Version May 2024
INTRODUCTION — Dissecting cellulitis of the scalp (DCS), also known as perifolliculitis capitis abscedens et suffodiens or Hoffman disease, is a chronic inflammatory disorder of the scalp characterized by boggy, suppurative nodules that are often associated with patchy hair loss (picture 1A-E). Follicular occlusion may be a key pathogenic event in the development of DCS. DCS may occur in association with other follicular occlusive disorders, such as acne conglobata, hidradenitis suppurativa, and pilonidal cysts [1].
Data on treatment options for DCS are limited. Oral antibiotics and oral isotretinoin are the most used treatments (algorithm 1). (See 'Treatment' below.)
The clinical features, diagnosis, and management of DCS will be reviewed here. An overview of the characteristics and diagnosis of hair loss is provided separately. (See "Evaluation and diagnosis of hair loss".)
Other follicular occlusive disorders are reviewed separately.
●(See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)
●(See "Pilonidal disease".)
CLASSIFICATION — DCS is a type of primary cicatricial (scarring) alopecia, a group of inflammatory disorders that target hair follicles and result in follicular destruction and permanent hair loss. A classification scheme proposed by the participants of a 2001 workshop on cicatricial alopecia sponsored by the North American Hair Research Society further classified DCS as a neutrophilic form of primary cicatricial alopecia based upon pathologic features [2]. (See "Evaluation and diagnosis of hair loss", section on 'Classification' and 'Histopathology' below.)
EPIDEMIOLOGY — The prevalence of DCS is unknown, but DCS appears to be an uncommon disorder. Adult males account for the majority of affected patients, with a typical age of onset between 20 and 40 years. Occasionally, DCS occurs in adolescents and females [3-7]. In a multicenter retrospective study of patients seen at specialist hair clinics, DCS accounted for only 3 percent of the 840 cases of cicatricial alopecia [8]. Among the patients with DCS, 76 percent were male, and the median age was 37 years.
Although the largest published case series have arisen from Asia and Europe, DCS likely occurs globally [5,7-14]. Although clinical experience suggests that Black males are the most frequently affected population in the United States, epidemiologic data are insufficient to confirm this conclusion [15-17].
An association of DCS with smoking has been proposed but has not been confirmed. In a case-control study with 33 patients with DCS and 304 controls, current smoking was more common among patients with DCS than among the controls (odds ratio 6.47, 95% CI 2.77-15.13) [18].
PATHOGENESIS — The etiology of DCS is unknown. A defect in follicular keratinization leading to obstruction of the follicle is suspected to contribute to the development of DCS. This theory is supported by the observation that DCS occurs in association with other disorders of follicular occlusion. (See 'Associated disorders' below.)
Proposed pathogenic events in DCS are as follows:
●Sebaceous and keratinous material accumulates within dilated hair follicles.
●Release of this material into the dermis triggers an intense neutrophilic inflammatory reaction followed by abscess and sinus tract formation.
●Secondary bacterial infection can occur, leading to exacerbation of the disease.
CLINICAL FEATURES — The major clinical features of DCS are suppurative nodules, interconnecting sinuses, hair loss, and a chronic course.
●Suppurative nodules and sinuses – DCS usually manifests as boggy, suppurative nodules on the vertex, parietal, and posterior scalp (picture 1A-E); however, other sections of the scalp can be affected. Drainage of pus or blood from involved skin is common. Because interconnecting sinuses are often present between nodules, the application of pressure to a nodule can result in drainage from a distant site. Patients often use head scarves, hats, or gauze dressings to hide these clinical manifestations. Pain or pruritus may be present [9,10,19].
Exudate from nodules of DCS is usually sterile; however, secondary infection can occur. Staphylococcus aureus [20], Pseudomonas aeruginosa [3], and anaerobic bacteria [21] have been isolated from sites of DCS.
●Hair loss – Hair loss in DCS is usually patchy and most prominent on the skin overlying nodules. Although hair loss can be reversible in early stages of disease, scarring alopecia can develop in persistent cases [22].
●Disease course – The clinical course of DCS is chronic. Patients frequently experience periodic flares of varying severity depending on the degree of inflammation. Hypertrophic or keloidal scarring may occur (picture 2).
ASSOCIATED DISORDERS — Other follicular occlusion disorders and other conditions may occur in association with DCS.
●Follicular occlusion tetrad – DCS is considered a component of the follicular occlusion tetrad, a group of four disorders (hidradenitis suppurativa, acne conglobata, DCS, and pilonidal sinus) thought to have follicular occlusion as a key pathogenic event. Patients with DCS may exhibit other disorders in the follicular occlusion tetrad [5,7,14,23]. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis" and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acne conglobata' and "Pilonidal disease".)
●Other disorders – Additional disorders, such as marginal keratitis [24], arthritis, spondyloarthropathy [25], keratitis-ichthyosis-deafness (KID) syndrome [26], and sternoclavicular hyperostosis, also have occurred in patients with DCS [1,27-29]. (See "Overview and classification of the inherited ichthyoses", section on 'KID syndrome' and "SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome".)
HISTOPATHOLOGY — Histopathologic features of DCS vary according to the stage of the disease and severity. Characteristic histologic findings of DCS are dense, predominantly neutrophilic, mixed-cell perifollicular infiltrates in the dermis. There may be abscesses in the dermis or subcutaneous tissue [1].
Follicular dilatation may be evident in early disease [15,22]. Granulomatous inflammation, scarring, and fibrosis are common in advanced or late-stage disease [30].
DIAGNOSIS — The diagnosis of DCS can usually be made based upon the patient history and physical examination, although a culture should be performed to rule out secondary infection. In addition, a biopsy may be necessary to confirm the diagnosis and rule out other forms of cicatricial alopecia if overlapping features are present. (See "Evaluation and diagnosis of hair loss", section on 'Cicatricial alopecia'.)
In general, the diagnosis should be suspected in patients with a chronic, relapsing eruption characterized by multiple boggy, suppurative nodules on the scalp. (See 'Clinical features' above.)
History and physical examination
●Patient history – The patient history should include an assessment of the duration of hair loss and associated symptoms. Patients with DCS typically mention chronic and recurrent scalp nodules associated with purulent or bloody drainage.
Given the association of DCS with other disorders in the follicular occlusion tetrad, patients should also be asked about a history of signs or symptoms of hidradenitis suppurativa, acne conglobata, or pilonidal cysts. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Clinical manifestations' and "Pilonidal disease" and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acne conglobata'.)
●Physical examination – The physical examination of the hair and scalp should include an assessment of the distribution and extent of involvement. Boggy nodules, typically 1 to 3 cm in diameter, involving the posterior and vertex scalp are typical of DCS. Palpation of the scalp aids in the detection of the classic boggy texture. Drainage of pus or blood and patches of alopecia overlying nodules are common findings.
The physical examination of the scalp may also help to assess for the likelihood of hair regrowth. A loss of follicular orifices suggests permanent scarring alopecia. General principles for the clinical evaluation of patients with hair loss are reviewed separately. (See "Evaluation and diagnosis of hair loss", section on 'Physical examination'.)
Performance of a full skin examination is helpful for identifying patients with concomitant hidradenitis suppurativa, acne conglobata, or pilonidal cysts. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis", section on 'Clinical manifestations' and "Pilonidal disease" and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acne conglobata'.)
●Dermoscopy – Dermoscopy may be a useful adjunctive procedure in the clinical assessment of patients with DCS. (See "Overview of dermoscopy of the hair and scalp".)
Common findings are as follows [31]:
•Early disease – Empty follicular openings, yellow dots, and black dots
•Advanced disease – Yellow, structureless areas and three-dimensional yellow dots imposed over dystrophic hair shafts
•End-stage disease – Confluent, ivory-white areas without follicular openings
Culture — A bacterial culture should be performed to rule out bacterial infection. However, in most cases, exudate associated with DCS is sterile. (See 'Active infection' below.)
Scalp biopsy — If the diagnosis of DCS is uncertain, a scalp biopsy should be performed to confirm the diagnosis and differentiate DCS from other cicatricial alopecias. (See "Evaluation and diagnosis of hair loss", section on 'Scalp biopsies'.)
●Technique – A 4 mm punch biopsy is usually adequate. The preferred site for a biopsy is within a boggy, suppurative, or tender nodule; the goal is to sample a clinically active (ie, inflamed) lesion.
Some dermatopathologists prefer to receive two scalp biopsy specimens to allow for examination of the tissue in both vertical and horizontal sections. However, a single biopsy can be sufficient.
●Interpretation – Classically, histologic examination of DCS reveals a perifollicular, neutrophil-predominant, mixed-cell inflammatory infiltrate. (See 'Histopathology' above.)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of DCS includes other inflammatory or nodular disorders that affect the scalp.
●Folliculitis decalvans – Folliculitis decalvans is an uncommon type of cicatricial alopecia that presents with multiple pustules and areas of scarring of the scalp. On examination, yellowish crusts or collarettes of scale at sites of ruptured pustules and tufted folliculitis (multiple hairs emerging from a single inflamed follicular orifice) are common findings (picture 3A-B). The deep-seated nodules characteristic of DCS are not a typical feature of folliculitis decalvans. (See "Folliculitis decalvans".)
●Acne keloidalis – Acne keloidalis is a form of cicatricial alopecia that most commonly presents with multiple fibrotic or keloid-like follicular papules on the posterior scalp (picture 4A-B). Patients with advanced disease may develop keloid-like plaques or nodules. Although scarring and keloids may occur as a consequence of DCS, fibrotic keloid-like papules or plaques are not the primary clinical feature in DCS. (See "Acne keloidalis nuchae: Pathogenesis, clinical manifestations, and diagnosis".)
●Bacterial folliculitis – Bacterial folliculitis is characterized by inflamed follicular papules or pustules (picture 5). Unlike DCS, large, boggy nodules or abscesses are not typical features of folliculitis. (See "Infectious folliculitis", section on 'Bacterial folliculitis'.)
●Pilar cysts – Pilar cysts present as solitary or multiple firm, slow-growing subcutaneous nodules on the scalp (picture 6). Occasionally, a pilar cyst may become inflamed or infected. The presence of multiple nodules that are boggy or suppurative helps to distinguish DCS from pilar cysts. (See "Overview of benign lesions of the skin", section on 'Pilar (trichilemmal) cysts'.)
●Kerion – Kerion is a severe manifestation of tinea capitis that results from an intense immune response to the infection. Patients develop an inflammatory plaque with pustules, crusting, or drainage (picture 7). Unlike DCS, kerion is most common in children. However, kerion mimicking DCS has been reported in adults and children [32-34]. (See "Tinea capitis", section on 'Clinical manifestations'.)
TREATMENT — Treatment of DCS is warranted given the chronic and progressive nature of the disease and the high likelihood for scarring and permanent alopecia. Our approach to the treatment of DCS is reviewed here. Other approaches may be reasonable.
Overview — The key treatment strategies for DCS are to reduce inflammation, reduce follicular occlusion, and prevent and treat secondary infection. Systemic antibiotics, oral isotretinoin, biologic tumor necrosis factor (TNF)-alpha inhibitors, and surgical excision are the mainstays of treatment. However, treatment efficacy data are limited, precluding conclusions on the relative efficacy of these treatments.
Occasionally, patients present with very painful or fluctuant nodules for which an immediate intervention is necessary for symptom relief. Adjunctive therapies, such as intralesional corticosteroid injection and incision and drainage, appear useful in this setting. (See 'Painful or very fluctuant lesions' below.)
In our experience, incorporation of an adjunctive topical antimicrobial agent has also seemed to help reduce risk for secondary infection. (See 'Adjunctive topical antimicrobial agents' below.)
Pretreatment assessment — The pretreatment assessment should include an evaluation for secondary infection.
Active infection — Because of the possibility of secondary infection in DCS, a bacterial culture should be performed prior to treatment. If the culture identifies pathogenic bacteria, an appropriate antibiotic should be selected to treat the infection. The patient can then transition to treatment directed at the underlying disease. (See 'Preferred initial therapy' below.)
Preferred initial therapy
Oral tetracyclines — Oral antibiotic therapy with doxycycline is our preferred initial treatment for DCS. The anti-inflammatory and antibacterial effects of tetracyclines may contribute to benefit. In addition, tetracyclines are generally well tolerated.
●Administration – We typically begin treatment for adults with doxycycline (at a dose of 100 mg twice daily) for a period of three months. Lower daily doses of doxycycline have also been utilized [9].
•Patients with a satisfactory response to doxycycline – If there is marked improvement after three months, we continue doxycycline for at least three additional months. Doxycycline may be continued at the same dose or reduced to a subantimicrobial dose (eg, 20 mg twice daily or 40 mg of immediate release/delayed release doxycycline once daily), with subantimicrobial dosing usually reserved for patients with milder disease presentations and complete resolution of disease activity. Treatment courses longer than six months may be necessary to reach optimal control for some patients who are responding to doxycycline. We stop doxycycline after there has been at least a three-month period of disease inactivity.
•Patients with an unsatisfactory response to doxycycline – If there is an unsatisfactory response after three months, we stop doxycycline and either start minocycline (at a dose of 100 mg twice daily) or proceed to oral isotretinoin. In our experience, some patients who have inadequate responses to doxycycline exhibit greater improvement with minocycline. For patients with severe disease, we often proceed directly to oral isotretinoin. (See 'Oral isotretinoin' below.)
As with patients responding to doxycycline, patients who achieve satisfactory responses after three months of minocycline therapy continue minocycline for an additional three months at the same dose or a reduced dose (eg, 50 mg twice daily). Minocycline can be stopped after a three-month period of disease inactivity. If there is no response to minocycline, we proceed to therapies for tetracycline-refractory disease. (See 'Tetracycline-refractory disease' below.)
•Patients who respond to tetracyclines but relapse – In our experience, patients who experience marked improvement with tetracyclines but relapse after cessation may benefit from a repeat course of antibiotic therapy or a transition to another therapy.
When relapses are delayed and occur infrequently (eg, one or fewer relapses per year), we often prescribe a three-month course of the previously effective antibiotic (eg, doxycycline 100 mg twice daily). For patients who respond to doxycycline, we often continue a subantimicrobial dose of doxycycline (at a dose of 20 mg of doxycycline twice daily or 40 mg [with 30 mg immediate release and 10 mg delayed release] of doxycycline once daily) as long-term maintenance therapy.
For patients with rapid or more frequent relapses, we often proceed to oral isotretinoin. (See 'Tetracycline-refractory disease' below.)
●Efficacy – Despite the frequent use of oral antibiotics for DCS, randomized trials evaluating antibiotic therapy are lacking. Partial responses to antibiotics may be common. In a retrospective study that included 10 patients with DCS treated with systemic antibiotics (six patients given doxycycline [at a dose of 200 mg per day for three months] and four patients given clindamycin and rifampin [both 300 mg twice daily for three months]), a complete response occurred in one patient, with the remaining nine patients having partial improvement [12]. In another retrospective study of 21 patients with DCS, four of five patients treated with doxycycline (mean daily dose of 100 mg per day) had "a great reduction in disease activity" [9].
Recurrence after cessation of antibiotic therapy may be common; in the study of 10 patients mentioned above, 9 had recurrence of disease activity [12].
●Adverse effects – Potential adverse reactions to tetracyclines include gastrointestinal symptoms (nausea, abdominal pain or discomfort); photosensitivity (particularly tetracycline and doxycycline); and, infrequently, pseudotumor cerebri. In addition, minocycline may cause dose-dependent vestibular effects, bluish skin dyspigmentation (usually following several months of therapy), lupus-like drug reactions, or drug reaction with eosinophilia and systemic symptoms (DRESS). (See "Drug reaction with eosinophilia and systemic symptoms (DRESS)".)
Tetracycline-refractory disease — The main treatments utilized for DCS that cannot be adequately controlled with tetracyclines include oral isotretinoin, oral clindamycin and rifampin combination therapy, biologic TNF inhibitors, and surgical excision. Efficacy data for these interventions are limited.
Approach to treatment — Oral isotretinoin is our treatment of choice for DCS that does not respond well to oral tetracyclines (algorithm 1). Although some authors suggest isotretinoin as the preferred initial therapy for moderate to severe DCS [35], we generally try doxycycline prior to proceeding to isotretinoin because of doxycycline's relatively favorable adverse effect profile. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Adverse effects'.)
Our approach to patients who cannot receive oral isotretinoin or who experience inadequate or transient responses to oral isotretinoin is as follows (algorithm 1):
●Patients who cannot receive or prefer to avoid oral isotretinoin – Either treatment with a biologic TNF inhibitor or combination treatment with oral clindamycin and rifampin is our preferred next step for patients with disease that responds poorly to tetracyclines but who cannot receive or prefer to avoid oral isotretinoin. (See 'Biologic TNF inhibitors' below and 'Clindamycin and rifampin' below.)
●Patients with disease that responds poorly to oral isotretinoin – Treatment with a biologic TNF inhibitor is our preferred next therapy after failure of oral isotretinoin, but long-term continuation of therapy may be necessary to maintain improvement. Surgical intervention is an alternative for patients who prefer a potentially curative procedural intervention and who are comfortable with the expected outcome of extensive scarring. (See 'Biologic TNF inhibitors' below and 'Surgical excision' below.)
●Patients who experience disease relapse after oral isotretinoin – Mild relapses (eg, few relatively small, boggy nodules) can often be managed with a course of doxycycline and intralesional corticosteroid injections. (See 'Oral tetracyclines' above and 'Painful or very fluctuant lesions' below.)
For moderate to severe relapses after oral isotretinoin, we tend to proceed to a biologic TNF-alpha inhibitor. Alternatively, our experience suggests that a repeat course of oral isotretinoin followed by long-term, low-dose isotretinoin (eg, 20 mg per day, increased to 1 mg/kg per day during flares) may also be beneficial. (See 'Biologic TNF inhibitors' below.)
Oral isotretinoin — The mechanism of benefit for oral isotretinoin in DCS is unclear but may relate to anti-inflammatory effects or inhibition of follicular occlusion. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Adverse effects'.)
●Administration – Adults are usually treated with 0.5 to 1 mg/kg of isotretinoin per day. Our typical initial regimen consists of 1 mg/kg per day of isotretinoin. We assess the response after three months (algorithm 1).
•Patients with a satisfactory response – Remission often occurs within three months in patients who respond to oral isotretinoin [10]. Our clinical experience suggests that treatment should be continued for at least four months after resolution or marked reduction of clinically active lesions. We usually stop isotretinoin once this has been achieved.
•Patients with an unsatisfactory response – If there is no evidence of response after three months, we stop oral isotretinoin.
If there is a partial response after three months, we continue isotretinoin for an additional three months prior to reassessing efficacy. In our experience, the addition of adjunctive, once-monthly intralesional corticosteroid injections can be helpful in this setting. (See 'Painful or very fluctuant lesions' below.)
If the response remains inadequate after six months, we stop isotretinoin.
Relapse several weeks to months after discontinuation of isotretinoin may be common; however, in some patients, the severity of disease may be lower than prior to treatment. The severity of relapse influences our selection of subsequent treatment. (See 'Approach to treatment' above.)
●Efficacy – Support for use of isotretinoin for DCS comes from retrospective studies and case series [9-11,35-41]. Data from several retrospective studies suggest partial or complete improvement rates of 75 to 100 percent of patients [42]. Examples of some of the largest retrospective studies include:
•In a retrospective study of 51 patients with DCS, 33 of 35 patients treated with isotretinoin (at a dose of 0.5 to 0.8 mg/kg per day) experienced complete remission after three months [10]. However, relapses were common after treatment.
•A retrospective multicenter study involving 72 patients with DCS treated with isotretinoin at an average dose of 0.25 to 0.5 mg/kg until a cumulative dose of 120 to 150 mg/kg demonstrated reduced inflammatory signs in 90 percent of patients [43].
•In a retrospective study that included 16 patients treated with oral isotretinoin (at a dose of 20 to 40 mg per day based upon a dose equivalent to 0.3 to 0.7 mg/kg), responses were complete in six patients, partial in six patients, and absent in four patients [7]. The median time to initial response was 2 weeks (range 0.7 to 8 weeks), and the average cumulative dose of isotretinoin was 5731 mg (range 280 to 19,920 mg).
●Adverse effects – Potential adverse effects of isotretinoin include dry skin and mucous membranes, hypertriglyceridemia, elevation of liver transaminases, vision changes, and teratogenicity. The drug is contraindicated in pregnancy. Adverse effects are reviewed in detail separately. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Adverse effects'.)
In the United States, participation in a Risk Evaluation and Mitigation Strategy program (www.ipledgeprogram.com) is required for isotretinoin prescriptions.
Clindamycin and rifampin — Combination treatment with oral clindamycin and oral rifampin may be beneficial for patients who have insufficient responses to tetracyclines but who prefer to avoid or cannot tolerate oral isotretinoin (algorithm 1). (See 'Approach to treatment' above.)
●Administration – Our typical regimen for adults is clindamycin (at a dose of 300 mg twice daily) and rifampin (at a dose of 300 mg twice daily) for three months. If the response is insufficient after three months, we cease treatment.
Patients with a satisfactory response continue treatment for an additional three months. If marked improvement is maintained, we then stop the antibiotics.
●Efficacy – Efficacy data are limited. In a retrospective study that included 10 patients with DCS treated with systemic antibiotics (four patients given clindamycin and rifampin [both 300 mg twice daily for three months] and six patients given doxycycline [at a dose of 200 mg per day for three months]), a complete response occurred in one patient, with the remaining nine patients having partial improvement [12]. Isolated case reports also suggest benefit of clindamycin and rifampin [1,9]. Recurrence of disease activity after treatment may be common.
●Adverse effects – Pseudomembranous colitis is a potential adverse effect of clindamycin. Rifampin is associated with multiple drug interactions and may cause orange or red staining of body secretions, gastrointestinal distress, hepatitis, hematologic abnormalities, influenza-like syndromes, and other conditions. Adverse effects of these antibiotics are reviewed separately. (See "Clindamycin: An overview", section on 'Toxicity' and "Rifamycins (rifampin, rifabutin, rifapentine)", section on 'Adverse effects'.)
Biologic TNF inhibitors — The biologic tumor necrosis factor (TNF) inhibitors adalimumab and infliximab may be beneficial for DCS that cannot be adequately treated with antibiotics or oral isotretinoin (algorithm 1). (See 'Approach to treatment' above.)
●Administration – We typically treat with adalimumab. The subcutaneous route of adalimumab is an advantage over the intravenous route of infliximab. Although a subcutaneously administered formulation of infliximab is available in some countries, published reports of infliximab benefit in DCS have assessed the intravenous formulation.
•Adalimumab – Our typical regimen for adults mirrors the dosing for hidradenitis suppurativa (ie, an initial 160 mg dose given subcutaneously, then 80 mg every other week starting at day 15) [12,44].
However, other regimens have been utilized (eg, an initial 80 mg dose given subcutaneously, followed by 40 mg at week 1, then 40 mg every other week) [45-47].
•Infliximab – Dosing regimens used for infliximab also vary. Some authors have utilized dosing similar to psoriasis dosing (at a dose of 5 mg/kg at weeks 0, 2, 6, and then every 8 weeks) [45,48], and others have used different regimens [1,12,49]. Higher doses (up to 10 mg/kg) may be necessary in severe, refractory cases.
Signs of improvement with TNF inhibitors are often evident within the first one to three months of treatment [12,44-47,50].
Best practice for the duration of biologic therapy is unclear. Because biologic treatment is not considered curative, we generally plan to continue treatment in patients who respond to biologic therapy. We reserve trials of treatment cessation to patients who have experienced long periods of complete remission (eg, >1 year).
●Efficacy – Case reports and small case series document improvement of refractory DCS with adalimumab [12,44-47,50] and infliximab [45,49,51]. In one retrospective study of eight patients treated with infliximab and one patient treated with adalimumab (alone or in conjunction with other systemic therapies), treatment was associated with reduced inflammatory nodules, reduced purulent drainage, and improvement in patient quality of life [48].
●Adverse effects – Potential adverse effects of biologic TNF-alpha inhibitors include injection site reactions, infusion reactions, neutropenia, serious infections, and other adverse effects. Adverse effects of these drugs are reviewed in detail separately. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects".)
Surgical excision — Surgical therapy for DCS involves the excision of skin in affected areas of the scalp. Surgical excision is generally performed by a dermatologic surgeon or plastic surgeon experienced in the treatment of this condition. The expected outcome of scarring must be considered carefully when proceeding with surgical excision.
Multiple cases of sustained remission following surgical excision of affected areas of the scalp (with staged excisions and/or skin grafts) have been reported [35,52]. Short-term use of TNF-alpha inhibitor therapy to calm inflammation prior to surgical excision has been reported in a patient with severe DCS [51].
Painful or very fluctuant lesions — Acute relief from the discomfort associated with an inflamed or suppurative nodule is sometimes necessary. Intralesional corticosteroid injections and incision and drainage are used to provide rapid, temporary symptom relief. These interventions do not alter the course of the disease and should not be used as primary treatment.
Selection between intralesional corticosteroid injection and incision and drainage is based upon the clinical presentation. Intralesional corticosteroid injection is our preferred intervention for painful, inflamed, nonfluctuant or minimally fluctuant nodules. We use incision and drainage for fluctuant lesions.
●Intralesional corticosteroid – Intralesional injection is best performed by clinicians experienced with this procedure. To minimize risk for corticosteroid-induced skin atrophy, the concentration and total volume of injection should be commensurate with the degree of inflammation or fibrosis, as well as the size of the individual lesion. (See "Intralesional corticosteroid injection".)
The typical dose range is 5 to 10 mg/mL of triamcinolone acetonide, depending on the severity of inflammation. Higher concentrations (eg, 10 to 40 mg/mL) may be useful for the treatment of associated hypertrophic scarring. (See "Keloids and hypertrophic scars", section on 'Treatment of hypertrophic scars'.)
A 30-gauge needle can be used for injection. We usually do not inject more than 40 mg of triamcinolone acetonide per treatment session to minimize risk for systemic adverse effects. (See "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)
●Incision and drainage – Techniques for incision and drainage are reviewed separately. (See "Techniques for skin abscess drainage".)
Adjunctive topical antimicrobial agents — Topical antibiotics and topical antimicrobial agents are not considered effective primary treatments for DCS. In one retrospective study, 8 of 11 patients treated with topical antibiotics (drugs not specified) had no response to treatment, and the remaining three patients had partial responses and recurrences of disease activity [12].
However, our clinical experience suggests that regular use of topical antimicrobial cleansers (eg, chlorhexidine, povidone iodine) as an adjunct to oral therapies for DCS may help to reduce risk for secondary infection. We typically instruct our patients to use an antimicrobial cleanser to wash the entire scalp during showering or bathing on a daily basis.
Other therapies — Other treatments associated with improvement in DCS in small numbers of patients include oral zinc sulfate, dapsone, intracavitary foam sclerotherapy, radiation therapy, and application of a pressure dressing. Additional study is necessary to confirm efficacy of these interventions.
●Pharmacologic therapies
•Antibiotics – In a retrospective study that included four patients treated with dapsone (at a dose of 50 or 100 mg per day) for DCS, two had a complete response, and two had a partial response [12]. The mean treatment duration was nine months. In a case report, combination treatment with dapsone (at a dose of 100 mg per day) and isotretinoin (at a dose of 80 mg per day) was associated with clinical improvement within four weeks after failure of isotretinoin monotherapy [53].
Benefit of azithromycin [9] and ciprofloxacin [54-56] has also been documented in case reports.
•Other biologic drugs – The interleukin (IL) 23 inhibitors tildrakizumab [57] and risankizumab [58,59] and the IL-17 inhibitor secukinumab [60] have appeared beneficial for individual patients with refractory DCS [60].
•Oral zinc sulfate – Improvement with oral zinc sulfate is described in case reports. In one case report, a patient treated with oral zinc sulfate for six months had disappearance of nodules and hair regrowth within the first three weeks, complete healing after three months of therapy, and sustained remission for at least five years [61]. In another report, an adolescent with DCS and acne conglobata had flattening of nodules within 4 weeks and hair regrowth after 12 weeks but required continued treatment with a lower dose of oral zinc sulfate to maintain improvement [62].
•Oral corticosteroids – Oral corticosteroids are not used as a primary treatment for DCS but are sometimes prescribed as adjunctive therapy for highly inflammatory presentations of DCS [7,35]. We do not use oral corticosteroids for DCS because the need to continue therapy for maintenance of benefit and the serious adverse effects associated with long-term systemic corticosteroid therapy. (See "Major adverse effects of systemic glucocorticoids".)
●Procedural therapies
•Lasers – Examples of laser interventions described as beneficial in case reports include laser hair reduction with a long-pulsed neodymium-doped yttrium aluminum garnet (Nd:YAG) [63] or pulsed diode [64] laser, laser resurfacing with a carbon dioxide (CO2) laser [65], and treatment with a 2940 nm multifractional erbium-doped yttrium aluminum garnet (Er:YAG) laser [66].
•Photodynamic therapy – Aminolevulinic acid photodynamic therapy was associated with improvement in case reports and small case series [67-70].
•Intracavitary foam sclerotherapy – Use of intracavitary foam sclerotherapy as a method of inducing fibrosis within fluid-filled subcutaneous cavities in DCS was associated with improvement in signs and symptoms of DCS in a case series of three patients. [71].
•Radiation – Near-complete or complete remission after x-ray epilation has been documented in case reports and small case series [35]. However, use of x-ray epilation for DCS has fallen out of favor due to long-term safety concerns.
•Pressure dressings – Resolution of a fluctuant nodule refractory to medical therapy with use of a pressure dressing for four months is documented in a case report [72].
PROGNOSIS AND FOLLOW-UP — Because DCS is a chronic disorder with frequent relapses, long-term follow-up is essential. Some hair regrowth may occur once the disease is satisfactorily controlled in sites where sufficient damage to the hair follicles has not occurred. Patchy scarring alopecia can develop in longstanding cases [22].
Rare complications include squamous cell carcinoma in longstanding disease [73] and calvarial osteomyelitis [74].
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Dissecting cellulitis of the scalp (DCS) is a chronic inflammatory disease of the scalp that can result in scarring and permanent hair loss. DCS most commonly affects adult males; however, other individuals can develop DCS. (See 'Epidemiology' above and 'Prognosis and follow-up' above.)
●Pathogenesis – The pathogenesis of DCS is unclear. The disease may result from a defect of follicular keratinization that leads to obstruction of hair follicles. DCS may occur in association with other follicular occlusive disorders. (See 'Pathogenesis' above and 'Associated disorders' above.)
●Clinical features – Patients with DCS typically develop multiple boggy, suppurative nodules on the vertex and posterior scalp with interconnecting sinus tracts (picture 1A-E). Purulent or bloody drainage is common. Hair loss is usually patchy. (See 'Clinical features' above.)
●Diagnosis – A diagnosis of DCS usually can be made based upon the patient history and physical examination. A bacterial culture should be performed to rule out secondary infection. When the diagnosis is uncertain, a scalp biopsy can be helpful for confirming DCS. (See 'Diagnosis' above.)
●Treatment – Data on the treatment of DCS are limited, and the ideal approach to treatment is unclear. (See 'Approach to treatment' above.)
•Initial treatment – For the initial treatment of DCS, we suggest a course of oral doxycycline rather than other treatments (algorithm 1) (Grade 2C).
For most patients with an inadequate response to doxycycline, we suggest a trial of minocycline prior to proceeding to other therapies (Grade 2C). Tetracyclines are generally well tolerated, and in our experience, some patients with inadequate responses to doxycycline have greater improvement with minocycline. However, proceeding directly to oral isotretinoin is a reasonable alternative, particularly for patients with severe DCS. (See 'Preferred initial therapy' above.)
•Relapse after cessation of tetracyclines – The frequency of relapse influences our approach to DCS that responds to tetracyclines but relapses after cessation (algorithm 1). For patients with infrequent relapses (one or fewer relapses per year), we suggest a course of the previously effective antibiotic rather than other therapies (Grade 2C). For patients with relapses treated with doxycycline, we suggest subsequent continuation of doxycycline at a subantimicrobial dose for maintenance therapy (Grade 2C).
We manage patients with a higher frequency of relapse (>1 relapse per year) or rapid relapse (eg, relapse within three months after treatment cessation) similarly to patients with disease refractory to tetracyclines.
•Disease refractory to tetracyclines – For patients with DCS that cannot be adequately controlled with oral tetracyclines, we suggest oral isotretinoin rather than other therapies (algorithm 1) (Grade 2C). Treatment with a biologic tumor necrosis factor (TNF) inhibitor (adalimumab or infliximab) or combination therapy with clindamycin and rifampin is an alternative next-line therapy for patients who cannot receive oral isotretinoin. (See 'Biologic TNF inhibitors' above and 'Clindamycin and rifampin' above.)
Surgical excision is an option for disease that cannot be satisfactorily managed with medical therapy. Surgical excision may lead to long-term remission but typically results in extensive scarring. (See 'Surgical excision' above.)
•Acute treatment of painful, fluctuant nodules – Adjunctive intralesional corticosteroid injection and incision and drainage may be helpful for achieving rapid symptom relief. These interventions do not alter the course of the disease and should not be used as primary treatment.
For patients with painful, nonfluctuant or minimally fluctuant nodules who require acute symptom relief, we suggest intralesional corticosteroid injection rather than incision and drainage (Grade 2C). For patients requiring relief from fluctuant, suppurative nodules, we suggest incision and drainage (Grade 2C). (See 'Painful or very fluctuant lesions' above.)
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