Canine Recurrent Flank Alopecia: A Complete Clinical Overview

Canine recurrent flank alopecia (CRFA) is a relatively frequent dermatosis, characterized by the cyclical or seasonal appearance of non-inflammatory alopecia areas, preferentially located on the flanks.

CRFA remains a condition with incompletely elucidated etiopathogenesis and although documentation exists in scientific literature, it deserves an updated synthesis. This article aims to provide an update on current knowledge about CRFA, based on data from scientific publications. We will successively address epidemiology, etiopathogenic hypotheses, clinical presentation and variations, diagnostic approach including differential diagnoses and complementary examinations, typical histopathological characteristics, critical evaluation of proposed therapeutic options, as well as the prognosis of this condition.

Definition and Nomenclature

Several denominations have been used to describe this clinical entity, including “seasonal flank alopecia”, “idiopathic cyclic flank alopecia” or “cyclic follicular dysplasia”. However, none of these terms is perfectly adequate. The alopecia is not always complete (sometimes just changes in color or texture of the coat), it is not strictly confined to the flanks (other areas can be affected), and the seasonal or recurrent character is not systematic in all affected individuals. The term “canine recurrent flank alopecia” is often preferred as it encompasses the most frequent location and the cyclic character often observed, while recognizing these variations. The first formal description of this condition in veterinary literature dates back to 1990 by Scott, who reported cases of fluctuating non-scarring alopecia in five spayed female dogs.

This condition, although visually striking for owners, is considered essentially cosmetic and is not associated with systemic signs or alteration of the animal’s general health.

Appearance giving the impression that the dog has been clipped

Epidemiology

Breed Predispositions

CRFA is described in many canine breeds, but a clear breed predisposition is reported, strongly suggesting an underlying genetic component. This observation repeated in various studies implies that hereditary factors make certain lineages more susceptible to developing the disease. The Boxer is the most frequently cited breed and seems particularly predisposed. Other breeds are also considered at increased risk, notably the English Bulldog, Airedale Terrier, Schnauzer (miniature, standard and giant), Bouvier des Flandres, Doberman, Labrador Retriever, Golden Retriever, Wirehaired Pointing Griffon, and the Affenpinscher. More recent studies have also included the Rhodesian Ridgeback and Staffordshire Bull Terrier among affected breeds. An atypical form of recurrent flank alopecia has been specifically studied in the Cesky Fousek.

CRFA also exists in light-coated breeds

Age of Onset

The age of onset of CRFA is variable, ranging from 1 to 11 years. However, the majority of cases develop the first clinical signs between 3 and 6 years. Specific studies on Boxers and Airedale Terriers have reported an average age of onset around 3.6 years, while another source mentions an average of 3.8 years. The average age at diagnosis is often around 4 years.

Distribution by Sex and Reproductive Status

Initially, some publications reported an overrepresentation of spayed females. However, subsequent observations and broader studies have clearly established that there is no predisposition linked to sex or reproductive status. Males and females, whether intact or neutered, can be affected by CRFA.

Seasonal and Geographic Influence

One of the most characteristic aspects of CRFA is its frequent seasonality. In the northern hemisphere, alopecia typically appears during months with the shortest daylight hours, usually between November and March or April. Regrowth then occurs spontaneously in spring or summer.

Significantly, an inverse correlation has been observed in the southern hemisphere (Australia, New Zealand, Brazil), where the onset of alopecia coincides with the months of short days (austral winter and spring). This observation constitutes a strong argument for the role of photoperiod as a major triggering factor. If classic seasonal environmental factors such as temperature or humidity were paramount, one would expect onset during the same calendar season (e.g., winter) in both hemispheres, which is not the case. The systematic coincidence with decreasing day length (and thus increasing night length) strongly suggests the involvement of a biological mechanism sensitive to light cycles, probably mediated by the pineal gland and associated hormones such as melatonin and prolactin.

However, it is important to note that this seasonality is not an absolute rule. Some dogs may present sporadic episodes, skip a season, or even develop alopecia that becomes permanent after several cycles.

Etiopathogenesis

Unknown Fundamental Cause

Despite breed predispositions and evocative seasonality, the exact etiology of CRFA remains unknown to date. Investigations conducted to identify an underlying systemic endocrine cause have proven unsuccessful. Thyroid profiles, adrenal function tests (to exclude hypercortisolism), and measurements of circulating growth hormones or sex hormones are generally within normal limits in dogs with CRFA. Nevertheless, the hypothesis of a localized alteration at the level of hair follicles, such as a change in the number or sensitivity of hormone receptors, cannot be formally ruled out and remains a possible lead.

Photoperiod Hypothesis

The influence of photoperiod (the daily duration of light exposure) is the etiopathogenic hypothesis best supported by clinical and epidemiological observations. The marked seasonality, correlated with the decrease in day length in both hemispheres, is the main indicator. This hypothesis is reinforced by anecdotal reports describing dogs developing lesions outside the usual season when kept in dark or low-light environments. Conversely, prevention attempts through light therapy (exposure to intense artificial light for 15-16 hours per day during at-risk months) have reportedly shown some success in isolated cases, although controlled studies are lacking to confirm this approach.

Role of Melatonin

Melatonin is a neurohormone primarily synthesized by the pineal gland during periods of darkness; its production is therefore inversely proportional to day length. It plays a fundamental role in regulating circadian and seasonal rhythms, including the hair cycle and seasonal shedding, in many mammalian species. The main hypothesis regarding CRFA postulates that insufficient endogenous melatonin production, or an alteration in its reception or signaling at the level of hair follicles in genetically predisposed individuals, could be a key factor in the pathogenesis. Melatonin could act directly on receptors present on follicular cells or indirectly by modulating the secretion of other hormones involved in the hair cycle, such as melanotropic hormone (MSH) or prolactin. The empirical use of melatonin as treatment is based on this hypothesis.

Role of Prolactin

Prolactin is another hormone whose secretion is influenced by photoperiod, often inversely to that of melatonin (an increase in melatonin tends to decrease prolactin levels). In certain species like sheep, the decrease in prolactin induced by increased melatonin is associated with the induction of winter coat. Studies in mice and sheep have shown that prolactin can have inhibitory effects on the anagen phase (growth) of the hair follicle, potentially reducing hair length, shortening anagen, inducing shedding (exogen), or prolonging the telogen phase (resting). Although no study has specifically evaluated the role of prolactin in CRFA, its involvement in the photoperiodic regulation of the hair cycle makes it a potential actor in the pathogenesis of this condition.

Genetic Factors

The strong predisposition observed in certain breeds (Boxer, Airedale, English Bulldog, etc.) is a major argument for a genetic component in CRFA. Genetic studies have begun to explore this path. A genome-wide association study was conducted on an atypical form of RFA (aRFA) in the Cesky Fousek. This study identified several chromosomal regions (loci) associated with the disease, suggesting a polygenic basis (involving several genes) rather than a single mutation. The analysis highlighted 144 potential candidate genes involved in four main metabolic pathways: collagen formation, muscle structure and contraction (potentially linked to the arrector pili muscle), lipid metabolism (which can influence follicular development signaling pathways such as WNT or SHH), and the immune system. Additionally, genes linked to circadian rhythm regulation and melatonin metabolism were among the candidates, reinforcing the link with photoperiod.

The identification of such diverse metabolic pathways (collagen, muscle, lipids, immunity) associated with aRFA suggests unexpected complexity. Rather than a simple direct hormonal deregulation of the hair cycle, the pathogenesis of CRFA might involve a more fundamental disruption of skin homeostasis or the very structure of the hair follicle. These structural or metabolic alterations, of genetic origin, could make the follicles abnormally sensitive to seasonal or hormonal triggers (photoperiod, melatonin, prolactin). This model goes beyond the simple causal chain “photoperiod → hormone → cycle arrest” and suggests a complex interaction between an inherited tissue susceptibility and triggering environmental factors.

It should be noted that another study specifically targeting the MLPH gene (associated with color dilution) in the Rhodesian Ridgeback did not find an association with CRFA in this breed. This indicates that the genetic basis may be heterogeneous across breeds or that the genes involved are different from those linked to pigmentation.

Follicular Mechanisms

Functionally, CRFA is considered an abnormality of the hair cycle, often described as hair cycle arrest. Histopathology suggests a major defect in the initiation or progression of the anagen phase (growth). This leads to an accumulation of hair follicles in the telogen phase (resting) or, after shedding of the telogen hair without immediate replacement.

The term “cyclic follicular dysplasia” is sometimes used, referring to the morphologically abnormal appearance of follicles observed histologically. Follicles may appear atrophic, deformed, with irregular basal structures. However, the term “dysplasia” (abnormal development) can be debated, with some preferring to focus on the functional aspect of cycle arrest.

Diagnosis

Clinical Approach

The presumptive diagnosis of CRFA is primarily based on a detailed history and thorough clinical examination. Key elements of the history include belonging to a predisposed breed, typical age of onset (young adult to middle-aged adult), seasonal and recurrent character of alopecia episodes (if present), and absence of general signs or pruritus.

The dermatological examination looks for cardinal clinical signs:

• Non-inflammatory and non-pruritic alopecia: This is an essential characteristic. The underlying skin is generally not red, thickened, or irritated, and the dog does not scratch.
• Typical location: The condition predominantly affects the flanks (lateral or dorso-lateral thoraco-lumbar region). It is often bilateral, but symmetry is not always perfect, and unilateral involvement, although rare, is possible.
• Appearance of lesions: The alopecic areas are generally well-demarcated, with clean edges, sometimes irregular or serpiginous, forming “map-like” patterns. The size of lesions is variable, ranging from a few centimeters to almost the entire thoraco-lumbar region.
• Hyperpigmentation: Dark coloration (black or brown) of the skin in alopecic areas is very frequent but not constant. Its absence does not allow exclusion of the diagnosis, as the capacity to hyperpigment varies according to breeds and individuals.
• Easy epilation: At the beginning of a shedding episode, hairs at the periphery of lesions or in affected areas can often be easily epilated by gentle traction (positive trichogram).

It is also necessary to be aware of atypical presentations that can complicate the initial diagnosis: involvement of the bridge of the nose or periocular region (particularly in Labrador and Golden Retrievers), more generalized involvement, or simple changes in color (for example, aurotrichia – hairs becoming golden) or texture of the coat on the flanks without visible alopecia. Rare cases associated with histological interface dermatitis have also been described.

Differential Diagnoses

Given that symmetrical non-inflammatory alopecia is a presenting complaint that can correspond to several conditions, it is crucial to establish a rigorous differential diagnosis to exclude other potential causes. The main categories to consider are:

• Endocrinopathies: Hypothyroidism and hypercortisolism (spontaneous or iatrogenic) are the major differentials. Unlike CRFA, these diseases are often accompanied by systemic signs (lethargy, polyuria-polydipsia, weight gain, etc.) and other cutaneous abnormalities (thin skin, comedones, recurrent pyoderma). Sex hormone imbalances are rarer but possible.
• Other non-inflammatory alopecias: Alopecia X (sharing clinical and sometimes histological similarities), color dilution alopecia, various breed-specific follicular dysplasias, telogen effluvium (massive shedding after stress) or anagen effluvium (shedding during the growth phase, rare), and pattern baldness should be considered.
• Infectious/parasitic causes: Although CRFA is non-inflammatory, generalized demodicosis or dermatophytosis can sometimes mimic symmetrical alopecia, especially at the beginning. Bacterial folliculitis can also occur secondarily in alopecic areas of CRFA.
• Others: Sebaceous adenitis (inflammation of sebaceous glands), post-clipping alopecia (no regrowth after shaving), alopecia areata (immune mechanism), post-injection cutaneous reactions (vaccine, medications) or traction alopecia (due to elastics for example) are other possible differentials, although often with a different distribution or clinical history.

Complementary Examinations

The confirmation of CRFA diagnosis and exclusion of differentials require complementary examinations:

• First-line examinations: Deep skin scrapings, trichograms (microscopic examination of hairs), skin cytology (search for bacteria, yeasts) and possibly fungal culture are essential to rule out demodicosis, dermatophytosis, or secondary infection.
• Blood and hormonal tests: A complete blood count and biochemical profile are useful to assess general health and look for indices of endocrinopathy. Specific hormone assays, at minimum total T4 and TSH, are necessary to exclude hypothyroidism. In case of suspected hypercortisolism, low-dose dexamethasone suppression tests or ACTH stimulation tests may be indicated.
• Skin biopsies: Histopathological examination of skin biopsies is considered the key step to confirm the suspicion of CRFA and exclude other dermatoses with similar presentation. It is recommended to perform several biopsies (6 to 8 mm diameter punch) taken within characteristic alopecic lesions. The timing of the biopsy is important, as histological lesions may vary according to the stage of evolution (shedding phase, established phase, regrowth phase). Ideally, biopsies should be performed when alopecia is well established.

It is crucial to understand that, although histopathology provides very suggestive elements, the lesions observed in CRFA (infundibular hyperkeratosis, atrophic/dysplastic follicles) are not strictly pathognomonic and can sometimes be found, to varying degrees, in other conditions such as certain endocrinopathies or follicular dysplasias. Therefore, the definitive diagnosis of CRFA does not rely solely on biopsy but on an integrative approach. It requires the convergence of several elements: a compatible clinical presentation (breed, age, seasonality, appearance of lesions), rigorous exclusion of differential diagnoses (particularly endocrine and parasitic) by appropriate examinations, and histopathological results compatible with non-inflammatory alopecia presenting the follicular characteristics described for CRFA.

Histopathology

General Characteristics

Histopathological examination of skin biopsies taken from alopecic areas in a dog with CRFA typically reveals non-inflammatory alopecia. Inflammatory infiltrate in the dermis or around follicles is generally absent or very discrete, which is an important criterion for differentiating CRFA from alopecias of inflammatory or infectious origin.

Follicular Abnormalities

The most characteristic changes concern hair follicles and their associated structures:

• Infundibular hyperkeratosis: This is one of the most constant and marked signs. It is a significant thickening of the cornified layer (keratin) at the upper portion of the hair follicle (infundibulum). This excess keratin can obstruct the follicular opening and sometimes extend to secondary follicles or sebaceous gland ducts.
• Infundibular dilatation: Infundibula may appear markedly enlarged, forming cystic structures filled with keratin lamellae.
• Follicular atrophy and dysplasia: The middle and deep portions of hair follicles (isthmus and bulb) are often atrophic, i.e., reduced in size. They may also present dysplastic aspects, with irregular, tortuous shapes, and poorly defined or deformed bulbar structures.
• “Witch’s feet” or “octopus” appearance: These imagery terms describe a particular appearance of atrophic/dysplastic follicles, characterized by irregular and branched epithelial projections extending from the base of the follicle into the surrounding dermis. This appearance is considered very suggestive of CRFA, although not exclusive.
• Hair cycle arrest: Analysis of the hair cycle phases reveals a clear predominance of follicles in telogen phase (resting phase) or catagen phase (regressive transition phase). Follicles in anagen phase (active growth phase) are rare or absent in biopsies performed during the alopecic phase. An increase in the number of kenogen phase follicles (empty follicles after telogen hair shedding, before the start of a new anagen cycle) is also a frequent finding, indicating a defect in the induction of the new growth phase. It should be noted that the distribution of phases can be very variable from one individual to another and depends heavily on the timing of the biopsy relative to the disease cycle. If the biopsy is performed late or during the regrowth phase, anagen follicles may be observed.

Other Findings

Other changes may be observed:

• Melanin aggregates: Clumps of melanin pigment may be present in the lumen of dilated infundibula, within follicular epithelial cells, or even in associated sebaceous glands.
• Epidermis and Dermis: The epidermis is generally of normal thickness, sometimes discreetly hyperplastic or hyperpigmented on the surface. The dermis shows no significant abnormalities, particularly no inflammation or fibrosis.

Comparison with Other Alopecias

It is important to note that certain histological characteristics of CRFA are not exclusive. The increase in kenogen phase follicles is a sign common to several hair cycle disorders, indicating difficulty initiating the anagen phase. Alopecia X, for example, also presents a strong predominance of follicles in telogen phase and a low percentage of anagens, sometimes making distinction difficult on histological basis alone. However, the marked dysplastic aspects, particularly the “witch’s feet” image, seem more characteristic of CRFA. The absence of marked inflammation allows CRFA to be differentiated from alopecias of infectious, parasitic, or immune origin (such as alopecia areata or sebaceous adenitis).

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Prognosis

Evolution and Recurrences

CRFA is, by definition, an often recurrent condition. In many dogs, episodes of alopecia occur cyclically, typically every year, in connection with seasonal changes in photoperiod.

However, the evolution is marked by significant interindividual variability:

• A non-negligible proportion of dogs (estimated at about 20% in one source) will experience only one episode of CRFA in their lifetime, without subsequent recurrence.
• Other dogs will present very regular cycles, with hair loss occurring at the same period each year.
• Some individuals may “skip” a season, not presenting alopecia in a given year, only to recur the following year.
• Finally, in some dogs, particularly those who have presented several recurrent cycles, alopecia may eventually become permanent, or regrowth between episodes may become increasingly incomplete.

Hair Regrowth

Spontaneous regrowth of hair is a frequent characteristic of CRFA. It generally occurs within 3 to 8 months after the onset of shedding, although longer periods, up to 14 or even 18 months, have been reported in some cases.

The quality of the regrown coat is often altered. New hairs may have a different color (often darker, but sometimes lighter or golden – aurotrichia) and/or modified texture (duller, drier, rougher) compared to the normal surrounding coat. As a result, even after regrowth, the previously alopecic area often remains visually identifiable.

The prognosis for complete regrowth, with hair of identical quality and color to the original, is therefore variable and largely unpredictable for a given individual.

Impact on Quality of Life

It is essential to reaffirm that CRFA is a strictly cosmetic disease. It does not affect the general health, well-being, or longevity of the dog in any way. The vital prognosis is excellent. The main impact is aesthetic for the owner.

This benign and often self-resolving nature fully justifies the conservative therapeutic approach (abstention or “benign neglect”) as a first-choice option. The absence of pain or associated systemic disease, combined with the high probability of spontaneous regrowth and uncertain efficacy of treatments such as melatonin (demonstrated in a controlled study), makes watchful waiting a medically sound strategy. It avoids interventions, costs, and potentially unnecessary constraints for a condition that does not alter the animal’s quality of life.

Conclusion

Canine recurrent flank alopecia (CRFA) is a dermatosis characterized by episodes of non-inflammatory alopecia, primarily affecting the flanks in a cyclical or seasonal manner. It preferentially affects certain breeds such as the Boxer, English Bulldog, and Airedale Terrier, suggesting a genetic predisposition. The exact etiopathogenesis remains unknown, but the influence of photoperiod is strongly suspected, potentially involving dysregulations in the production or signaling of melatonin and/or prolactin at the level of hair follicles. Recent genetic studies suggest a complex polygenic basis involving various metabolic pathways beyond simple hormonal regulation. Diagnosis is based on an evocative clinical picture (breed, seasonality, appearance of lesions), rigorous exclusion of differential diagnoses (particularly endocrinopathies and parasites), and compatible histopathological examination (infundibular hyperkeratosis, atrophic/dysplastic follicles, absence of inflammation, hair cycle arrest). The vital prognosis is excellent, but complete coat regrowth and prevention of recurrences remain unpredictable.