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. 2024 May;65(5):514–519.

Nasal planum diseases in dogs

Tim Chan 1,✉, Andrea TH Lam 2
PMCID: PMC11017923  PMID: 38694745

Introduction

A broad range of diseases can affect the nasal planum in dogs, alone or in addition to other cutaneous manifestations; these include keratinization, infectious, immune-mediated, and neoplastic disorders (Table 1). The initial (primary) lesion and distribution, breed predisposition, and presence of other cutaneous signs are helpful in determining the etiology. This article describes key clinical features of diseases that primarily or frequently target the nasal planum in dogs.

Table 1.

Diseases that affect the nasal planum in dogs.

Disease Initial (primary) lesion and distribution on nasal planum Other clinical features Signalment
HNPK Hyperkeratosis — dorsal aspect May progress to crusts, bleeding ulcers from secondary infection or trauma Young dogs (1 to 2 y)
Labrador retriever and greyhound
INH Hyperkeratosis — dorsal aspect May progress to crusts, bleeding ulcers from secondary infection or trauma Middle-aged to older dogs
No strong breed predisposition
American cocker spaniel, English bulldog, miniature poodle, miniature schnauzer, and Doberman pinscher are overrepresented
MCP Erythema, swelling, crust — alar folds and perinasal junction Chronic lesions are fissures, erosions, depigmentation, and loss of nasal planum architecture
Other mucocutaneous locations may be affected (lips, perioral)
Antibiotic-responsive
German shepherd
Cryptococcosis Nodule — nasal planum and bridge of nose Progresses to ulcers, draining tracts
Spread to other organs and systemic disease common
Active dogs (e.g., hunting)
Vitiligo Noninflammatory depigmentation with intact nasal planum architecture (“cobblestone”) — multifocal Multifocal lesions
Considered a cosmetic condition in dogs
Young dogs (median: 2 y)
Rottweiler, Doberman pinscher, and collie appear to be overrepresented
UDS Depigmentation, erythema, swelling — diffusely affecting entire nasal planum Progresses to crusts, erosions/ulcers, alopecia
Other areas include periocular skin and lips
Ocular disease precedes dermatologic signs in vast majority
Middle-aged dogs
Akita, Samoyed, Siberian husky
DLE Diffuse depigmentation, erythema — dorsal half of the nasal planum common Progresses to erosions, ulcers, crusts
Atrophic scarring and dyspigmentation are chronic
Nasal planum commonly the only area affected
Generally, large-breed dogs
German shepherd and its crosses
PF Pustule, purulent crust — dorsal aspect and bridge of nose Progresses to healing depigmentation and loss of nasal planum architecture
Other areas of both commonly affected
Middle-aged to older dogs
Chow chow, shar-pei, and Akita are overrepresented
MCLE Erosions and ulcers — symmetrical ± perinasal Progresses to crusts, secondary depigmentation, and loss of nasal planum architecture
> 1 perimucosal region often affected
German shepherd
AISBD Erosions and ulcers (blisters) — no clear distribution, multifocal Progresses to crusts (hemorrhagic), healing depigmentation, and loss of nasal planum architecture
> 1 region often affected
German shepherd (MMP)
Alar fold arteriopathy Linear ulcer/fissure — rostrolateral alar folds Crust (hemorrhagic), healing (secondary) depigmentation German shepherd
Dermal arteritis of the nasal philtrum Deep, V-shaped ulcer — center of the nasal philtrum Progresses to crust (hemorrhagic), healing (secondary) depigmentation, and loss of nasal planum architecture Saint Bernard
Cutaneous histiocytosis Nodule, swelling — no predilection site May develop crusts, erosion/ulcers, loss of nasal planum architecture on nodule/swelling
Lesions are commonly multifocal
Systemic histiocytosis is described
Bernese mountain dog is predisposed to systemic histiocytosis
ECTL Variable clinical phenotype — depigmentation may extend beyond border of nasal planum Nasal planum seldom the only area affected Older dogs
SCC Nodule — usually asymmetrical, no known predilection site May develop crusts, erosions/ulcers, draining tracts on nodule Older dogs

HNPK — Hereditary nasal parakeratosis; INH — Idiopathic nasodigital hyperkeratosis; MCP — Mucocutaneous pyoderma; UDS — Uveodermatologic syndrome; DLE — Discoid lupus erythematosus; PF — Pemphigus foliaceus; MCLE — Mucocutaneous lupus erythematosus; AISBD — Autoimmune subepidermal blistering diseases; MMP — Mucous membrane pemphigoid; ECTL — Epitheliotropic cutaneous T-cell lymphoma; SCC — Squamous cell carcinoma.

Diagnostic procedures

The initial lesion is crucial to understanding the pathogenesis but is easily missed due to rapid progression to chronic, secondary lesions that offer less diagnostic value. A thorough history aids in establishing the type and distribution of the initial lesion. For instance, depigmentation of the nasal planum can occur at the onset of disease (e.g., vitiligo), before secondary lesions, such as ulceration or crusting, appear. Conversely, in other cases, secondary depigmentation may develop as a result of healing following erosion or ulceration.

A physical examination warrants careful attention to the lesion type and location within the nasal planum. Lesions include hypopigmentation or depigmentation, erythema, erosions, ulcers, crusts, loss of architecture (“cobblestone” appearance), fissures, and nodules. Certain diseases also have characteristic anatomical distributions of lesions on the nasal planum, including the dorsal ridge, alar folds, and philtrum; or are multifocal to diffuse.

Cytology helps confirm the presence of microorganisms and may reveal neoplastic cells or acantholytic keratinocytes. Microbial culture and susceptibility testing can further support an infectious cause and guide antimicrobial selection. However, detection of microorganisms does not always indicate an infectious etiology, as bacteria and Malassezia are common secondary occurrences to any inflammatory process affecting the nose. Primary infections typically do not present exclusively as nasal lesions, except in specific instances such as certain dermal and subcutaneous mycoses.

Physical examination and cytology or culture are often inadequate for definitively diagnosing most nasal planum diseases, except for those with a distinct clinical phenotype, such as dermal arteritis of the nasal philtrum. Therefore, the authors recommend skin biopses for histopathological evaluation. Ideally, 2 punch biopsies (4 to 6 mm) of early lesions should be taken to capture the pathomechanistic role of the disease. Older lesions often lack primary histological changes of the underlying process and are more likely to have microbial overgrowth. For the best chance of a definitive diagnosis, it is imperative to sample fully affected skin rather than attempt to straddle the margin between normal and abnormal skin, especially if using a small biopsy punch. Similarly, sampling solely from an ulcer may not provide a conclusive answer due to the absence of epidermis. Key features for each disease are presented in Table 1.

Keratinization disorders

Hereditary nasal parakeratosis

Hereditary nasal parakeratosis is an autosomal recessive disorder of the SUV39H2 gene in Labrador retriever and greyhound dogs that causes aberrant keratinocyte terminal differentiation of the nasal planum (1,2). Lesions usually appear in puppies and young dogs and consist of adherent scale, hyperkeratosis, and fissures on the dorsal ridge of the nasal planum, which may predispose to secondary infections (1,2). Affected dogs are otherwise healthy.

Idiopathic nasal or nasodigital hyperkeratosis

Idiopathic nasal or nasodigital hyperkeratosis causes proliferative hyperkeratosis on the dorsal ridge of the nasal planum, with or without paw pad involvement (3). Lesions are considered cosmetic and asymptomatic, but occasional deep fissuring can predispose to secondary Malassezia or bacterial infections. Overrepresented breeds include American cocker spaniel, English bulldog, miniature poodle, miniature schnauzer, and Doberman pinscher (3).

Infectious causes

Mucocutaneous pyoderma (MCP)

Mucocutaneous pyoderma is a bacterial dermatitis commonly affecting German shepherd dogs and their crosses (4). Early lesions are erythema, swelling, purulent exudate, and crusts, followed by ulcers, fissures, hypopigmentation/depigmentation, and loss of normal architecture. Predilection sites include the alar folds and perinasal areas. The nasal planum can exclusively be affected, but other mucocutaneous junctions, e.g., lip margins, periocular region, and vulva, may be involved (4). Cytological examination of erosions or exudate typically reveals numerous bacteria and inflammatory cells. Mucocutaneous pyoderma responds to topical or systemic antibiotics (e.g., cephalexin, 25 to 30 mg/kg, PO, q12h), empirically or based on culture and susceptibility testing. Mucocutaneous pyoderma shares clinical and histopathological features with discoid lupus erythematosus, but the latter has cytotoxic interface dermatitis that MCP lacks. As such, distinguishing between these 2 diseases often relies on clinical differentiation first involving an antibiotic trial.

Subcutaneous and cutaneous mycoses

Nasal planum lesions as the sole clinical sign is rare for most mycotic infections except cryptococcosis (5). Cryptococcus neoformans and C. gattii are dimorphic fungi present in pigeon feces, soil, and plant matter (5). These are considered primary fungal pathogens as they can cause infection in immunocompetent individuals through inhalation of blastospores from the environment (5). Clinically, cryptococcosis presents as deep nodules that form a characteristic “beak-shaped” bump encompassing the nasal planum and bridge of the nose. Ulceration and draining tracts may develop on the nodules. The condition is more common in cats than dogs (5). Yeast or spherules of Cryptococcus are typically numerous on cytological and histological evaluation (5).

Immune-mediated or autoimmune diseases

Vitiligo

Vitiligo is putatively an acquired autoimmune disease that targets melanocytes in the skin, resulting in depigmented macules and patches without affecting the nasal planum architecture (6) (Figure 1 A). Leukoderma and leukotrichia are commonly seen in other areas of the body. This is considered a cosmetic disease in dogs. The few reports of canine vitiligo report overrepresentation in rottweiler, Doberman pinscher, and collie dogs (6). Early signs are usually noticed in young dogs (median age: 24 mo) (6). The clinical features are normally sufficient for diagnosis, but skin biopsies of areas of early depigmentation for histopathological examination can provide a definitive diagnosis (6).

Figure 1.

Figure 1

Clinical lesions of diseases that commonly target the nasal planum in dogs. A — Vitiligo in a German shepherd. Varying degrees of hypopigmentation to complete depigmentation are noted. In contrast to discoid lupus erythematosus (DLE), the normal “cobblestone” architecture is entirely intact. B — Early DLE with secondary infection in a Labrador retriever. Note the loss of pigment affecting the nasal planum. Architecture has not yet been entirely effaced, but a layer of crust has formed over the dorsal ridge, along with mild erosion. C — Chronic DLE in a mixed-breed dog. Depigmentation is well-established. There is almost complete loss of normal “cobblestone” appearance to the nasal planum and expansion of the nares due to prior destruction of the nasal tissues during the active phase of disease. D — Pemphigus foliaceus in a Labrador retriever cross. Note the heavy crusts on the nasal planum, with erosions and ulcers affecting the rostral aspect of the nose. E — Nasal arteritis in a Saint Bernard. Note the well-demarcated, wedge-shaped ulcer located directly over the nasal philtrum.

Photographs courtesy of Dr. Andrea Lam (A, B, D, and E) and Dr. Jennifer Schissler (C).

Uveodermatologic syndrome (VKH-like syndrome)

Akita, Samoyed, and Siberian husky dogs are believed to be predisposed to uveodermatologic syndrome, an immune-mediated disease that targets melanocytes or antigens in both skin and ocular tissues (6). The median age of onset is 3 y (6). Ocular disease (uveitis, vision loss) precedes dermatologic signs in most cases (6,7). Diffuse depigmentation of the entire nasal planum is the first cutaneous change, often with erythema and swelling, followed by erosions/ulcers, crusts, and alopecia of the surrounding haired skin (6). The nasal planum is most commonly affected but the periocular skin and lips are also common predilection sites (6). Skin biopsies for histopathological examination should be done on early, active inflammatory lesions (depigmentation, erythema, swelling) (6).

Facial discoid lupus erythematosus (DLE) and mucocutaneous lupus erythematosus (MCLE)

Facial discoid lupus erythematosus is the most common form of chronic cutaneous lupus erythematosus (8). The nasal planum is typically the sole predilection site, which helps distinguish DLE from other diseases. Diffuse depigmentation is usually the first sign, due to cytotoxic interface dermatitis resulting in pigmentary incontinence. Later, depigmented lesions progress to ulcers that form a thick layer of crusts, followed by atrophic or hypertrophic scarring and further dyspigmentation in more chronic stages (8) (Figure 1 B, C). Facial DLE tends to affect middle-aged to older, large-breed dogs, with German shepherd dog and its crosses being overrepresented (8). A rare subtype that may or may not involve the nasal planum, generalized DLE, has been described (9). Mucocutaneous lupus erythematosus is another type of chronic cutaneous lupus erythematosus that also primarily affects middle-aged German shepherd dogs (10). Nasal lesions are not the predominant area affected, accounting for only 20% of cases in one study of 21 dogs (10). In addition, more than half of affected dogs exhibit involvement in > 1 perimucosal site (10). Skin biopsies of areas of early depigmentation are recommended.

Pemphigus foliaceus (PF)

Pemphigus foliaceus is an autoimmune, superficial pustular dermatosis that classically targets the dorsal aspect of the nasal planum, bridge of the nose, pinnae, periocular area, and foot pads (11). However, a truncal variant of PF may spare the nasal planum. Many dog breeds have been reported to develop PF, but the chow chow, shar-pei, and Akita are overrepresented (11,12). This condition usually occurs in middle-aged to older dogs, though dogs of any age may be affected. Intact pustules are fragile and therefore transient, and rarely appreciated grossly, especially on the nasal planum. It is more common to observe crusts with underlying purulent exudate and erosions (Figure 1 D). Cytological examination of intact pustules or purulent exudate underneath a crust may reveal acantholytic keratinocytes, suggestive of PF. However, as staphylococcal pyoderma and pustular dermatophytosis can also cause acantholysis, it is important to rule out both types of infection first. Skin biopsies for histopathology are highly recommended to definitively diagnose PF once infectious etiologies have been ruled out, as treatment involves immunosuppression. Punch biopsies (4 to 6 mm) should encompass intact pustules (when present) or adherent crusts. To optimize preservation of lesions and improve chances of definitive diagnosis, refrain from scrubbing skin or clipping hair before biopsy recovery.

Autoimmune subepidermal blistering diseases (AISBD)

Autoimmune subepidermal blistering diseases are a rare group of diseases driven by autoantibody-mediated disruption of proteins involved in maintaining structural integrity of the basement membrane zone, resulting in vesicle (blister) formation. Autoimmune subepidermal blistering diseases that commonly affect the nasal planum include mucous membrane pemphigoid, bullous pemphigoid, and junctional epidermolysis acquisita (13). The primary lesion is a vesicle, which is fragile and transient, quickly evolving into erosions and ulcers. Hemorrhagic crusts can form over ulcers, but purulent crusting is not a feature. Other body sites are almost always affected. The German shepherd dog is overrepresented for mucous membrane pemphigoid (14). The authors suggest using an appropriately sized punch biopsy or performing a wedge biopsy to extract an intact vesicle whenever feasible. Alternatively, sampling the inflamed edge of a ruptured vesicle for histopathological examination is recommended for definitive diagnosis.

Nasal alar arteriopathy

Nasal alar arteriopathy is a vasculopathy observed primarily in middle-aged German shepherd dogs, characterized by a linear ulcer/fissure on the rostrolateral alar fold (15). Its etiology is unknown but it is suspected to be an immune-mediated vasculopathy with a strong breed predisposition. Profuse arteriolar bleeding can be seen and presents a challenge during tissue biopsy sampling. As a result, empirical treatment with topical and/or systemic immunomodulatory drugs can be considered.

Dermal arteritis of the nasal philtrum

Dermal arteritis of the nasal philtrum presents clinically as a distinct, deep, V-shaped or wedge-shaped ulcer on the nasal philtrum, most commonly affecting Saint Bernard dogs (Figure 1 E). Similar to nasal alar arteriopathy, the clinically distinct phenotype, strong breed predisposition, and challenge in performing biopsies often necessitate a clinical diagnosis and empirical treatment with immunomodulatory drugs.

Histiocytosis

Cutaneous reactive histiocytosis is an inflammatory, lymphohistiocytic, proliferative disorder of unknown etiology, likely involving antigen-driven immunoregulatory disruption (16). Nodules with or without ulcerations on the nasal planum and other areas of the body are common and may wax and wane. Multiple nodules are more common than solitary lesions (16). Systemic reactive histiocytosis is a generalized histiocytic disorder with a known familial occurrence in the Bernese mountain dog (16). Cutaneous nodules in both cutaneous and systemic forms are similar, and hence diagnostic imaging and sampling of internal viscera are warranted to differentiate them. Diagnosis involves deep-tissue biopsies of nodules for cultures to exclude infectious causes and for histopathological evaluation.

Neoplasia

Cutaneous epitheliotropic T-cell lymphoma

The clinical presentation of cutaneous epitheliotropic T-cell lymphoma is highly diverse. Older dogs are predisposed (17). The nasal planum is commonly affected (~28%) but seldom the only location involved (17). Due to the phenotypic variability, initial lesions may include depigmentation, erythema, loss of architecture, crusts, and plaques. Interestingly, depigmentation may not follow a symmetrical pattern, and may extend beyond the border of the nasal planum to cause hypopigmentation/ depigmentation of the rostral muzzle, lips, and in some cases, mucosa. Impression smear cytology of affected sites may reveal numerous lymphocytes, but the authors recommend skin-punch biopsies to demonstrate epitheliotropism.

Squamous cell carcinoma

Squamous cell carcinomas make up 5% of cutaneous tumors in dogs and usually appear as a single nodule on the nose that may ulcerate and bleed (18). Older dogs are more commonly affected. Punch or excisional biopsy or debulking surgery are recommended.

Conclusion

Many diseases can cause lesions of the nasal planum in dogs, but very few affect the nasal planum only, without involving other areas of the body. The initial lesion type and location within the nasal planum are useful clinical clues that help highlight unique features of these diseases. Cytological evaluation of lesions is recommended as an initial diagnostic step to rule out secondary infections; however, most cases warrant histopathological evaluation to reach a definitive diagnosis.

Footnotes

The Veterinary Dermatology column is a collaboration of The Canadian Veterinary Journal and the Canadian Academy of Veterinary Dermatology (CAVD). The CAVD is a not-for-profit organization, with a mission to advance the science and practice of veterinary dermatology in Canada, in order to help animals suffering from skin and ear disease to live the lives they are meant to. The CAVD invites everyone with a professional interest in dermatology to join (www.cavd.ca). Annual membership fee is $50. Student membership fees are generously paid by Royal Canin Canada.

Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (kgray@cvma-acmv.org) for additional copies or permission to use this material elsewhere.

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