The differential diagnosis for LPP includes discoid lupus erythematosus (DLE), central centrifugal cicatricial alopecia (CCCA), folliculitis decalvans, and dissecting cellulitis.1
DLE typically causes discrete, indurated lesions of central hypopigmentation (erythematous when active), along with slight atrophy and a rim of hyperpigmentation. This is in contrast to the perifollicular erythema and lack of atrophy that you’ll see in LPP. In addition, patients with DLE will have telangiectasias, while those with LPP will not.
CCCA is typically non-inflammatory, but can sometimes have symptoms such as mild itching. As the name implies, the hair loss associated with this disease starts in the central scalp and works its way centrifugally to the periphery, whereas in LPP, the alopecia can be patchy or diffuse, or can involve only the frontal scalp.2
Folliculitis decalvans is a form of scarring alopecia characterized by inflammatory perifollicular papules and pustules. Such lesions would not be observed in a patient with LPP. Bacterial culture will identify Staphylococcus aureus in most patients with untreated folliculitis decalvans.6
Dissecting cellulitis presents with tender, fluctuant nodules on the scalp that commonly suppurate and drain. The scarring hair loss that results could be mistaken for LPP, but a history of active, inflamed, nodular lesions will help to distinguish this condition from LPP.
A biopsy is required to confirm the diagnosis of LPP.2 A 4 mm punch biopsy should be performed, and optimally, 2 adjacent biopsies are taken so that they can be sectioned both vertically and horizontally.2 The biopsy should be done adjacent to a patch of alopecia that still has most of the hair follicles present. This is important because a biopsy of an area of scalp completely scarred with no remaining hair follicles will not demonstrate the pathognomonic patterns of inflammation that will allow for an accurate diagnosis.
In early-stage LPP, histopathology will reveal a lichenoid interface inflammation with hypergranulosis, hyperkeratosis, and hyperacanthosis, whereas in later stages, inflammation may be minimal or absent, with fibrous tracts taking the place of destroyed hair follicles.7