In the horny layer anucleated cornified keratinocytes (corneocytes) adhere tightly to each other thanks to intercellular lipids. They are protected from the environment by a lipid barrier formed by an emulsion of sebum from the sebaceous glands and sweat from the apocrine glands. Due to the enzymatic action of the cholesterol-chymase, which digests the intercellular lipids in the most superficial layer of the horny layer, the outer corneocytes detach individually and are lost in the environment, whilst new keratinocytes from the deeper epidermal layers differentiate to corneocytes and come to the surface. This turnover is perfectly in balance in the normal epidermis, and individually detached corneocytes are too small to be appreciated macroscopically. In "dry seborrhea" corneocytes detach in large aggregates which are macroscopically appreciated as "scales" or "dandruff". An increased horny layer production, a defective lipid barrier or a decreased destruction of the stratum corneum are the main caused of dry seborrhea.
A. Excessive production
In most cases dry seborrhea is caused by an excessive production of the cutaneous horny layer, due to a congenital defect, a reaction to external or internal injury, or to metabolic causes.
Mild to moderate inherited dry seborrhea is often seen in particular breeds, such as e.g., the doberman. In these animals small white scales may be easily seen on the dorsum and treated with shampoos containing a combination of sulphur 2% and salicylic acid 2%. Oral or topical essential fatty acids may have a useful cosmetic effect in these cases. American cocker spaniels and, to a lesser extent, European cocker spaniels, may suffer from primary idiopathic seborrhea. In these animals the epidermal turnover is much higher than that of normal beagles. Clinically affected animals show excessive scaling, especially in the interdigital areas, as well as follicular casts. This condition may be alleviated with administration of vitamin A (600-800 IU/kg BID) or retinoids (isotretinoin or etretin 1-2 mg/kg BID).
Ichthyosis is a congenital disease characterized by hyperkeratosis, which may be extreme in severe forms. One form of ichthyosis, epidermolytic hyperkeratosis, is characterized by epidermal hyperproliferation. Retinoids and keratolytic shampoos (sulphur-salicylic acid) may decrease the severity of the clinical signs, however no cure is possible.
ii) Reaction to external injury
Against damage from the environment, the epidermis is able to react with hyperplasia and increased cell turnover. The cells reach the skin surface before they are completely differentiated and a defective horny layer is produced. Cells may still have their nuclei (parakeratosis) and form an excessively thick stratum corneum (hyperkeratosis), which may be lost in large scales (dandruff), caused by both excessive production of corneocytes and defective digestion of intercellular lipids. External noxae are represented by physical trauma and infectious agents.
a. Physical trauma. Thickening of the epidermis and of the horny layer is an important means of defense against several physical traumas, such as mechanical pressure and friction (e.g., licking, scratching) or sun light. Avoidance of such traumas leads to normalization of the skin.
b. Infectious agents. The same process occurs as means of defense against infectious agents, such as bacteria, Malassezia or Cheyletiella or Sarcoptes mites, and as reaction to their irritant products (bacteria and yeasts) or feeding activity (mites). By increasing the epidermal turnover and surface scaling, the body tries to eliminate these pathologic agents from the skin surface.
iii) Reaction to internal injury
A dry seborrhea may be the result of inflammatory infiltrates located within the epidermis. This infiltrate may form pustules and collarettes or may be represented by an interface dermatitis.
a. Pustules and collarettes. Diffuse exfoliative diseases, such as superficial spreading pyoderma and pemphigus foliaceus feature large and dry collarettes which may appear as scales. Collarettes are the borders of broken pustules and vesicles, where the bottom of the primary lesion has dried out or healed. Usually these lesions are distributed in a cyclic-polycyclic or serpiginous pattern, and may present some mild exudation at the borders, witness of their origin. In these cases performing an impression cytology from these exudative areas may lead to the diagnosis. In case of pyoderma intracellular bacteria are seen in degenerated neutrophils and a systemic and topical shampoo therapy are advised. In case of pemphigus, acantholytic cells admixed with healthy neutrophils may suggest the diagnosis, which has to be confirmed by a skin biopsy. Therapy is based on immunosuppressive drugs.
b. Lymphocytic exocytosis. Rare diseases such as epitheliotropic lymphoma, feline thymoma-associated-paraneoplastic dermatitis and some forms of erythema multiforme (the so-called old dog EM) all feature macroscopically cutaneous scaling and microscopically an interface lymphocytic infiltrate in the epidermis. The cause of the desquamation is not clear, it is proposed that sublethal damage to the basal keratinocytes may result in alternate keratinization. For this group of diseases the diagnosis is always histological.
iv) Metabolic causes
Zinc deficiency and amino acid deficiency (as present in metabolic epidermal necrolysis--also called hepatocutaneous syndrome or necrolytic migratory erythema--and in generic dog food dermatosis) may lead to an epidermal hyperproliferation with defective keratinocyte maturation and horny layer formation. Histologically thick layers of hyper-and parakeratosis are observed, clinically evident as tight adherent scales. The localization of the desquamation is very similar for all of these diseases, i.e., around the eyes, lips, food pads, however the reason for this is unknown. The diagnosis of these diseases usually is histological. Two genodermatoses caused by zinc deficiency are known: the lethal acrodermatitis of the bull terrier and the zinc responsive dermatosis. The first one is a fatal diseases restricted to bull terriers in which a defective zinc absorption is associated to hyperkeratotic ulcerative skin lesions and immunodeficiency. The zinc responsive dermatosis is a milder disease a seen in northern breeds which may be controlled with zinc sulphate administration (10 mg/kg BID, mixed with food). Generic dog food dermatosis may be cured by feeding a well balanced diet. The lesions of metabolic epidermal necrolysis are mostly mainly associated to end-stage liver degeneration or glucagonoma and may be temporarily improved by administering amino acids (e.g., eggs).
B. Defective lipid barrier and skin dehydration
i). Essential fatty acid deficiency
This condition is extremely rare and has been reported mainly in experimental settings. A deficiency in cutaneous desaturase enzymes, leading to insufficient conversion of essential fatty acids may be present in some atopic dogs. In animals with deficiency of EFA the coat may become dull and show excessive dry scaling. Fatty acids are part of the intercellular lipis and of the superficial lipid film, which protects the epidermis from water loss. Thus a defective protective barrier may lead to epidermal dehydration and scale formation. Essential fatty acids of both groups (omega 6 and omega 3) may improve coat condition in these dogs, however it is often necessary to administer them for a long period of time (minimum 2 weeks, often months) before seeing the results.
ii). Water balance disturbances
In animals which live in very dry climates or in houses with heating or air-conditioning an excessive epidermal water loss may lead to an abnormal desquamation. The same may happen if the animal is washed too frequently with aggressive shampoos (e.g., benzoyl peroxyde), which increase the transepidermal water loss. In these cases environmental humidity should be corrected and a conditioner can be applied to the animal's coat.
iii). Sebaceous gland alterations
Sebum is a very important constituent of the superficial epidermal lipid film and it contains antibacterial products. The deficiency of the surface lipids may favour epidermal dehydration and the decrease of antibacterial factors may favour bacterial colonisation. In both situations a dry seborrhea may be observed (see above). There are at least three common causes of sebaceous glands alterations.
a. Sebaceous adenitis. In this disease, sebaceous glands are the target of pyogranulomatous to granulomatous inflammation and in some cases they eventually disappear completely from the dermis. A decreased or absent production of sebum can lead to abnormal desquamation, particularly in the follicular infundibulum. This is seen macroscopically with a typical form of scaling surrounding the hair shafts, the so-called "follicular casts" seen in sebaceous adenitis. The diagnosis of this disease is histological. The therapy is based on the daily use of 70% propylenglycole spray on the coat or on the administration of retinoids.
b. Leishmaniasis. Dogs affected by the scaling cutaneous form of leishmaniasis often have histologically a granulomatous infiltrate in the sebaceous glands and clinically show large grey "asbestiform" scales which tightly adhere to the cutaneous surface and to the hair shafts. These scales may be the result of the inflammatory infiltrate in the sebaceous glands, however they are different from those of sebaceous adenitis, maybe due to the presence of the parasites in the superficial dermis and to an interface dermatitis. The diagnosis of leishmaniasis is based on the observation of the parasite in skin biopsies, bone marrow or lymph-node smears, on serological tests or on PCR. The therapy is based on injectable antimonials and often life long allopurinol administration.
c. Hyperadrenocorticism. In this endocrine disease sebaceous gland hypotrophy and hypoproduction are seen. The skin feels very dry and dry seborrhea may be observed. Furthermore the epidermis is very thin and a lamellar keratosis is common. Other signs typical of hyperadrenocorticism, such as polyuria, polydypsia, polyphagia, pendulous abdomen, panting, thin skin and non-inflammatory symmetrical alopecia lead to the diagnosis, which has to be confirmed by specific hormonal tests and diagnostic imaging procedures.
C. Decreased horny layer destruction
Some types of ichthyosis, due to decreased horny layer destruction, have been described in man. In these diseases there is a proven epidermal lipids defects, such as e.g. deficiency of cholesterol sulphatase in recessive X-linked ichthyosis. Similar conditions are very rarely described in domestic animals, and are mostly fatal.
3. GREASY SEBORRHEA
In greasy or oily seborrhea there is an excessive sebum production or a cornification defect leading to an alternate epidermal lipid metabolism. The coat feels greasy and dirties the hands when touching it. Greasy seborrhea may be congenital or acquired.
A localised congenital sebaceous gland hypertrophy may be seen in sebaceous or compound nevi. The surface of these lesions is greasy and often hyperkeratotic. The clinical diagnosis is confirmed by a skin biopsy. Therapy is palliative, topical products (benzoyl peroxide shampoo, human exfoliative cleansing products) or oral retinoids may be administered to temporarily decrease the signs.
Some breeds, such as some terriers, may develop an idiopathic greasy seborrhea on their dorsum, which may be controlled with twice weekly-twice monthly sebolytic shampoos (tar based) or oral isotretinoin (1-2 mg/kg SID).
Acquired greasy seborrhea may be the result of Malassezia infection or of a hormone producing testicular tumour.
i) Malassezia infection
Cutaneous yeast infection often complicates primary skin diseases, such as allergy or endocrine diseases. The skin is initially erythematous (inflammation due to irritant yeast metabolites, such as zymogen) and with time turns hyperpigmented, thickened and covered by yellowish waxy scales. This condition may be very pruritic, is initially limited to the ventral areas of the neck, axillae and groin, but may involve most of the body. A typical "cheesy" smell accompanies this infection. Diagnosis is obtained with the cytological examination of apposition samples or of material collected with a superficial scraping and smeared on a glass slide. Histologically a hyperplasia of the epidermis and of the adnexa is observed. Therapy is usually based on the administration of ketoconazole (5-10 mg/kg BID) and chlorhexidine (better or associated to miconazole) biweekly shampoos for 3 to 4 weeks. Identification and correction of the underlying disease is essential for prevention of recurrences.
ii) Testicular tumours
Some hormone producing testicular tumours may cause sebaceous gland hyperplasia and a greasy seborrhea similar to that observed in Malassezia infection. Furthermore most of the times this skin condition is complicated by this yeast infection.