Primary cicatricial alopecias (CA) are commonly classified according to the type of inflammatory infiltrate present. CAs can be predominately lymphocytic, such as with CCCA, neutrophilic, or mixed.3
Folliculitis keloidalis shows mixed lymphocytic and neutrophilic infiltration with histological findings similar to CCCA.3
Interestingly, folliculitis keloidalis and CCCA occur concurrently in some patients, but further study is needed to determine the significance of this relationship.1
Histologically, AGA demonstrates miniaturization of terminal hairs into vellus-like hairs and an absence of inflammation.4
The clinical presentation, histopathology, and treatment response appear to be similar between men and women with CCCA. Therefore, current practices to diagnose and treat female patients should also be used for male patients with CCCA.1
Timely management of CCCA can halt or slow disease progression in most cases, but hair regrowth depends on the extent of damage and scarring in the follicle.5
Clinical features of CCCA and AGA are presented in . African American men presenting with hair loss on the vertex and concurrent symptoms of pruritus, scaling, erythema, pustules, papules, or tenderness warrant evaluation for CCCA with biopsy confirmation. AGA can affect the vertex, but is usually asymptomatic, with additional hair loss in the frontal or bitemporal hairline or crown ().5
On average, CCCA in men presents at an earlier age than AGA. In the study by Sperling et al,1
the average age was 29 years; the average age in the current study was 30 years. However, more cases are needed to confirm this observation.
Comparison of clinical features and treatments for central centrifugal cicatricial alopecia versus androgenetic alopecia
Androgenetic alopecia on the vertex. Note the symmetrical hair loss similar to CCCA.
Currently, there are no published studies that establish an effective treatment regimen for CCCA. It is typically treated more aggressively than AGA with anti-inflammatory agents, such as potent topical corticosteroids, applied daily to the scalp6
and/or intralesional corticosteroids at the periphery of the affected area monthly for the first six months, then symptomatically thereafter.5
Aggressive cases may require a minimum of six months of treatment with oral tetracycline or doxycycline due to their anti-inflammatory properties.6
Much longer treatment periods may be required. Antifungal shampoos can be used to control scaling and inflammation.5
However, severely damaged follicles may not recover, and follicular scars are incapable of hair regrowth.6
AGA is commonly treated with 2% or 5% minoxidil or finasteride 1mg, which typically results in increased hair density.4
Hair transplantation for AGA can produce dramatically positive results, but will be unsuccessful in patients with active inflammation from CCCA.5
The cause of CCCA remains unknown, but hair grooming practices, such as chemical processing with relaxers; heat styling; and hairstyles that increase traction, such as braids and extensions,6
have been implicated, particularly in women. Genetic inheritance factors have also been suggested, which may be a more likely explanation in men because they less commonly use the above hair grooming practices. However, there is no published literature that definitively establishes the cause(s).5
Therefore, it is important to obtain a thorough medical history including hair grooming practices and scalp biopsy when clinical suspicion necessitates further investigation.