its respiratory, gastrointestinal, and neurological components, which facilitates its attribution to that disease. Demonstration of the virus in paw pad epidermis has moreover been proposed as a means of antemortem diagnosis (Gröne et al., 2004a).
5.2 Leishmaniasis
In canine leishmaniasis due to Leishmania infantum, cutaneous lesions constitute the most frequent clinical manifestation, with exfoliative dermatitis representing the dominant form (Saridomichelakis et al., 2014). Nasodigital hyperkeratosis and onychogryphosis are among the characteristic signs (Koutinas et al., 2014), alongside ulcerations of the extremities and scaly desquamation (Ferrer et al., 1988). Definitive diagnosis relies on the combination of macroscopic appearance, exclusion of the main differential diagnoses, histopathology, demonstration of the parasite, and complete response to antileishmanial treatment (Saridomichelakis et al., 2014). However, species such as Leishmania major may produce ulcerative lesions of the muzzle, feet, and paw pads, sometimes without seropositivity, which then requires the use of molecular biology (Baneth et al., 2016). Furthermore, ischemic dermatopathy and vasculitis lesions have been reported in association with leishmaniasis, of which they may constitute a manifestation (García et al., 2025). Given its Mediterranean distribution, this hypothesis must be considered in light of the animal’s geographic origin and stays in endemic areas.
Paw pad thickening in a dog with leishmaniasis
6 Dysimmune Dermatoses
Immune-mediated dermatoses occupy a particular place, as paw pad involvement is both frequent and sometimes the initial manifestation. Pemphigus foliaceus is the most common representative, while cutaneous lupus, drug reactions, and vasculopathies complete the autoimmune and ischemic spectrum of podal involvement.
6.1 Pemphigus Foliaceus
Pemphigus foliaceus is the most common autoimmune dermatosis in dogs. It produces pustules, crusts, erosions, scales, and alopecia affecting mainly the muzzle, face, inner surface of the pinnae, and trunk (Ihrke et al., 1985b; Mueller et al., 2006). Paw pad involvement is common, present in nearly one-third of cases, and manifests as erythematous swelling of the margins, fissuring, and villous hypertrophy (Ihrke et al., 1985b; van den Broek and Horváth-Ungerböck, 2011). Pemphigus foliaceus limited to the paw pads has moreover been described, producing a picture of hyperkeratinization and villous hypertrophy that could be mistaken for “hard pad disease” (Ihrke et al., 1985a). The coexistence of vasculitis lesions prolongs the time to remission (Zhou et al., 2021).
Diagnosis is supported by cytology, which reveals acantholytic keratinocytes, and by histopathology, which shows subcorneal or intragranular pustules rich in acanthocytes. The major autoantigen is desmocollin 1 (Bizikova et al., 2011; Bizikova et al., 2022). Treatment relies on corticotherapy at an immunosuppressive dose, possibly combined with azathioprine, the combination not having demonstrated superiority over corticotherapy alone in a series of ninety-one dogs (Mueller et al., 2006). Oclacitinib has moreover been proposed as an emerging option (Jordan et al., 2024).
Podal lesions in a dog with pemphigus foliaceus
6.2 Cutaneous Lupus Erythematosus
The spectrum of canine cutaneous lupus erythematosus has expanded considerably since the initial description of discoid lupus, and a canine adaptation of the Gilliam and Sontheimer classification now distinguishes several variants: vesicular cutaneous lupus, exfoliative cutaneous lupus, mucocutaneous lupus, and facial or generalized discoid lupus (Olivry et al., 2018). Several of these forms affect the extremities: vesicular cutaneous lupus produces annular and polycyclic erosions on glabrous areas, including the abdomen and inner thighs, while mucocutaneous lupus affects the junctions and may extend to the extremities (Olivry et al., 2018). Paw pad involvement is possible in the context of systemic lupus, whose cutaneous manifestations, less common, appear at the periphery of the spectrum (Olivry et al., 2018). Most of these variants have a favorable prognosis once diagnosed, which justifies knowing how to recognize them in order to institute appropriate immunomodulatory treatment early.
6.3 Drug Reactions and Erythema Multiforme
Drug-induced cutaneous reactions and erythema multiforme deserve a place in the differential diagnosis of acute, erosive, or ulcerative podal involvement. Canine erythema multiforme encompasses a spectrum ranging from erosive and vesiculobullous forms to a recently individualized hyperkeratotic variant: described in seventeen dogs, most often middle-aged to older males, this variant produces erythematous annular and linear macules and plaques covered by firm, adherent crusts, with histology showing panepidermal cytotoxic dermatitis and ortho- and parakeratotic hyperkeratosis; it is distinguished from classic erosive erythema multiforme and does not respond to antimicrobials, but does respond to immunosuppressants in just over half of cases (Banovic et al., 2023). Severe forms include Stevens-Johnson syndrome and toxic epidermal necrolysis, acute and serious dermatoses in which paw pad involvement, ulcerative and painful, manifests as extensive epidermal detachment often triggered by a drug. Recognition of these entities requires discontinuation of the suspected drug and supportive care, and clearly distinguishes their prognosis from that of chronic hyperkeratoses.
Alongside purely immune-mediated drug reactions, certain podal lesions result from direct iatrogenesis. Systemic retinoids such as acitretin count among their adverse effects cracking and fissuring of the paw pads, which overlap with the picture of cheilitis and exfoliative dermatitis (Koch et al., 2012). Tyrosine kinase inhibitors used in oncology, including toceranib, expose the patient to lameness, skeletal pain, dermatitis, pruritus, and pigmentation disorders (Koch et al., 2012).
6.4 Vasculopathies and Ischemic Dermatopathies
Familial cutaneous vasculopathy of the German Shepherd Dog illustrates ischemic paw pad involvement. Described in puppies, it combines swelling, depigmentation, and ulceration of the paw pads with crusting of the ear tips and tail tip, focal depigmentation of the nasal planum, and fever and lethargy (Weir et al., 1994). Histology reveals multifocal nodular dermatitis in which neutrophils and mononuclear cells surround foci of dermal collagenolysis, accompanied by degenerative and inflammatory vascular lesions; the mode of transmission is autosomal recessive (Weir et al., 1994). A case associating this vasculopathy with generalized demodicosis has also been reported (Fondati et al., 1998). Ulceration of the central paw pads is a warning sign. More generally, ischemic dermatopathy and vasculitis may complicate other conditions, foremost among which is leishmaniasis (García et al., 2025), and should be considered when confronted with a well-demarcated podal ulceration accompanied by distal extremity lesions.
7 Mechanical, Traumatic, and Neoplastic Conditions
This final group encompasses conditions whose common feature is that they do not result from a systemic derangement, but from physical trauma, repeated mechanical stress, or neoplastic proliferation. Their recognition is important, as it entirely redirects management, from surgical intervention to simple paw pad protection.
7.1 Corns and Paw Pad Keratomas
A corn presents as a focal, circular, hard, and hyperkeratotic lesion, typically located at the center of digital paw pads (Utzmann et al., 2025). It is preferentially located on the third and fourth digits and on the forelimbs, affects primarily Greyhounds and related breeds, and occurs predominantly in males (Guilliard et al., 2010). Its frequency is far from negligible in this population: reported at between 2.4 and 5.9% in retired racing Greyhounds, it represents their most common dermatological condition (Guilliard and Doughty, 2022). It causes chronic, sometimes severe lameness, aggravated on hard surfaces, and mediolateral digital pressure consistently elicits pain (Guilliard and Doughty, 2022). The proposed mechanisms are mechanical in nature, involving repeated trauma or pressure, or penetration of a foreign body; the viral hypothesis, once supported by the identification of a papillomavirus in two Greyhounds (Anis et al., 2016), is now considered unlikely, as the infection was not found in a series of eighteen Greyhounds nor on histological examination of more than one thousand corns (Guilliard and Doughty, 2022). Treatment remains challenging: surgical excision carries a recurrence rate exceeding half of cases, distal digital ostectomy is considered only in carefully selected cases, and tenotomy of the superficial digital flexor tendon, by altering the phalanx loading, provides immediate pain relief (Guilliard et al., 2010; Guilliard and Doughty, 2022; Martinez et al., 2021).
7.2 Burns and Physical-Chemical Injuries
Involvement of a single paw pad may also result from trauma by an object, such as a shard of glass, and heals as a rule without complication in an otherwise healthy animal, within a few weeks depending on the extent of the wound (Utzmann et al., 2025). In contrast, simultaneous involvement of multiple paw pads suggests environmental injury: thermal burns from a hot surface, road, or beach in summer; chemical burns from irritants; or barrier disruption by road salt and winter moisture (Utzmann et al., 2025). The topographic distribution and mono- or multifocal nature of the involvement therefore remain, here again, key orienting factors. In sporting and working dogs, intense pad use is a specific risk factor: in sled dogs, exertional pododermatitis is common, and an emollient balm applied before and after exercise significantly reduces the development of erythema, abrasions, and fissures (Bouvier et al., 2020).
7.3 Paw Pad Tumors
Tumors arising from the paw pad itself are rare but must be included in the differential diagnosis of a solitary podal nodule or thickening. Malignant melanoma of the paw pad, a poorly documented entity, behaves aggressively: in a multicenter series of twenty cases, the overall metastatic rate exceeded half of the dogs, and median survival was approximately two hundred forty days (Jeon et al., 2022). A primary cutaneous ganglioneuroblastoma of the paw pad has also been described, manifesting as lameness and foot licking associated with thickening of a digital paw pad (Salvadori et al., 2019). Thus, any unilateral and persistent nodular podal lesion warrants histological investigation before being attributed to a benign cause.
7.4 Calcinosis and Mineral Deposits
Calcinosis cutis deserves consideration when confronted with a firm nodule at pressure points or in the podal region. Circumscribed calcinosis is a nodule resulting from dystrophic calcification, with lesions arising most often at sites of repeated or previous trauma: pressure points, paw pads, and areas of injury (Hnilica and Patterson, 2017). It more often affects young rapidly growing dogs, with the German Shepherd Dog, Boston Terrier, and Boxer being predisposed; it produces firm, well-circumscribed, generally solitary nodules of 0.5 to 7 cm, located in the subcutaneous tissue, from which a whitish, chalky, or pasty material may exude (Hnilica and Patterson, 2017). These nodules are non-painful, except precisely when they are located within the paw pads. Diagnosis combines cytology, which shows calcific fragments and granulomatous inflammation, histopathology, and, when needed, radiography to demonstrate calcific deposits lodged deep within the metacarpal or metatarsal paw pads (Hnilica and Patterson, 2017). Surgical excision is curative. It must be distinguished from diffuse calcinosis cutis, which is observed primarily in the context of hyperadrenocorticism (Miller et al., 2013).
8 Common Symptomatic Management of Hyperkeratosis and Fissures
Whatever its cause, fissured podal hyperkeratosis calls for transversal symptomatic management aimed at softening the stratum corneum, restoring the barrier, and protecting the paw pad from weight-bearing, while etiological treatment, when available, is conducted in parallel. This practical dimension, often the only one accessible in incurable hereditary or idiopathic forms, deserves to be addressed on its own terms.
The first approach is keratolytic and moisturizing. Urea at high concentrations, from forty to fifty percent, is a keratolytic agent of choice for hyperkeratotic dermatoses: it dissolves intercellular matrix proteins, loosens the stratum corneum, and simultaneously hydrates the underlying epidermis, while enhancing the penetration of associated active ingredients (Starace et al., 2020). Salicylic acid at concentrations of around ten percent, combined with regular trimming of excess horn, markedly reduces paw pad hyperkeratosis and associated lameness (De Lucia et al., 2019). Emollient balms based on essential fatty acids and essential oils, applied daily, improve the condition of the stratum corneum and prevent fissuring (Catarino et al., 2018; Viaud et al., 2025).
The second approach is barrier support and mechanical protection. In split paw pad dermatosis as well as in hereditary hyperkeratoses, paw pad protection measures — boots and bandages — combined with barrier-reinforcing treatment provide benefit where no single treatment prevents relapses (Utzmann et al., 2025). In working dogs, preventive application of a balm before exercise limits the development of lesions (Bouvier et al., 2020).
The third approach targets secondary infection and fissure inflammation. Surface cytology guides the choice of a topical antiseptic or antifungal agent, whose efficacy in reducing bacterial and yeast loads on the foot has been demonstrated (Ortalda et al., 2016); antiseptic and keratolytic shampoos and soaking of crusted lesions usefully complement this care (van den Broek and Horváth-Ungerböck, 2011). Given the chronic and recurrent nature of most of these conditions, owner education, explanation of the importance of daily topical care, and a follow-up schedule determine compliance and long-term outcome.
Pain and lameness management must not be neglected, even though it constitutes the primary reason for the consultation. Deep fissures and burns are painful and warrant appropriate analgesia and relative rest; in the specific case of corns, when conservative and surgical measures fail, tenotomy of the superficial digital flexor tendon provides immediate relief by altering the phalanx loading pattern (Martinez et al., 2021; Guilliard and Doughty, 2022).
Conclusion
Paw pad dermatoses share a common final pathway — hyperkeratosis — which makes them clinically similar and diagnostically deceptive. Thus, systematic reasoning takes priority over pattern recognition: characterizing the elementary lesions, determining whether involvement extends beyond the paw pad, distinguishing involvement of the cornified pad from that of the interdigital spaces, placing the clinical picture in its context of breed, age, geographic origin, and systemic signs, then confirming by histopathology and, as appropriate, by genetics, serology, molecular biology, or hepatic workup. Ultimately, prognosis ranges from a purely cosmetic condition, such as nasodigital hyperkeratosis, to the fatal outcome of hepatocutaneous syndrome, which gives diagnostic rigor direct prognostic and therapeutic significance. When etiological treatment is unavailable, rigorous symptomatic management of the stratum corneum, the barrier, and pain remains, in itself, a tangible benefit for the animal.
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References
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