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Sebaceous Adenitis THE FACTS NOT FICTION
Just what is Sebaceous Adenitis ?
To understand this owners need to imagine hair anatomy as such we commence with these facts:
Most omnivores and herbivores (horses, cattle, pigs, rats, mice e.g.) have simple hair follicles (HF)s, in which primary and secondary HFs are arranged individually and each infundibulum contains one hair shaft (HS). Carnivores (dogs, cats e.g.) have compound follicles. Extending vertically from the epidermis to the base of the HF, the anagen HF can be divided into three major anatomic regions:
1. The infundibulum which extends from the opening of the HF to the point (approx. the opening of the sebaceous gland duct). 
2. The isthmus which extends from the lower end of the infundibulum to the interface between the completely cornified inner root sheath (IRS) and the first non-cornified cell of Huxley`s layer. In the isthmus of a telogen follicle the outer root sheath (ORS) undergoes trichilemmal cornification (a telogen follicle has no IRS). 
3. The inferior portion which extends from the last cell in which trichohyalin granules can be seen to the base of the HF. It is composed of a suprabulbar and a bulbar region. In the suprabulbar region IRS differentiation can be identified with the Huxley layer being the inner layer and the Henley layer being the outer layer. The bulbar region is composed of matrix cells with intermingled melanocytes. The inferior portion regresses during catagen and is thus only present in anagen follicles. From the outside to the inside the anagen HF can be conceptualized as an outer tube (ORS) surrounding an inner tube (IRS). Between the outer and the inner tube histologically barely visible cells, called the companion layer, are located. The two tubes surround the hair shaft (HS). Together with the IRS and the companion layer the HS arises from the germinative cells of the follicle (known as matrix cells) by trichogenic (cortex) and medullary (medulla) cornification, respectively. The matrix cells are located at the base of the follicle and form the bulb. Within a concavity of the bulb the dermal papilla (DP) is located surrounded by a thin basement membrane. In the catagen stage the inferior portion of the HF regresses and the DP becomes devaginated. 
Histologically an increased number of apoptotic cells in the outer sheath and partial replacement of the inner sheath by trichilemmal cornification is visible. Catagen can only be appreciated in longitudinal sections of skin biopsies. In the telogen stage the inner sheath cornification is completely replaced by trichilemmal keratin produced by the ORS. 
In the majority of these dysplastic disorders a HF is formed during organogenesis and the clinical picture first becomes evident when the HF starts to cycle (usually within the first 1 to 3 years of life). Nevertheless, a genetic basis for these diseases is assumed. In the majority of these cases a hair shaft of insufficient structural quality is formed and thus the hair shaft breaks easily if it penetrates the follicular ostium. Any inflammatory skin disease may generate a telogen arrest, of unknown mechanism .Perifolliculitis is seen mainly in leishmaniasis and sebaceous adenitis and could also lead to a telogen arrest. Granulomatous perifollicular reaction is very often seen in leishmaniasis. Leishmaniads are not always visible. Alopecia is more or less prominent. The face and ears are frequently involved. Seborrhoea may be severe and hyperkeratosis could contribute to the loss of hair. Sebaceous adenitis is characterized by the destruction of sebaceous glands by a granulomatous reaction, without hair follicle involvement. Lesions are more or less nummular, particularly in short-haired dogs, and seborrhoea may be severe, particularly in long haired dogs (Samoyede) in which alopecia is less prominent. Alopecia due to chemotherapy and postclipping alopecia are also due to telogen arrest The hair cycle is influenced by genetics, intrinsic and extrinsic factors. Alopecias associated with hair cycle abnormalities seem to occur because the hairs remain in telogen and fail to re-enter anagen. There are many causes of alopecia. There are many diseases that appear to be associated with hair cycle abnormalities. These include endocrine dermatoses, alopecia X, some patterned alopecias, cyclic flank alopecia, post clipping alopecia, and anagen/telogen defluxion. Many nutrients are used to stimulate hair growth, including biotion and paprika. The addition of paprika (Capsicum tetragonum) to the food increases the intensity of hair colouration and stimulates the hair growth, particularly during shedding in fact I today advised an owner to include this to the daily diet of their Havanese whose coat has been lost with unknown veterinary cause. It is also possible to prevent the reddening of the coat of dogs with black coats by enriching the diet with tyrosine. The response time varies according to the hair cycle. If the majority of hairs are in the telogen phase they are replaced more quickly. The hairs that redden during shedding remain red even after supplementation of aromatic amino acids.Some dogs may have a preferential loss of guard hairs resulting in the appearance of a “puppy coat” but It is important for all owners to realize that, with few exceptions, histopathology cannot differentiate endocrine diseases from other causes of non-inflammatory alopecia. Hair loss can be divided into two basic categories: traumatic and non-traumatic. Traumatic alopecia is often associated with pruritus in which the dog is scratching the hair out. Often linked with food intolerances. Occasionally its caused by parasitic infestations but other times it is not , it’s the differentiating between the two that matters . Then there is the simplistic that as human beings we have all been to the hairdressers or barbers and they’ve told us that we have split ends, have you ever given thought to this matter of fact diagnosis?, The reality is that you haven’t even given it a thought because you hear it so often in all walks of life, rather like this new buzzfeed sweeping the Havanese breeding internet known as SA (sebaceous adenitis ) Granulomatous sebaceous adenitis is a genetic disease characterized by destruction of the sebaceous glands, which gradually disappear, causing keratinization disorders in the hair follicle with alopecia and the formation of hair flanges. The lesions appear gradually and can be localized in any region of the body . All breeds can contract this disease, but there are some clear breed predispositions The treatment requires localized care (keratin modulation shampooing) and general treatments: essential fatty acids corticotherapy, cyclosporine, synthetic retinoids , so let’s take a look at it and why all of a sudden it is becoming a greater deal than it factually is ! After all surely by now all owners realise that food plays a fundamental role in cutaneous homeostasis and in the treatment of many inflammatory dermatoses. The study of the diet is therefore an integral part of the dermatological history. The correction of dietary imbalances (with respect to zinc and essential fatty acids in particular) is a necessary factor in good dermatological therapy.
It is important to challenge ideas that impede the management of chronic pruriginous dermatitis on a daily basis. These include the harmfulness of food based on their origin, the value of IgE doses of dietary allergens, the absence of flea infestation opportunities and the harmfulness of short-term corticosteroid therapy.
The treatment of keratinization disorders or allergenic dermatites involves the use of nutrients that reinforce the skin barrier function, or even play an anti-inflammatory role. The future is open to the possible use of food for prophylactic purposes (probiotics, essential fatty acids, etc) in animals at risks of skin disease. Is SA simply being used as a big bad wolf by some new to the breed and as we are fully aware it is not a new disease by any meansSo lets get back to basics of hair anatomy, so here goes ………………….lets start with the norm of split ends after all it happens in all mammals with hair ,Trichoptilosis- a longitudinal splitting of the hairs (split ends) may be an acquired disorder from over grooming, but has been reported as a hereditary disorder in three Golden Retrievers. Medullary trichomalacia- is an unusual disorder where the medulla vacuolates. This may be an acquired disorder but was reported in six German Shepherd Dogs. Hairs on these dogs felt thicker and stiffer and broke easily. However I have also seen this in Havanese , because new owners don’t realise it exists it appears an anomaly. ! This will usually resolve with the next shed cycle but may recur. I must stress that SA is currently and in my honest opinion (and frankly this is all you shall get ) being used by some to make themselves appear vastly more knowledgeable than they really are. This is more about creating ripples in mill ponds , a need to fulfil a vacant hole within the lives of some and herein lies much ado about nothing. Don’t get me wrong and don’t misinterpret what I am saying BUT, SA has been around for decades and in many breeds . What most don’t realise is that disease often follows a specific pattern, they are usually linked with another disorder , often as in life bad things come in pairs… Congenital hypotrichosis- is a term used for animals that are born without their normal haircoat or who have non-colour linked alopecia with in the first month of life. This has been described in American Cockers, Belgian Shepherds, German Shepherds, toy and miniature Poodles, Whippets, Beagles, French Bulldogs, Rottweilers, Yorkshire Terriers, Labradors, Bichon Frise, Lhasas and Basset Hounds. These dogs may develop hyperpigmentation and seborrhea and may also have abnormal dentition just as shorter leg stature in dogs is linked with early onset cataracts . Inherited alopecias have few known specific therapies. Dietary manipulations, bathing and nutritional supplements have been proposed but have not been shown to be absolutely effective, I tend to advise on Melatonin for acquired or hereditary hair loss. With colour linked hair loss. Clinical signs are usually first seen at 4 weeks of age. This is the time breeders should start to notice that something isn’t quite right. The first change may be a lack of luster in the black hairs that would normally shine noticeably. As the alopecia progresses an excessive scaliness may occur in affected areas. Colour-linked alopecias are inherited alopecias that occur at a young age in specific coat colours. Black hair follicle dysplasia- occurs in bi-colour or tricoloured coats in the black haired regions only. The disorder appears to be an autosomal recessive disorder of pigment transfer and hair cuticles which leads to hair breakage. This disorder has been seen in Bearded Collies, Border Collies, Basset Hound, Papillion, Saluki, Beagles, Jack Russells , American Cockers, Schipperke, Cavalier King Charles Spanies, Dachshund, Gordon Setter, Large Munsterlander and Pointers. Colour dilute alopecia (colour mutant alopecia)- occurs in diluted coats (blue, fawn), but not all dogs with a blue or fawn coat will be affected. This disorder appears to be a polymorphic disorder of melanin transfer and storage leading to large clumps of melanin that break the hair cuticle. If you have a dog that has recurrent ear infections of the skin and/or ears then ask your vet to check that it isn’t a hypothyroid dog these are sometimes the only clinical signs observed. It pays to understand disease ALL disease, it may not be your rise to fame but it should give owners a far better understanding of the health status of the breeds they enjoy. Hyperestrogenism may occur in association with cystic ovaries, testicular tumors, or from exogenous estrogen supplementation. Estrogen is a known inhibitor of anagen initiation; therefore, bilaterally symmetrical alopecia sparing the head and distal extremities is a common clinical presentation of hyperestrogenism. Other dermatological signs include comedones, seborrhea, hyperpigmentation, and recurrent infections. Now lets look at one most will never have heard of , ALOPECIA X This condition has gone by many names including adult-onset hyposomatotropism, growth hormone-responsive alopecia, pseudo-Cushings disease, castration-responsive alopecia, biopsyresponsive alopecia, and, more recently, adrenal hyperplasia-like syndrome. This is a common condition seen in Poodles and the Nordic and “plush-coated” breeds. The pathomechanism of the alopecia is not known but appears to involve a defect in anagen initiation or maintenance. The alopecia develops in adult dogs between 1 and 10 years of age and occurs equally in males and females regardless of their neuter status. The alopecia may first appear as a primary loss of guard hairs progressing to complete alopecia of the neck, tail, perineal region, caudal thighs, and ultimately the trunk. Histopathology can be used to confirm that the alopecia is non-inflammatory and help rule out inflammatory causes of alopecia such as sebaceous adenitis, which can also be seen in quite a few breeds.

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