What is Dr. Zubair Khalid's research focus?

Dr. Zubair Khalid specializes in molecular virology, mRNA vaccine development, and computational biology, with a focus on avian pathogens like IBDV and Avian Reovirus.

Where is Dr. Zubair Khalid currently working?

Dr. Zubair Khalid is a Postdoctoral Research Associate at the University of Maryland (UMD), specifically within the Department of Animal and Avian Sciences.

Keratosis Pilaris Causes: Follicular Plugging Explained

Name: Keratosis Pilaris Causes: Follicular Plugging Explained
Creator: Dr. Zubair Khalid

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

Keratosis pilaris causes rough, sandpaper-like bumps because keratin and dead corneocytes accumulate inside the upper part of the hair follicle and form a plug. The plug is not dirt, not acne bacteria, and not an infection. It is a disorder of follicular keratinization, meaning the follicle lining produces and retains keratin faster than it can shed it [1][2].

This article explains the biology behind that plug, the genes and environmental factors that drive it, and why the same word ("follicular disease") means something very different when a veterinarian uses it about a dog or cat. The species comparison matters because owners often search for their own skin condition and land on pet health pages, or the reverse. The two are related in concept but distinct in cause.

This article is educational and is not a substitute for veterinary diagnosis or treatment.

What Keratosis Pilaris Actually Is

Keratosis pilaris is a common, benign, hyperkeratotic skin condition. It appears as small, folliculocentric papules, meaning each bump sits on a hair follicle, with variable perifollicular erythema (redness around the follicle) [3]. The lay description "plucked chicken skin" captures the texture well [1].

It is best understood as a family of follicular disorders rather than a single disease. Keratosis pilaris simplex is by far the most common form. Other variants include keratosis pilaris rubra, erythromelanosis follicularis faciei et colli, and the keratosis pilaris atrophicans spectrum, which includes ulerythema ophryogenes (keratosis pilaris atrophicans faciei) [3][4]. These variants share the same core problem, abnormal follicular keratinization, but differ in location, degree of redness, and whether inflammation leads to scarring or hair loss.

The condition is usually harmless. It can still prompt multiple visits to primary care and dermatology because of appearance and persistent roughness [1]. That gap between "benign" and "bothersome" is the reason it draws so much clinical attention.

The Core Mechanism: How a Follicular Plug Forms

The follicular infundibulum is the bottleneck

Every hair follicle has an upper funnel-shaped segment called the infundibulum. This is the region between the skin surface and the point where the sebaceous duct joins the follicle. The infundibulum is lined by stratified squamous epithelium that continuously keratinizes, the same way surface skin does.

In normal skin, corneocytes (flattened dead keratinocytes) detach from each other and shed into the follicle canal, then out onto the skin surface. In keratosis pilaris, that desquamation process fails. Keratin and corneocytes build up, adhere to the follicular lining, and form a cone-shaped plug that distends the follicular opening [1][5].

Why the plug becomes visible

The retained plug creates a firm, raised papule. Because the plug sits at the follicular orifice, each bump has a hair emerging from it or trapped beneath it. The surrounding redness comes from perifollicular inflammation and vascular changes, not from infection [3].

The result is a rough, goosebump-like field of skin. Friction, dryness, and cold weather worsen the texture because they impair the already fragile barrier and slow normal shedding.

The plug is keratin, not pus

A keratin plug is composed of keratin protein and dead corneocytes. It is sterile in the sense that it does not require bacteria to form. This is the single most important distinction from bacterial folliculitis, where infection and neutrophilic inflammation drive the lesion. A keratosis pilaris bump is a shedding problem first. A folliculitis bump is an infection problem first.

Genetic Causes of Keratosis Pilaris

Keratosis pilaris is strongly hereditary. It is described as a benign genetic skin disorder, and inherited mutations have been implicated in its etiology [3][5]. Two gene families dominate the current literature.

Filaggrin (FLG) loss-of-function mutations

Filaggrin is a structural protein critical to the epidermal barrier. Loss-of-function mutations in FLG are a well-established genetic contributor to keratosis pilaris [3]. A Finnish cross-sectional study of 502 patients with atopic dermatitis found that keratosis pilaris was significantly associated with the filaggrin loss-of-function mutation 2282del4 (p < 0.000, OR 4.917, 95% CI 1.961 to 12.330) and with palmar hyperlinearity (p < 0.000, OR 4.664, 95% CI 2.072 to 10.496) [6].

That same study found no link between keratosis pilaris and disease severity, asthma, or atopic sensitization [6]. The authors also noted that keratosis pilaris prevalence was generally low in the Finnish cohort and that this may reflect the lower frequency of the tested FLG mutations in Finland compared with central Europe or Asia [6]. This is a useful reminder that gene frequency varies by population, so keratosis pilaris prevalence varies too.

The clinical implication is straightforward. A defective barrier protein means the follicle lining cannot shed corneocytes normally, so plugs form more easily.

ABCA12 mutations

ABCA12 encodes a transmembrane transporter that is essential for lipid transport in the epidermis and for normal keratinocyte differentiation. A study of one keratosis pilaris family identified a novel heterozygous missense mutation in ABCA12, designated c.6694G>T (p.Asp2232Tyr), in the affected proband and in affected family members. The mutation was absent in healthy family members and in population-matched controls [7].

Functional prediction tools suggested the mutation produces a damaged protein, and the affected region sits in the extra-membrane domain, which is conserved across species. Immunofluorescence showed upregulated ABCA12 expression in the relevant skin [7]. This supports a model in which disturbed lipid handling and keratinocyte differentiation contribute to follicular plugging.

Inheritance pattern and syndromic associations

Keratosis pilaris and ulerythema ophryogenes are hereditary disorders of hair follicle keratinization that involve follicular inflammation and subsequent atrophy [4]. The pattern in families is consistent with autosomal dominant transmission, which is why the condition often appears in multiple generations of the same family.

Keratosis pilaris can also appear as one feature of a broader genetic syndrome. The combination of keratosis pilaris, ulerythema ophryogenes, and monosomy 18p has been reported repeatedly and has been proposed as a distinct syndrome (Zouboulis syndrome) [4]. A separate case report described widespread severe keratosis pilaris and ulerythema ophryogenes in a woman with partial monosomy of the short arm of chromosome 18 [8]. Investigators have argued that this association may help pinpoint a genomic region and gene responsible for follicular keratinization [8].

Keratosis pilaris atrophicans faciei can also be difficult to distinguish from frontal fibrosing alopecia, and genetic testing has been explored as a way to improve diagnostic accuracy in that overlap [9]. Atypical keratosis pilaris-like follicular lesions have been described in Bethlem myopathy, a collagen VI-related myopathy, with histopathologic correlation showing how the skin lesions develop in that rare neuromuscular disease [10].

Environmental and Acquired Triggers

Genes set the stage. Environment and barrier status determine how visible the condition becomes.

Dry skin and barrier impairment

Dry skin is the most consistent aggravating factor. General cutaneous measures for keratosis pilaris center on hydrating the skin, avoiding long baths or showers, and using mild soaps or cleansers [3]. Each of those measures addresses barrier water loss. When the stratum corneum loses water, corneocyte shedding becomes even less efficient, and plugs become more prominent.

Atopic dermatitis and the barrier connection

The relationship between keratosis pilaris and atopic dermatitis is real but more nuanced than many people assume. Keratosis pilaris associates with epidermal barrier defects in atopic dermatitis, but its role in disease severity and concomitant atopic disease varies between populations [6]. In the Finnish cohort, keratosis pilaris was infrequent in atopic dermatitis patients overall, and the association tracked with specific FLG mutations rather than with atopic dermatitis severity [6].

Keratosis pilaris may be associated with ichthyosis vulgaris and palmar hyperlinearity, and less likely with atopic dermatitis itself [3]. Palmar hyperlinearity is a visible marker of the same barrier defect that produces keratosis pilaris, which is why the two travel together [6].

Medication-induced keratosis pilaris-like eruptions

A distinct category of acquired follicular plugging occurs as an adverse cutaneous reaction to drugs. BCR-ABL tyrosine kinase inhibitors used to treat chronic myeloid leukemia produce a characteristic eruption resembling keratosis pilaris, especially nilotinib and dasatinib [11]. The pathogenesis of this reaction is still unknown [11].

A case report described an asymptomatic keratosis pilaris-like eruption appearing one month after starting imatinib for chronic myeloid leukemia, which is uncommon for that particular drug [11]. A separate report described a patient who developed red bumps and patchy hair loss on the arms, chest, shoulders, back, and legs two months after starting nilotinib, with the eruption classified as keratosis pilaris atrophicans [12]. That report stressed the importance of distinguishing keratosis pilaris-like eruptions from more severe drug hypersensitivity eruptions that would require stopping the medication, and of classifying these eruptions by morphology rather than lumping them all together as "chemotherapy eruption" [12].

Keratosis pilaris-like reactions have also been reported with chromatin remodeling complex inhibition in uveal melanoma, described as a novel constellation of adverse reactions in a small case series [13]. These drug-triggered cases share the follicular plugging phenotype but have an external cause rather than an inherited one.

Human Keratosis Pilaris Versus Canine Follicular Dysplasia Versus Feline Acne

Veterinary and human follicular conditions are frequently confused because they all involve hair follicles. The mechanisms and clinical behavior differ substantially.

Feature	Human keratosis pilaris	Canine follicular dysplasia	Feline acne
Primary problem	Abnormal keratinization of the follicular infundibulum with keratin and corneocyte plugs [1][2]	Abnormal hair follicle development and cycling, not a simple shedding defect	Follicular plugging and inflammation of the chin and lips, often with secondary bacterial involvement
Genetic basis	Inherited FLG and ABCA12 mutations, autosomal dominant pattern [3][6][7]	Breed-associated in predisposed breeds such as Siberian Husky and Doberman	Multifactorial, with plugging, sebum, and grooming behavior contributing
Typical appearance	Small folliculocentric papules with variable perifollicular erythema, "plucked chicken skin" [3][1]	Poor coat, patchy alopecia, scaling, recurrent skin problems in predisposed breeds	Blackheads, comedones, swollen chin, papules and pustules on the chin
Role of infection	Not primarily infectious	Secondary bacterial infection common	Secondary bacterial infection common
Species	Humans	Dogs	Cats

The key distinction is the target of the abnormality. Human keratosis pilaris is a keratinization and desquamation disorder of the follicular infundibulum [1][2]. Canine follicular dysplasia is a developmental and cycling disorder of the follicle itself, which is why it produces hair loss and coat failure rather than a field of rough bumps. Feline acne is a plugging and inflammatory disorder of the chin and lip follicles, and it frequently involves secondary bacteria.

Bacterial folliculitis is a third entity that is often mistaken for all of the above. In bacterial folliculitis, the follicle is invaded by bacteria and the lesion is driven by infection and neutrophilic inflammation. The bumps may look similar at arm's length, but the cause, the diagnostic approach, and the treatment are different.

Why the Distinction Matters for Pet Owners

If you are a pet owner reading about keratosis pilaris, the practical takeaway is that your dog or cat almost certainly does not have it. Keratosis pilaris is a human condition. When a veterinarian says "follicular disease" about your pet, they are describing a different category of problem, and the workup reflects that.

Follicular dysplasia in dogs is breed-associated. Siberian Huskies and Dobermans are among the breeds recognized as predisposed, and affected dogs typically show coat abnormalities, scaling, and recurrent skin issues rather than the small rough bumps seen in human keratosis pilaris. Feline acne concentrates on the chin and lips, and it often improves with attention to bowl hygiene and chin cleaning, though persistent or infected cases need veterinary care.

The reason this matters is that treatments do not transfer between species. A keratolytic approach that helps a human with keratosis pilaris is not automatically appropriate for a dog with follicular dysplasia or a cat with acne. Some topical agents are toxic to cats. Some human products contain ingredients that are not labeled for veterinary use. The correct first step for any pet with a follicular skin problem is a veterinary examination, not a trial of a human skin product.

If you have keratosis pilaris yourself and also own pets, keep your own topical products away from your animals, particularly cats, and wash your hands after application.

Common Myths and Questions About Keratosis Pilaris Causes

Myth: Keratosis pilaris is caused by poor hygiene

Keratosis pilaris is a genetic and keratinization disorder [3][5]. Hygiene has no role in causing it. Scrubbing harder can worsen the barrier and make the texture more prominent.

Myth: Keratosis pilaris is a form of acne

Acne and keratosis pilaris both involve follicles, but keratosis pilaris is a disorder of follicular keratinization, not a sebaceous gland and bacterial process [1][2]. The plugs are keratin and corneocytes, not infected sebaceous material.

Myth: Keratosis pilaris is contagious

It is inherited, not transmitted [3][5]. You cannot catch it from another person or pass it to a pet.

Myth: It always clears up on its own

Keratosis pilaris is chronic and tends to fluctuate with weather, humidity, and barrier status. The literature describes it as a chronic condition in the context of treatment trials [14]. It often improves with age, but it does not reliably resolve.

Myth: A flare means something serious is happening

Most keratosis pilaris is benign. The exception is a keratosis pilaris-like eruption that appears after starting a new medication, particularly a tyrosine kinase inhibitor. In that situation, the eruption must be distinguished from a severe drug hypersensitivity reaction, and the prescribing physician needs to be involved [12].

Practical Implications for Owners and Keepers

If you have keratosis pilaris

The general cutaneous measures described in the literature are hydrating the skin, avoiding long baths or showers, and using mild soaps or cleansers [3]. These steps target the barrier defect that drives plugging. Beyond that, treatment selection is a medical decision. Keratolytic agents, topical retinoids, corticosteroids, lasers, and microdermabrasion all appear in the clinical literature as options, and the choice depends on the variant, the location, and the degree of redness [3]. This article does not cover human treatment selection.

If your pet has a follicular skin problem

Get a diagnosis before treating. Follicular dysplasia, bacterial folliculitis, and feline acne look different under magnification and have different causes. A veterinarian can perform skin cytology, skin scrapings, and hair evaluation to sort them out. According to AAHA and AVMA guidance, routine wellness visits are the right setting to raise chronic skin concerns, and recurring skin problems warrant a specific diagnostic plan rather than repeated empirical treatment.

If you are a breeder or breed enthusiast

Follicular dysplasia in dogs is breed-associated. If you work with Siberian Huskies, Dobermans, or other breeds with recognized follicular dysplasia, document coat and skin changes early and discuss them with your veterinarian. Breed predisposition does not mean every dog in a breed will develop the condition, and it does not replace individual evaluation.

What Is Still Uncertain

The pathogenesis of drug-induced keratosis pilaris-like eruptions remains unknown [11]. Researchers have not yet mapped exactly how tyrosine kinase inhibitors and chromatin remodeling complex inhibitors trigger follicular plugging.

The full genetic architecture of keratosis pilaris is also incomplete. FLG and ABCA12 are established contributors [3][6][7], and the monosomy 18p association points to a candidate genomic region [4][8], but other genes in the epidermal barrier and keratinization pathways are likely involved. The Finnish study authors explicitly noted that mutations in other locations of the FLG gene or in other epidermal genes may explain population differences in prevalence [6].

The relationship between keratosis pilaris and atopic dermatitis also remains population-dependent rather than universal [6]. Clinicians should interpret prevalence data with the population in mind.

Limitations and When to Contact a Veterinarian

This article is educational and is not a substitute for veterinary diagnosis or treatment. Individual cases need a veterinarian who can examine the skin, take a history, and run appropriate tests.

Contact a veterinarian promptly if your pet has any of the following:

New or worsening hair loss, especially patchy or symmetric
Persistent scaling, crusting, or greasy coat changes
Redness, swelling, or pain around hair follicles
Pustules, draining tracts, or foul odor from the skin
Chin swelling, blackheads, or recurrent chin lesions in a cat
Itching that disrupts sleep, appetite, or behavior
Skin lesions that do not improve after basic hygiene and grooming measures
Any skin reaction that appears after starting a new medication, in pets or in people

For people, contact a physician if a keratosis pilaris-like eruption appears after starting a new drug, if the skin becomes painful or blistered, or if the condition causes significant distress.

Frequently Asked Questions

What is the main cause of keratosis pilaris?

The main cause is abnormal keratinization of the follicular infundibulum, which produces plugs of keratin and corneocytes [1][2]. Inherited FLG and ABCA12 mutations and dry skin make the plugging worse [3][6][7].

Is keratosis pilaris genetic?

Yes. It is a hereditary condition with an autosomal dominant pattern, and inherited mutations in FLG and ABCA12 have been implicated [3][6][7].

Does dry skin cause keratosis pilaris?

Dry skin does not cause it on its own, but it aggravates the plugging. Barrier hydration is a core general measure for managing the condition [3].

Is keratosis pilaris the same as follicular dysplasia in dogs?

No. Keratosis pilaris is a human keratinization disorder of the follicular infundibulum [1][2]. Canine follicular dysplasia is a developmental and hair cycling disorder seen in predisposed breeds such as Siberian Huskies and Dobermans.

Can pets get keratosis pilaris?

Keratosis pilaris is a human condition. Pets develop different follicular diseases, including follicular dysplasia in dogs and feline acne in cats.

Is keratosis pilaris an infection?

No. It is not primarily infectious. The plug is made of keratin and corneocytes, not bacteria [1][2]. Bacterial folliculitis is a separate condition driven by infection.

Can medication cause keratosis pilaris?

Yes. Tyrosine kinase inhibitors used for chronic myeloid leukemia can cause a keratosis pilaris-like eruption, especially nilotinib and dasatinib [11]. Similar reactions have been reported with chromatin remodeling complex inhibition [13].

When should I see a doctor about keratosis pilaris?

See a physician if the condition is distressing, if it is not responding to basic skin care, or if a keratosis pilaris-like eruption appears after starting a new medication, since drug-related eruptions must be distinguished from severe hypersensitivity reactions [12].