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13 Lugovic PDF
13 Lugovic PDF
Review
University Hospital Center, Zagreb; 3Department of Neurosurgery, Dr Josip Benčević General Hospital, Slavonski
Brod, Croatia
Table 1. Differential diagnosis of the scalp hair folliculitis according Camacho et al.2
Other
Superficial Deep Superficial Deep Predominantly
possibilities Predominantly
(generally (generally (generally (generally lymphocytic
(spongiotic granulomatous
suppurative) granulomatous) suppurative) granulomatous)
folliculitis) Primary Secondary
Fungi: Demodicosis Acne vulgaris Acne vulgaris Pruritic Keratosis Demo- Perioral
Dermatophytes folliculitis of pilaris and dicosis dermatitis
Pityrosporum Favus and Rosacea and perioral Lupoid pregnancy keratosis Vitamin C
Candida kerion dermatitis rosacea spinulosa deficiency Acneiform
Acne Fox-Fordyce eruption
Bacteria Tinea barbae Eosinophilic conglobata disease Keratosis Vitamin A secondary to
(Bockhart`s pustular folliculitis Keloidal acne pilaris deficiency syphilis
impetigo) Majocchi`s of the neck Infundibulo- atrophicans
Secondary trichophytic Toxic erythema folliculitis Due to
syphilis granuloma of the newborn Perforating Lichen lithium
folliculitis planopilaris
Viruses: Furuncle Follicular mucinosis
Herpes simplex Toxicoderma: Pityriasis
zoster Carbuncle Mechanical and Halogens rubra pilaris
Molluscum chemical traumas Lithium
contagiosum Sycosis
Toxicodermas: Pseudofolliculitis
Acneiform Halogens
syphilis Steroids
Pseudofolliculitis
follicular orifice1. Inflammatory diseases of the scalp Thus, folliculitis can be classified according to his-
hair follicle frequently manifest as folliculitis, which tological features and/or presence of microbiological
may lead to cicatricial or non-cicatricial alopecia, de- agents. There are several characteristic histopathologic
pending on whether or not the perifollicular infiltrate patterns of hair scalp folliculitis2. In acute folliculitis,
or the etiologic agent spares the hair follicle2,3. It is moderate neutrophil infiltrate can be seen infiltrating
often difficult to make an adequate diagnosis of scalp follicular epithelium, with the formation of micro- or
hair folliculitis and it usually requires considerable macro abscesses. Tissue necrosis may be discrete and
time and effort to recognize and treat the disease. is usually limited to the follicular infundibulum and
Besides the noninfectious causes, there are numer- the adjacent dermis, or it may be significant, affect-
ous infective pathogens that may cause folliculitis, ing the entire pilosebaceous complex. In chronic fol-
including bacteria, viruses and fungi. Diabetes mel- liculitis there is moderately dense lymphocytic infil-
litus, hyperhidrosis, maceration, tight-fitting clothes, trate, usually a granulomatous infiltrate with a foreign
particularly in obese people, inadequate use of topical body reaction around the keratin. The inflammation is
corticosteroids and halogenated compounds, skin care nodular, poorly defined and composed of neutrophils,
products and topical hydrocarbons, such as oils or tars lymphocytes, histiocytes, and giant cells. Plasmacytic
(occupational exposure) may precipitate exacerbation chronic folliculitis predominantly occurs in facial fol-
of folliculitis. In addition, immunocompromised pa- licles, such as perioral dermatitis, keloidal acne and
tients, such as HIV/AIDS patients, may present with solid facial edema, folliculitis decalvans and carbun-
various types of folliculitis. cle2,4.
Other histological forms of folliculitis are pre- covered by grayish scales. Hairs break at 4-6 mm and
dominantly eosinophilic folliculitides and spongiotic if they are plucked and placed on a black surface, one
folliculitides with characteristic features of infundib- can see the surrounding white ‘frosted sheath’ (spores
ulofolliculitis. One distinct form is follicular mucino- of the mosaic ectothrix). Hairs fluorescence in Wood’s
sis, which often histologically presents in spongiotic light and can therefore be easily identified 2.
folliculitis as keratinocytes get separated by mucin Trichophytic ringworm tinea of the scalp (black dots
deposits, but dermal mucin deposits can also be found tinea) affects only several follicles and manifests with
in lupus erythematosus and Fox-Fordyce disease. De- multiple small alopecic areas, which sometimes merge
struction of the hair follicle can sometimes ensue, at into a larger polycyclic patch with the characteristic
the ‘end-stage’ of folliculitis. Suppurative and granu- interior composed of healthy hair. The most specific
lomatous folliculitis generally destroys the follicle sign is the presence of ‘black dots’, which is very fragile
leading to cicatricial alopecia. The presence of keratin hair infested by endothrix parasite, broken at the level
is important as well. Prominent plugs of keratin with- of infundibulum or slightly above. Dermatopatho-
in the dilated follicular orifice lead to chronic-stage logical features of tinea tonsurans are chronic der-
perifolliculitis. matitis with vasodilatation, lymphocytic perivascular
infiltrates with occasional spongiosis. Special staining
Folliculitis Due to Infective Agents may reveal the fungus in the corneal layer, ecto- or
The majority of infectious folliculitides are caused endothrix arthrospores and Adamson’s fringe.
by bacteria and fungi (such as pityrosporum, demodex, Kerion Celsi is an inflammatory tinea of the scalp,
or other agents)5-7. These clinical variants of folliculitis generally caused by zoophilic, geophilic or anthropo-
can be diagnosed by adequate sampling, swabs, KOH philic dermatophytes, accompanied by severe inflam-
examination/or fungal cultures of expressed follicu- matory reaction. It starts as tinea tonsurans and soon
lar content. Thereby, diagnosis of these skin changes becomes indurated and covered with squamous crusts
includes identification of the infection, while therapy and pustules. In a few weeks it becomes red, painful
includes treatment of the infection. and warm, from small disseminated pustular plaques
Viral folliculitis is rare. Folliculitis due to herpes to plaques up to 10 cm. Deep suppurative folliculitis
simplex hominis and varicella-zoster may occasionally af- and perifolliculitis occasionally reaching the hypoder-
fect the pilosebaceous structures, affecting the beard mis can be seen on histopathologic examination. Over
area in males (‘viral sycosis’), manifesting as a group of time, the infiltrate becomes lymphocytic.
erythematous papulovesicles or umbilicated vesicles. Favus is folliculitis caused by T. schoenleinii and it
is currently prevalent in Spain. It begins with small
Fungal Folliculitis erythematosquamous patches with slight infiltration.
Dermatophytes, saprophytes such as Pityrospo- Underneath the scales, there are pseudopustular yel-
rum and Candida sp. may cause various folliculitides. lowish elements in the initial phase of the ‘scutulum’
Dermatophytic folliculitis is very common and can be of the ‘favic cup’, somewhat elevated and umbilicated
caused by all dermatophytes except for E. floccosum, T. centrally, sulfur yellow in color with soil-like consis-
concentricum and M. persicolor. In vitro cultures can be tency, since they are made up of mycelia and epithelial
used for identification of these keratinophilic fungi. detritus. The underlying epidermis is emanating rather
We can therefore visualize whether the hair is invaded unpleasant odor caused by detritus, exudate, pus and
by concentric destruction, or by perforation with ‘per- secondary bacterial infection. Affected hair is luster-
forating organs’, indicating T. mentagrophytes. There less, gray, dry, and fluorescent under Wood’s light.
is variation in clinical presentation of dermatophytic Pityrosporum folliculitis may be seen on the skin in
folliculitis. periphery of the scalp. This is a superficial pustulosis
Microsporous ringworm tinea of the scalp (great which most frequently affects the back and the upper
gray patch tinea) is a non-inflammatory tinea ton- part of the thorax, typical sites for Pityrosporum or-
surans of the scalp characterized by typical large biculare, although it can sometimes affect upper limbs
round or polycyclic plaques and small satellite patches as well.
tory infiltrates around thick, compact, keloidal col- oid scars, predominantly located on the face, throat,
lagen bands, which correspond to destroyed follicles shoulders, chest, back, gluteal region, or beside scalp
or sometimes peripilar granulomas. Therapy includes area. In the areas with apocrine glands, like the axil-
topical steroids, antibiotics, retinoids, cryotherapy, e lae and the groin, this causes hidradenitis suppurativa
tc. or dissecting cellulitis in the scalp region. Histologic
Tufted hair folliculitis manifests with a ‘tuft’ of examination shows deep folliculitis, progressing to-
hair made up of 5 to 20 hairs, which appear normal wards the formation of abscesses and, with subse-
in the follicular openings that remain in the alopecic quent reepithelialization of the follicular unit, leaving
plaque13. It also appears to be caused by S. aureus, a sinus and fibrosis. Hidradenitis suppurativa, dissect-
although it is possibly related to immunodeficient ing cellulitis and acne conglobata often coexist as a
states or is of ‘nevoid origin’. It manifests as exudative follicular occlusion triad.
patches on the parietal or occipital areas, which tend Acne necrotica (acne varioliformis, necrotizing
to progress peripherally leaving cicatricial alopecia in lymphocytic folliculitis) is a rare, chronic pruritic
the center. Histologically, there is a perifollicular in- eruption of multiple follicular papules which rapidly
filtrate composed of lymphocytes, eosinophils, plas- progress into umbilicated vesiculo-papules or pus-
mocytes and neutrophils with inflammation around tules, sometimes with a central crust, mostly located
the upper portion of the follicle, which does not affect in the temporal areas, nape and the frontal implan-
the bulb. Topical antiseptics and systemic antibiotics tation line2. Most patients are adult women. Over
(erythromycin, tetracyclines and doxycycline) improve weeks, it slowly involutes, leaving a varioliform scar1.
the inflammatory component. Use of shampoos with Histopathologically, there is epidermal damage with
mineral oils and keratolytics is also advised. mixed dermal inflammatory infiltrates in more ad-
Erosive pustular dermatitis is a pustular dermatosis vanced crusted lesions, while lymphocytic perifolli-
with erosions and crusts covering the scalp, generally cular infiltrates and other adnexal structures in early
caused by S. aureus, or rarely S. epidermidis, Pseudomo- lesions sometimes cause spongiosis. Excoriated bacte-
nas aeruginosa, coagulase negative staphylococcus, rial folliculitis or rarely herpes simplex virus is con-
diphtheroids, coliforms and Proteus mirabilis. Candida sidered in its etiopathogenesis. Isotretinoin has good
sp. and other fungi have also been cultured in some therapeutic results and corticosteroids often bring
cases, but these seem to reflect secondary coloniza- immediate improvement. Topical therapy is generally
tion14,15. Follow-up is very important since carcinoma- ineffective, although potent topical corticosteroids or
tous transformation may occasionally occur. Despite benzoyl peroxide may be helpful1.
the nonspecific histological features, there is chronic Acneiform eruptions can sometimes be seen on
perifollicular inflammatory infiltrate composed of the scalp, such as in case of chloracne. Chloracne are
lymphocytes, plasmocytes and giant cells15. It has been caused by the exposure to chlorinated compounds
suggested that exposure to ultraviolet light may be a which can be found in industry, usually in electrical
predisposing factor. Treatment includes nonsteroid conductors, and therefore may represent an occupa-
anti-inflammatory agents, topical and systemic antibi- tional disease. Clinically, it manifests with cysts and
otics. Superficial bacterial folliculitis usually responds comedones that are usually open, covering temporal
well to antiseptic baths such as povidone iodide and areas, cheeks, throat and retroauricular region16. The
chlorhexidine gluconate, to astringent aluminum sub- treatment includes topical/oral antibiotics, topical/
acetate compresses and to topical antibiotics (poly- oral retinoids excision, laser ablation, and drug with-
myxin B sulfate, neomycin sulfate, fusidic acid and drawal.
mupirocin). Deep folliculitis requires treatment with Lichen planopilaris is a form of lichen planus locat-
systemic antibiotics (e.g., cephalosporins, azithromy- ed on the scalp, characterized by perifollicular erythe-
cin, semisynthetic penicillins). ma and small keratotic pruriginous follicular papules
Acne conglobata represent a chronic inflammatory resulting in small alopecic plaques17-19. It is more com-
process which manifests with nodules, cysts, abscess- mon in the hair implantation line, both the frontal
es, draining sinus tracts, comedones and multiple kel- hair implantation line and the occipital line, although
it can also appear on any other part of the scalp. The lar plugs on the nose and cheeks, which later expand
disease occurs more frequently in women between to the scalp, neck and extremities causing atrophy in
age 30 and 602. There are three different types of these areas. The atrophic aspect of the cheeks and ci-
the disease according to clinical manifestations and catricial alopecia on the scalp, eyebrows and eyelashes
histopathologic features: keratotic follicular papules make all these children look very much alike. At the
and inflammatory lichenoid infiltration in the folli- beginning, it is accompanied with milium cysts on
cular epithelium; violaceous or erythematous plaques, the cheeks, or possible atopy, corneal opacities, pho-
some with follicular prominence and an inflammatory tophobia, conjunctivitis, keratitis, blepharitis and pal-
lichenoid infiltrate and follicular papules associated moplantar hyperkeratosis. Oral retinoids have been
with perifollicular and interfollicular inflammatory reported to lead to improvement.
infiltrate resulting in fibrosing alopecia 2. Eosinophilic pustular folliculitis (Ofuji’s syndrome)
Rarely, patchy cicatricial alopecia of the scalp is as- is a rare dermatosis of unknown etiology, character-
sociated with non-scarring alopecia of the axillary and ized by recurrent episodes of eruptive sterile follicular
pubic areas, and grouped spinous follicular papules re- papulopustules in seborrheic areas, accompanied by
sembling keratosis pilaris on the trunk and extremi- leukocytosis and eosinophilia. It is most common in
ties (Piccardi-Lassueur-Graham-Little syndrome). men and the general population in the third decade of
Pityriasis rubra piliaris is characterized by multiple life, in which the papulopustules tend to form round
follicular papules, sometimes with a central black cor- ring-shaped or polycyclic plaques with peripheral pro-
neal plug, which generally accompanies or precedes gression and central clearing, with residual scaling and
seborrheic dermatitis of the scalp20,21. This disease pigmentations. The histopathologic features include
manifests with a yellow-orange erythematosquamous infundibular follicular pustules mainly composed of
plaques, often developing on the scalp, with obvious eosinophils and polynuclears. Topical corticosteroids
islands of sparring and palmoplantar hyperkeratosis. or tacrolimus ointment can be prescribed.
Clinically it shows multiple follicular papules with Follicular mucinosis (alopecia mucinosa) on the scalp
a central corneal plug on the lateral surfaces of the is characterized by the presence of follicular papules
thighs and arms, gluteal region and forearms. There and indurated plaques associated with alopecia. The
is a corneal plug which occludes the pore and dilates disease is accompanied with mycosis fungoides and
the follicular ostium, hyperkeratosis, dermal vasodi- angiolymphoid hyperplasia with eosinophilia, less fre-
latation with chronic perivascular and periadnexal in- quently with chronic discoid lupus erythematosus and
flammatory infiltrate. Therapy may include systemic Goodpasture’s syndrome. There is another form of
retinoids, topical corticosteroids and retinoids, mild idiopathic or primary origin (mainly affects children
keratolytic agents, etc. and young adults) presenting by grouped follicular
Keratosis pilaris atrophicans is characterized by papules. They show a tendency to coalesce into more
different clinical presentations which may be classi- or less well defined erythematous plaques with dilated
fied in two groups: hair keratosis and pseudopelade. follicular orifices on the surface of these plaques, as
There are hair keratoses that cause atrophy in glabrous well as alopecia.
skin of the face, such as folliculitis atrophicans faciei Follicular mycosis fungoides is characterized by the
and atrophoderma vermiculatum; however, keratosis presence of infiltrated follicular papules located on the
follicularis spinulosa decalvans should be referred as face, neck, trunk and extremities, and sometimes on
pseudopelade or ‘scarring follicular keratosis’2,22. The the scalp25. Histopathologically, there are perifollicu-
difference between keratosis pilaris and these four der- lar and intrafollicular infiltrates of atypical lympho-
matoses is the greater inflammatory component seen cytes with convoluted nuclei. One must differentiate
in the latter, as well as intense clinical erythema 23. this disease from follicular lymphomatoid papulosis,
Keratosis follicularis spinulosa decalvans, a type of especially type B or lymphocytic papulosis. It should
X-linked recessive genodermatosis, causes cicatricial be treated with nitrogen mustards and/or electron
alopecia of the scalp and eyebrows during infancy or therapy, but also with topical corticosteroids, photo-
adolescence2,24. It begins with corneal filiform follicu- therapy, etc.
16. Rodríguez-Pichardo A, Camacho F. Chlo- 22. Baden HP, Byers HR. Clinical findings, cutaneous pa-
racne as a consequence of a family accident with chlorinated thology, and response to therapy in 21 patients with keratosis
dioxins. J Am Acad Dermatol 1990;22:1121. pilaris atrophicans. Arch Dermatol 1994;130:469-75.
17. Matta M, Kibbi A-G, Khattar J, Salman SM, 23. Oranje AP, Van Osch LDM, Oosterwijk JC.
Zaynoun ST. Lichen planopilaris: a clinicopathologic Keratosis pilaris atrophicans. One heterogeneous disease
study. J Am Acad Dermatol 1990;22:594-8. or a symptom in different clinical entities? Arch Dermatol
18. Mehregan DA, Van Hale HM, Muller SA. Li- 1994;130:500-2.
chen planopilaris: clinical and pathologic study of forty-five 24. Puppin D, Aractingi S, Dubertret L,
patients. J Am Acad Dermatol 1992;27:935-42. Blanchet-Bardon C. Keratosis follicularis spinulosa
19. Oremović L, Lugović L, Vučić M, Buljan M, decalvans: report of a case with ultrastructural study and un-
Ožanić-Bulić S. Cicatricial alopecia as a manifestation successful trial of retinoids. Dermatology 1992;184:133-6.
of different dermatoses. Acta Dermatovenerol 2006;14:245- 25. Pereyo NG, Requena L, Galloway J,
52. Sangűeza OP. Follicular mycosis fungoides: a clinicohis-
20. Clayton BD, Jorizzo JL, Hitchcock MG, topathologic study. J Am Acad Dermatol 1997;36:563-8.
Fleischer AB, Williford PM, Feldman SR, 26. Khumalo NP, Jessop S, Gumedze F, Ehrlich
White WL. Adult pityriasis rubra pilaris: a 10-year case R. Hairdressing and the prevalence of scalp disease in Afri-
series. J Am Acad Dermatol 1997;36:959-64. can adults. Br J Dermatol 2007;157:981-8.
21. Drago F, Maietta G, Parodi A, Rebora A. Ker- 27. Ogunbiyi A, George A. Acne keloidalis in females:
atosis pilaris decalvans non-atrophicans. Clin Exp Dermatol case report and review of literature. J Natl Med Assoc
1993;18:45-46. 2005;97:736-8.
28. Parish LC, Witkowski JA, Mirensky Y. Recent
advances in antimicrobial therapy of bacterial infections of
the skin. Curr Opin Dermatol 1993;1:263-70.
Sažetak
Folikulitis vlasišta je relativno česta pojava u dermatološkoj praksi koja zbog nedostatka jasnih smjernica predstavlja
značajan dijagnostički i terapijski izazov. Općenito se upalne bolesti pilosebacealnog folikula u vlasištu najčešće manife-
stiraju kao folikulitis. Postoje brojni infektivni agensi koji mogu uzrokovati folikulitis vlasišta, kao što su bakterije, virusi
i gljive, kao i mnogi neinfektivni uzroci. Nekoliko neinfektivnih bolesti mogu imati sliku folikulitisa u vlasištu, kao što
su folliculitis decalvans capillitii, perifolliculitis capitis abscendens et suffodiens, erozivni pustularni dermatitis, lichen
planopilaris, eozinofilni pustularni folikulitis i drugo. Klasifikacija folikulitisa također je nejasna i kontroverzna. Tako se
navode različiti oblici folikulitisa i nekoliko njihovih klasifikacija. Prema ključnim varijacijama histoloških nalaza postoje
tri skupine folikulitisa: infektivni folikulitis, neinfektivni folikulitis i perifolikulitis. Dijagnoza folikulitisa povremeno
zahtijeva histološku potvrdu i ne može se osnivati samo na kliničkoj pojavi lezija vlasišta. U ovom članku su obuhvaćene
moguće upalne bolesti folikula vlasišta s mogućim diferencijalnim dijagnozama i pripadajućim histološkim značajkama.
Ključne riječi: Folikulitis; Koža glave; Perifolikulitis