Nasal hyperkeratosis is characterized by excessive keratin accumulation and thickening of the nasal planum. I see many cases
with just nasal hyperkeratosis and I suspect that some cases that have combined symptoms of nasodigital hyperkeratosis have
different underlying etiologies. To some degree it occurs commonly in older dogs and has been described as being a senile
change. The disease may occur in young or middle aged dogs. Nasal hyperkeratosis has also been seen in dogs with dry eye or
blocked lacrimal ducts. Fissures may occur in affected sites. Some cases will have a more yellowish crusting character to
the hyperkeratosis and this should raise the index of suspicion about underlying inflammatory disease. Generally these cases
do not depigment or loose normal markings. Other differential diagnosis includes pemphigus foliaceus and erythematosus, distemper
virus, zinc responsive dermatosis, genetic dog food dermatosis and lupus erythematosus and leishmaniasis. Asymmetrical cases
may be due to infectious disease and unilateral blocked tear ducts or nasal glands (xeromyteria). Xeromycteria is due to damage
or absence of the nasal gland that functions to keep the nasal planum moist. Biopsy may be indicated to primarily rule out
other differentials. Treatment consists of topical moisturizers such as petrolatum, propylene glycol and vitamin E. In refractory
cases lactic acid moisturizers may be tried. In the most difficult cases a combination of urea/lactic acid and salicylic acid
(Kerasolv, DVM Pharmaceuticals) or tretinoin gel may be helpful. Douxo ® Seborrhea Spot-on with 1% phytosphingosine as a spot
on application twice weekly has also proven to be a palliative treatment in many cases.
Labrador retrievers are also affected by hereditary nasal parakeratosis.(Page, Paradis et al. 2003; Peters, Scott et al. 2003)
This is believed to be an autosomal recessive trait and in one report 16 of 18 dogs shared common ancestors but none of the
sires or dams of affected dogs were affected. (Page, Paradis et al. 2003) This clinically will appear as nasal hyperkeratosis
though cytology and biopsy is characterized by parakeratosis and multiple intracorneal serum lakes and superficial interstitial-to-interface
lymphoplasmacytic dermatitis.(Peters, Scott et al. 2003). Treatment is similar to other nasal hyperkeratotic syndromes but
some may also respond to antibiotics and tacrolimus.
Footpad Hyperkeratosis – Hard Pad Disease
Footpad hyperkeratosis can be seen as a separate entity or in association with nasal hyperkeratosis. There are different types
of hard pad disease seen. The first is a crusting, thickened pad. These cases are most common in pemphigus foliaceous, zinc
responsive dermatosis, distemper infections and metabolic epidermal necrosis. These pads may be painful and cause lameness.
Rare cases of pemphigus foliaceus present with just pad disease but most commonly these cases will have other lesions suggesting
this etiology. Biopsies are the most helpful diagnostic procedure. Treatment will depend on the underlying cause. The second
form is pads that have excessive fronds of normal appearing keratin. This is most obvious at the margins of the pads and represents
overgrowth of the normal keratin mounds of the pads. Inflammation and exudate are not present. Lameness and pain are not detected.
This condition appears more as if the pads just grow abnormally fast, do not desquamate normally or if there is conformational
issues (improper wear). Familial footpad hyperkeratosis has been seen in Irish setters and the Dogue de Bordeaux and may have
an autosomal recessive inheritance. Other breeds also seem to be over represented and these include the Kerry blue terrier,
Labrador retriever and Golden retriever. The author has also seen this entity in a litter of Akitas. In the familial form
of the disease symptoms are usually present by 6 months of age. Clinically all pads are usually affected and can create severe
lameness with crusting, fissures and pronounced compact keratin that in some cases can produce horns. Histopathology shows
moderate to severe hyperplasia with marked papillated and diffuse hyperkeratosis.
Treatment is symptomatic with topical emollients such as propylene glycol, phytosphingosine and keratolytics as mentioned
in the nasal hyperkeratosis section. If papilloma virus is detected treatment with Imiquimod (Aldara, 3 M) or interferon may
be helpful. Trimming excess pad tissue can also be of value.