Dissecting cellulitis of the scalp (DCS) also known as perifolliculitis capitis abscedens et suffodiens (PCAS) is a chronic, relapsing, inflammatory dermatosis consisting of edematous sterile pustules and nodules resulting in sinus tracts and scarring alopecia. Although first described as infectious in 1903, DCS is primarily an inflammatory process that can precede a secondary infection; this is similarly true of the other conditions within the follicular occlusion tetrad: hidradenitis suppurativa (HS), acne conglobata, and pilonidal sinus.1,2
DCS has a greater incidence in black men between the ages of 20 and 40, but it can occur in other demographics, including women and children.3 DCS has a predilection for the vertex scalp, although the entire scalp can be involved, and produces boggy or fluctuant pustules and nodules Figure 1.2 Patients commonly complain of pain and of a disfiguring appearance that contributes to the reduction in quality of life. The disease may wax and wane over several years, later producing dermal fibrosis, sinus tracts, and hypertrophic scarring with scarring alopecia. There is an increased risk of squamous cell carcinoma in patients with long-standing disease.4 The prevalence of DCS is unknown as it is recognized as a rare disease by the National Institute of Health, however research and data on HS indicates a prevalence of 0.3 to 4%, and practice patterns suggest DCS is less common than HS and therefore likely falls on the lower end of that range.5,6
The etiology of DCS is undefined, though it certainly is instigated or exacerbated by follicular occlusion, where keratinous plugging of the pilosebaceous apparatus causes dramatic secondary inflammatory changes to proinflammatory stimuli. The follicles in DCS frequently occlude, dilate, rupture, and keratin debris as well as bacteria stimulate relapsing and remitting episodes of inflammatory and infectious nodules, draining abscesses, and ultimately sinus tracts and alopecia. Histology is characterized by infiltration with dense neutrophils, lymphocytes, histiocytes, and plasma cells, as well as granulomas, scarring, and fibrosis seen in later stages. The differential diagnosis includes cysts, furuncles, acne keloidalis nuchae, and folliculitis decalvans, among others.6 Treatment of DCS is variable depending on severity ranging from topical therapies to systemic monoclonal antibodies, with most patients requiring a multimodal approach as seen in Table 1. This review provides evidence for the treatment of DCS utilizing current literature.
Corticosteroids reduce inflammation in DCS; for mild cases, topical corticosteroids (TCS) like clobetasol, betamethasone, and fluocinolone should be applied twice daily for up to three weeks at a time to avoid long term TCS side effects like hypopigmentation and atrophy. Intralesional triamcinolone acetonide is the standard of care for active DCS lesions. Dosing ranges from 3.33 mg/mL to 10 mg/mL of intralesional triamcinolone, and roughly 0.1 mL to 0.5 mL per lesion.7 Oral corticosteroids are less commonly prescribed for DCS, and have been shown to be useful at doses up to 50 mg daily and tapered down for flares, or at lower doses as bridging therapy to starting another longer-term treatment option like isotretinoin.7
Although no reports specifically for DCS, topical benzoyl peroxide 10% and clindamycin solution 1% daily have shown improvement in HS, another member of the follicular occlusion tetrad with similar pathophysiology. As in HS, benzoyl peroxide and topical clindamycin should be utilized together to prevent colonization with clindamycin resistant bacteria.8 Oral antibiotics primarily act as anti-inflammatory agents that can also prevent and treat secondary infections caused by DCS, and usually lead to gaps of little to no disease activity without significant flares. Patients anecdotally request antibiotics due to their efficacy, however, clinicians must balance the risk of chronically altering patient’s microbiota along with increasing the chance of antibiotic resistance. Case reports indicate success with rifampicin 300 mg twice daily for four months that led to reduction in lesions within weeks prior to starting isotretinoin.9 Similarly, clindamycin 300mg twice daily also lead to a significant and rapid improvement prior to starting isotretinoin.10 Combination oral rifampicin 300 mg and clindamycin 300 mg, both twice daily, increases overall efficacy in HS and reduces the risk of antibiotic resistance, and again while not studied in DCS the similar pathophysiology suggests this regimen would be similarly efficacious in DCS11,12 One case report exists utilizing doxycycline 50 mg every other day in addition to various other therapies for DCS.13
DCS has a greater incidence in black men between the ages of 20 and 40, but it can occur in other demographics, including women and children.3 DCS has a predilection for the vertex scalp, although the entire scalp can be involved, and produces boggy or fluctuant pustules and nodules Figure 1.2 Patients commonly complain of pain and of a disfiguring appearance that contributes to the reduction in quality of life. The disease may wax and wane over several years, later producing dermal fibrosis, sinus tracts, and hypertrophic scarring with scarring alopecia. There is an increased risk of squamous cell carcinoma in patients with long-standing disease.4 The prevalence of DCS is unknown as it is recognized as a rare disease by the National Institute of Health, however research and data on HS indicates a prevalence of 0.3 to 4%, and practice patterns suggest DCS is less common than HS and therefore likely falls on the lower end of that range.5,6
The etiology of DCS is undefined, though it certainly is instigated or exacerbated by follicular occlusion, where keratinous plugging of the pilosebaceous apparatus causes dramatic secondary inflammatory changes to proinflammatory stimuli. The follicles in DCS frequently occlude, dilate, rupture, and keratin debris as well as bacteria stimulate relapsing and remitting episodes of inflammatory and infectious nodules, draining abscesses, and ultimately sinus tracts and alopecia. Histology is characterized by infiltration with dense neutrophils, lymphocytes, histiocytes, and plasma cells, as well as granulomas, scarring, and fibrosis seen in later stages. The differential diagnosis includes cysts, furuncles, acne keloidalis nuchae, and folliculitis decalvans, among others.6 Treatment of DCS is variable depending on severity ranging from topical therapies to systemic monoclonal antibodies, with most patients requiring a multimodal approach as seen in Table 1. This review provides evidence for the treatment of DCS utilizing current literature.
Corticosteroids reduce inflammation in DCS; for mild cases, topical corticosteroids (TCS) like clobetasol, betamethasone, and fluocinolone should be applied twice daily for up to three weeks at a time to avoid long term TCS side effects like hypopigmentation and atrophy. Intralesional triamcinolone acetonide is the standard of care for active DCS lesions. Dosing ranges from 3.33 mg/mL to 10 mg/mL of intralesional triamcinolone, and roughly 0.1 mL to 0.5 mL per lesion.7 Oral corticosteroids are less commonly prescribed for DCS, and have been shown to be useful at doses up to 50 mg daily and tapered down for flares, or at lower doses as bridging therapy to starting another longer-term treatment option like isotretinoin.7
Although no reports specifically for DCS, topical benzoyl peroxide 10% and clindamycin solution 1% daily have shown improvement in HS, another member of the follicular occlusion tetrad with similar pathophysiology. As in HS, benzoyl peroxide and topical clindamycin should be utilized together to prevent colonization with clindamycin resistant bacteria.8 Oral antibiotics primarily act as anti-inflammatory agents that can also prevent and treat secondary infections caused by DCS, and usually lead to gaps of little to no disease activity without significant flares. Patients anecdotally request antibiotics due to their efficacy, however, clinicians must balance the risk of chronically altering patient’s microbiota along with increasing the chance of antibiotic resistance. Case reports indicate success with rifampicin 300 mg twice daily for four months that led to reduction in lesions within weeks prior to starting isotretinoin.9 Similarly, clindamycin 300mg twice daily also lead to a significant and rapid improvement prior to starting isotretinoin.10 Combination oral rifampicin 300 mg and clindamycin 300 mg, both twice daily, increases overall efficacy in HS and reduces the risk of antibiotic resistance, and again while not studied in DCS the similar pathophysiology suggests this regimen would be similarly efficacious in DCS11,12 One case report exists utilizing doxycycline 50 mg every other day in addition to various other therapies for DCS.13
