4. Mixed cicatricial alopecias

#### 4.1. Acne keloidalis

initial lesion is erythema follicular pustule and papule. These can be painful and itchy. Later, new pustules are observed and accumulated to form pustular milier abscess (Figure 2). Consequently, cicatricial alopecia plaques have been formed [67]. Tufted folliculitis is characterized by having more than one hair on dilated orificial follicles. It is often seen in folliculitis decalvans [67, 68]. Concurrently DLE, LPP, acne keloid, and tinea capitis can occur during the course. In order to diagnose folliculitis decalvans, biopsy must be taken from pustules. Although pathognomonic findings are absent in the histopathological evaluation, follicular neutrophilic pustules in the early stages, plasma cells in chronic period are seen. As a response to follicular damage, foreign matter granules can be formed and consequently common fibrosis occurs. Careful histological and clinical evaluation should be carried out even after the diagnosis since the disease can overlap with other alopecias. Diagnosis should take into consideration of dissecting folliculitis, acne keloid, erosive pustular dermatosis,

Bacterial cultures should be taken from each patient and antibiotic resistance should be determined prior treatment. Long-term antibiotics targeting S. Auerus must be used. Tetracycline, coloxylin, erythromycin is used as first-line therapy. Antibiotic treatment is initiated as in acne and reduced according to the response. The disadvantage of antibiotic therapy is recurrence. Clindamycin and rifampicin is used in combination in unresponsive patients. Other effective choice of therapy is isotretinoin. It can be administered intralesionally in fast progressive cases. Other treatments include dapsone, hydroxychloroquine, adalimumab, infliximab. Wigs can be recommended as cosmetic camouflage in patients with cicatricial

Described by Hoffman in 1908, it is also known as perifolliculitis capitis abscedens et suffodiens. It forms follicular occlusion triad along with acne conglobate and hidradenitis

acne necrotica, DLE, CCCPA, LPP, and pseudopelade [67, 68].

Figure 2. Folliculitis decalvans; pustules on the scalp are noticed.

alopecia [36, 69, 70].

186 Hair and Scalp Disorders

3.2. Dissecting cellulitis

Acne keloidalis was first described in 1869 by Kohn. This disease is also known as folliculitis keloidalis nuchae or folliculitis keloidalis. The term acne keloidalis is somewhat of a misnomer since the condition is neither a kind of acne nor keloidal in nature. Acne keloidalis is most often seen in African Americans. The prevalence in American football players is 15%. Mechanical trauma, infections, autoimmunity, and drugs are the causes in its etiopathogenesis [76–78]. It is clinically developed in the early stages on the occipital scalp and on the nape of the neck as reddish-brown colored papules with smooth surface. Occasionally, these papules transformed into nodules and plaques. Pustules and abscesses are rarely occurred. Intrafollicular and perifollicular lymphocytes and plasma cell infiltrates are histopathologically involved in the early lesions. In the advanced stages, follicular destruction develops. Sebaceous glands disappear. Differential diagnosis should include folliculitis decalvans, acne necrotica, and dissecting folliculitis [1, 76].

First-line therapy of acne keloidalis is prevention. Preventing trauma and infections is important. In mild cases, combination of potent topical corticosteroids with topical antibiotics is advantageous. Oral tetracycline may be added to the monthly injections of intralesional corticosteroids. Partial response can be obtained by cryotherapy and laser therapy. Effective lasers include carbon dioxide, 1064 nm Nd:YAG or 810 nm diode. Surgical excision may be needed for common keloidal plaques. Surgical approaches include excision with primary closure or secondary intention healing. Deep surgical excision is more efficient. Surgical excision is an effective option [36, 79, 80].

#### 4.2. Acne necrotica

Acne necrotica is also known as folliculitis necrotica. It is a mysterious disease not understood by many dermatologists. Infections are routinely mentioned in its etiology but evidence cannot be demonstrated. Drugs and food allergies are also thought to be the cause. Mechanical factors such as itching only spread the disease. Most of patients are women. Lesions are generally observed on the scalp along face and hairline. They are rarely occurred on nose and cheeks [4, 81, 82]. Initial lesions are umbilicated follicular papules. Not long after, they transformed into pustules. Consequently, varioliform scars may develop. Initially perivascular and perifollicular lymphocytic infiltrate, subepidermal edema is apparent. In the advanced stages, necrosis is observed in the follicular epithelium and epidermis [3, 81]. Neutrophiles can be seen in superficial dermis. Differential diagnosis should also include folliculitis decalvans, dissecting folliculitis, colitis, eczema herpeticum, and molluscum contagiosum [81, 82].

Treatment with oral tetracycline, antistaphylococcal antibiotics may be effective. They should be used in long term. In patients not having complete response, topical or intralesional corticosteroid can be added. Isotretinoin treatment may prolong the remission period [4, 43].

#### 4.3. Erosive pustular dermatosis

The disease was first described in 1979 by Pye et al. and about 100 cases have been reported so far [83]. The disease most commonly occurs in elderly and females. Sun damage, local trauma (surgery, cryotherapy, herpes zoster), and autoimmunity are blamed in its etiology. Lesions with crusts and pustules on atrophic skin are clinically observed. The number of pustules can vary remarkably, and in some cases they are absent. Pain and pruritus in the lesions are not observed. However, cicatricial alopecia may develop in the advanced stages. Histopathology is uncharacteristic and not very helpful in confirming the diagnosis [84, 85]. Histopathological examination is crucial to exclude other diseases. Histopathology shows subcorneal pustules, epidermal atrophy, and erosions. In addition, these findings can be accompanied by a polymorphous dermal inflammatory infiltrate and in some cases leukocytoclastic vasculitis might be present. The differential diagnosis should consider tinea capitis, Gram-negative folliculitis, pyoderma gangrenosum, DLE, pemphigus vulgaris, and SCC. High-potency topical steroids reduce the inflammation significantly [1, 85].

Steroids must be used more than 6 months for better responses. Other treatment options include tacrolimus, dapsone, calcipotriol, and acitretin. Sun protection is reported to be effective since disease etiology includes actinic damage [86, 87].

#### 5. Conclusion

Cicatricial alopecia forms an important group of disorders that end up with scarring and persistent hair loss. An elaborate physical examination, skin biopsies and blood tests can be helpful in order to establish the accurate diagnosis and to suggest the most appropriate treatment for the hair loss. Many patients do not respond to the first treatment they receive and the condition frequently relapses when treatment is stopped. Some clinics offer surgical treatment, such as scalp reduction surgery and hair transplantation, but it may not be suitable for all patients. Patients often have significant psychosocial impact and management of these patients should address not only their physical but also psychological aspects.
