Folliculitis Decalvans: Symptoms, Types, Causes and Treatment

Folliculitis decalvans is a rare but often distressing scalp disorder that can have a profound impact on a person's quality of life. It is marked by chronic inflammation, scarring, and irreversible hair loss, primarily affecting adults but sometimes seen in other age groups. This comprehensive article explores the symptoms, types, causes, and treatments of folliculitis decalvans, aiming to provide clarity and support to those affected by this challenging condition.

Symptoms of Folliculitis Decalvans

When it comes to folliculitis decalvans, early recognition of symptoms is crucial for managing the disease and preventing significant hair loss. The condition is notorious for its persistent, sometimes painful presentation and can be easily mistaken for other scalp disorders in its initial stages.

Symptom	Description	Area Affected	Source(s)
Follicular pustules	Small pus-filled bumps around hair follicles	Scalp (vertex/occiput)	1 2 4 8
Scarring alopecia	Irreversible hair loss with smooth, shiny patches	Scalp (mainly)	1 2 4 8
Follicular tufting	Multiple hairs emerging from a single dilated follicular opening	Scalp	2 6 8
Erythema	Redness and inflammation, often around follicles	Scalp/perifollicular	1 2 4
Crusting/Erosions	Yellowish crusts and erosions, sometimes hemorrhagic	Scalp lesions	1 2 4
Pain/Itching	Discomfort, burning, or itching sensations	Scalp	2 4

Table 1: Key Symptoms

Follicular Pustules and Redness

The hallmark of folliculitis decalvans is the presence of follicular pustules—small, pus-filled bumps that form around hair follicles. These pustules are often accompanied by diffuse or perifollicular erythema (redness), reflecting the underlying inflammation 1 2 4.

Scarring Alopecia

Over time, the chronic inflammation leads to irreversible hair loss and the development of smooth, shiny patches where the hair does not regrow—this is known as cicatricial or scarring alopecia. The loss of follicular ostia (the small openings where hair emerges) is characteristic, rendering the affected scalp areas bald and scarred 1 2 4 8.

Follicular Tufting

A striking sign seen in many cases is follicular tufting, where clusters of 5–20 hairs emerge from a single, dilated follicular orifice. This occurs due to damage and subsequent healing of the follicular opening, resulting in multiple hair shafts sharing a single infundibulum 2 6 8.

Crusting, Erosions, and Discomfort

Lesions may develop yellowish or hemorrhagic crusts, and erosions can appear due to persistent inflammation and scratching. Patients frequently report pain, itching, or a burning sensation, which can significantly affect daily comfort 1 2 4.

Extent and Progression

The disease often begins in the vertex (top) or occipital (back) area of the scalp but can expand, sometimes involving up to 50% of the scalp. Severity can range from discrete patches to extensive, thickly scarred areas 2.

Types of Folliculitis Decalvans

Folliculitis decalvans, while generally recognized as a single entity, actually presents in several distinct forms and overlaps with other scalp and skin disorders. Understanding these types is vital for accurate diagnosis and tailored treatment.

Type/Variant	Key Features	Population/Area	Source(s)
Classic FD	Scalp pustules, scarring alopecia, tufting	Adults (mainly scalp)	1 2 4 8
Tufted Folliculitis	Multiple hair tufts in scarring patches	Subtype of FD (scalp)	2 6 8
Folliculitis Spinulosa Decalvans	Pustules, keratotic papules, scarring, wider body involvement	Young adults, scalp + body	5
FD-like on Limbs	Pustular plaques, scarring alopecia, limited to limbs	Rare, older adults	3
FD-LPP Overlap	Biphasic presentation, features of both FD & LPP	Adults, sometimes pediatric	7 9

Table 2: Types and Variants

Classic Folliculitis Decalvans

The classic type is characterized by pustules, erythema, follicular tufting, and scarring alopecia, mainly limited to the scalp, particularly the vertex and occipital regions. It is most frequently seen in young and middle-aged adults 1 2 4 8.

Tufted Folliculitis

Tufted folliculitis is now considered a clinicohistological variant of FD. It is marked by the presence of multiple hair tufts (5–20) in a single follicular opening, which is a result of clustering and fibrosis of adjacent follicular units. This form is differentiated from classic FD mainly by the prominence and number of tufts 2 6 8.

Folliculitis Spinulosa Decalvans

A rarer form, folliculitis spinulosa decalvans, presents not only with scalp pustules and scarring but also with follicular keratotic papules affecting other parts of the body, such as the cheeks, chest, abdomen, and limbs. This variant is more common in younger adults and may be associated with other atypical findings (e.g., dental anomalies) 5.

FD-like Lesions Beyond the Scalp

Though FD is primarily a scalp disorder, rare cases have reported similar pustular, scarring lesions confined to the limbs. These cases mimic the histological and clinical features of FD but spare the scalp, suggesting a broader spectrum of disease 3.

Overlap with Lichen Planopilaris

Recently, cases have been reported where patients display both folliculitis decalvans and lichen planopilaris (LPP) features, sometimes sequentially or even concurrently. This biphasic presentation suggests an overlap syndrome, complicating both diagnosis and management 7 9.

Causes of Folliculitis Decalvans

Despite extensive research, the precise cause of folliculitis decalvans remains elusive. Several factors, including bacterial infection, immune dysregulation, and alterations in the scalp microbiome, are believed to contribute to its development.

Cause/Factor	Role in FD	Evidence/Notes	Source(s)
Staphylococcus aureus	Frequently isolated; possible trigger	Not always sole pathogen	1 2 10
Biofilm Formation	May persist in follicles, promoting chronicity	Observed in scalp biopsies	11
Immune Dysfunction	Deficient host response, abnormal inflammation	Impaired barrier, dysbiosis	1 2 7 10
Genetic Predisposition	Not well-defined	Few familial cases reported	5
Physical Trauma/Surgery	Occasionally precedes onset	Role not fully understood	2
Microbiome Instability	Persistent abnormal flora, even in non-lesional skin	May explain recurrences	10

Table 3: Factors Involved in FD

The Role of Staphylococcus aureus

S. aureus is frequently isolated from the lesions and even non-lesional scalp skin of FD patients. While its presence is strongly linked to the disease, not all patients improve with anti-staphylococcal therapy, and the bacteria can lack typical virulence factors, suggesting it is a trigger but not the sole cause 1 2 10.

Biofilm Hypothesis

Recent studies have found evidence of bacterial biofilms—communities of bacteria encased in a protective matrix—within the deeper parts of hair follicles in FD patients. These biofilms may contribute to the persistence of inflammation and resistance to treatment, making eradication difficult 11.

Immune System Abnormalities

A defective or dysregulated immune response is increasingly recognized in FD. This can manifest as a deficient barrier function, allowing bacteria to invade deeper layers and persist. Autoimmune processes and abnormal inflammatory responses (notably neutrophil-predominant inflammation) are often observed in scalp biopsies 1 2 7 10.

Microbiome Instability

FD is associated with a persistent, abnormal subepidermal microbiota, even after apparent clinical improvement. This unbalanced flora may serve as a reservoir for recurrence, underlining the importance of the skin’s microbial ecosystem in the disease 10.

Other Factors

Physical trauma, such as hair restoration surgery, has occasionally preceded FD onset, but its causal significance is unclear. Genetic predisposition remains speculative, with only a few familial cases and no definitive genetic markers identified 2 5.

Treatment of Folliculitis Decalvans

Managing folliculitis decalvans is challenging due to its chronic nature, frequent relapses, and the risk of scarring. Treatment focuses on halting disease progression, controlling symptoms, and preventing recurrence.

Treatment	Main Action/Goal	Notes/Effectiveness	Source(s)
Systemic Antibiotics	Eradicate S. aureus, reduce inflammation	Rifampicin + clindamycin, tetracyclines most effective	1 12 13
Topical Antibiotics	Local bacterial suppression	Variable results, often adjunct	1 13
Intralesional/Topical Steroids	Reduce inflammation	Controls symptoms, slows progression	1 4 12 15
Dapsone	Anti-inflammatory, antibacterial	Effective in severe/refractory cases	16
Calcineurin Inhibitors (Tacrolimus)	Immune modulation	Can halt progression, relapses on discontinuation	15
Photodynamic Therapy	Antimicrobial, anti-inflammatory	Case reports of success	14
Botulinum Toxin A	Alternative anti-inflammatory	Used in resistant cases	4
Maintenance/Combination Therapy	Prevent relapses	Often necessary long-term	1 12 16

Table 4: Treatment Options

Systemic and Topical Antibiotics

Antibiotics are the mainstay of FD treatment, targeting S. aureus and reducing inflammation. Combination regimens, such as rifampicin with clindamycin or tetracyclines, have shown the best results, especially for moderate to severe cases. Topical antibiotics may be used for localized disease but are less effective alone 1 12 13.

Anti-inflammatory Agents

Steroids, both topical and intralesional, help reduce inflammation and halt progression. They may be used alone for mild disease or with antibiotics for more extensive involvement. Tacrolimus, a calcineurin inhibitor, has also shown promise in controlling inflammation, though disease relapses are common upon discontinuation 1 4 12 15.

Dapsone and Alternative Therapies

Dapsone, with its dual anti-inflammatory and antibacterial properties, can be effective for severe or refractory FD, especially at moderate doses with long-term maintenance. Relapses often occur after stopping therapy, so ongoing, low-dose treatment may be required 16.

Other options include photodynamic therapy (light-based antimicrobial/anti-inflammatory treatment), which has shown benefit in case reports, and botulinum toxin A, which can be considered for resistant cases 4 14.

Maintenance and Long-term Management

Given the chronic and relapsing nature of FD, maintenance therapy—whether with low-dose antibiotics, anti-inflammatories, or a combination—is often necessary. Close monitoring is essential to adjust treatment and prevent irreversible scarring 1 12 16.

Conclusion

Folliculitis decalvans is a complex, chronic scalp disorder that can result in permanent hair loss and significant psychosocial distress. Early recognition and comprehensive management are key to minimizing its impact.

Key Takeaways:

• Symptoms: Include follicular pustules, scarring alopecia, follicular tufting, erythema, crusting, and discomfort, mainly on the scalp 1 2 4 8.
• Types: Classic FD, tufted folliculitis, folliculitis spinulosa decalvans, FD-like lesions on limbs, and FD–lichen planopilaris overlap exist 2 3 5 6 7 8 9.
• Causes: Multifactorial, involving S. aureus, biofilms, immune dysfunction, and microbiome instability; trauma and genetic factors may play a role 1 2 5 10 11.
• Treatment: Focuses on antibiotics (rifampicin, clindamycin, tetracyclines), steroids, dapsone, tacrolimus, and adjunct therapies; long-term maintenance is often required 1 4 12 13 14 15 16.

Understanding the nuanced presentation and underlying mechanisms of folliculitis decalvans is vital for optimizing care and improving outcomes for those affected by this challenging condition.