Some sources consider acne vulgaris part of the differential diagnosis for an acneiform eruption. From Wikipedia, the free encyclopedia. Can Fam Physician. Andrews' Diseases of the Skin: Clinical Dermatology. Page February MeSH : D Disorders of skin appendages L60—L75 , — Hirsutism Acquired localised generalised patterned Congenital generalised localised X-linked Prepubertal.
Perioral dermatitis Granulomatous perioral dermatitis Phymatous rosacea Rhinophyma Blepharophyma Gnathophyma Metophyma Otophyma Papulopustular rosacea Lupoid rosacea Erythrotelangiectatic rosacea Glandular rosacea Gram-negative rosacea Steroid rosacea Ocular rosacea Persistent edema of rosacea Rosacea conglobata variants Periorificial dermatitis Pyoderma faciale. Folliculitis Folliculitis nares perforans Tufted folliculitis Pseudofolliculitis barbae Hidradenitis Hidradenitis suppurativa Recurrent palmoplantar hidradenitis Neutrophilic eccrine hidradenitis.
Acrokeratosis paraneoplastica of Bazex Acroosteolysis Bubble hair deformity Disseminate and recurrent infundibulofolliculitis Erosive pustular dermatitis of the scalp Erythromelanosis follicularis faciei et colli Hair casts Hair follicle nevus Intermittent hair—follicle dystrophy Keratosis pilaris atropicans Kinking hair Koenen's tumor Lichen planopilaris Lichen spinulosus Loose anagen syndrome Menkes kinky hair syndrome Monilethrix Parakeratosis pustulosa Pili Pili annulati Pili bifurcati Pili multigemini Pili pseudoannulati Pili torti Pityriasis amiantacea Plica neuropathica Poliosis Rubinstein—Taybi syndrome Setleis syndrome Traumatic anserine folliculosis Trichomegaly Trichomycosis axillaris Trichorrhexis Trichorrhexis invaginata Trichorrhexis nodosa Trichostasis spinulosa Uncombable hair syndrome Wooly hair Wooly hair nevus.
In a viral folliculitis, a lower concentration of inflammation is noticeable. In some cases, hyperplasia of epidermis, necrosis of follicular epithelia or sebaceous gland can be visible. Fungal folliculitis is commonly seen in adult women living in warm and humid climates. Immunosuppression, diabetes and antibiotic use can be predisposing factors. The cause is mostly Malassezia globosa Malassezia furfur. Inside the dilated hair follicle due to keratin plug, numerous yeasts are visible Figure 3. Around hair follicle mild chronic inflammation including eosinophils can be seen.
The rupture of follicle transforms chronic inflammation to acute inflammation consequently abscess formation and granulation tissue can be seen [ 4 ]. In the syphilitic folliculitis, plasma cells are dominant [ 6 ]. There are some possible and practical methods for finding the cause of folliculitis such as: Gram staining for bacteria , PAS or silver stain for fungi and immunohistochemistry for viral causes. However, the sensitivity of these methods can be low. The more sensitive and specific methods such as fresh tissue culture, PCR, etc.
Folliculitis can also be classified according to microanatomic structure of the skin which is involved. Most of bacterial folliculitis involves the superficial part of hair follicle that is why they are called superficial bacterial folliculitis. The superficial folliculitis caused by S. In deep folliculitis tenderness, warmth, and erythema are visible in a wide area. Nodules are formed. They are most commonly seen in buttocks, axilla, and legs.
Furuncle: deep folliculitis includes only one hair follicle. More than one furuncle combines to form carbuncle [ 5 ]. This term means that there is an acneiform dilatation in the hair follicle e. In demodex folliculitis, besides the mites located inside the hair follicle, follicular spongiosis, perifollicular lymphohistiocytic inflammation also draws attention.
An isolated folliculitis is generally self-limited. In old and advanced lesions of all folliculitis perifollicular fibrosis can be visible. When clinically folliculitis is among the differential diagnosis but histopathologically the lesion is not seen in biopsy sections, deeper and serial sections must be taken. When histopathologically folliculitis diagnosis is made but no microorganism is detected, additional histochemical and immunohistochemical stains can be implemented. Acneiform lesions should be thought primarily when no microorganisms detected microscopically and by applying additional methods culture, etc.
On the other hand, for diagnosis of acneiform lesions a hundred percent clinical correlation is required. During investigation if a microorganism is detected, cure rate is very high with appropriate treatment topical antibiotic, topical antifungal, and systemic antiviral drugs. Eosinophils are predominant in some kinds of folliculitis.
When eosinophils are predominantly seen in folliculitis, the first step should not be searching for microorganisms. Bacteria and yeast fungi can accompany this clinic course. Ofuji disease eosinophilic pustular dermatosis is a rare disease generally detected in Japan, characterized by pruritic follicular papules and pustules located on the face and scalp [ 5 ]. Histopathologically follicle infundibulum is surrounded by inflammation which is predominantly composed of eosinophils and few lymphocytes. The follicle can be ruptured but granuloma formation is not expected.
Eosinophilia in peripheral blood and increased serum IgE levels can be detected in eosinophilic folliculitis. There is also a self-limiting variant of eosinophilic folliculitis presenting on the scalp of children with numerous papules and pustules. In the year , Brunstig described folliculitis decalvans a component of the follicular occlusion triad.
Other components of the triad include: acne conglobata a kind of nodulocystic acne and hidradenitis suppurativa acne inversa or apocrine acne. The histology of these disorders is similar. In all three disorders, abscess formation, suppurative granulomas, and finally sinus tracts are formed as a result of follicular hyperkeratinization [ 3 ]. Generally, culture is negative in these three disorders. Acne conglobata : giant comedones, cysts, and nodules are located on the neck and chest. These lesions leave large irregular scars and can end up with epidermal cysts.
Hidradenitis suppurativa is actually a wrong nomenclature because apocrine and eccrine sweat glands are generally affected secondarily. It favors axilla and groins. Histopathologically, the hair follicle is dilated and the apocrine gland duct is plugged with keratin. Some authors accept pilonidal sinus as a component of follicular occlusion triad. In pilonidal sinus disease, hair shafts are embedded in fibrosis they continue growing and elongating inside fibrosis Figure 4.
Histopathologically dense suppurative inflammation, fragmented hairs, abscess formation, and necrosis are seen one within the other. Acne keloidalis nuchae and acne conglobata component of follicular occlusion triad are frequently seen together and generally seen in the black race. Acne keloidalis nuchae favors posterior part of scalp and neck. Lesions end up with scars. In the beginning, discrete papules and pustules are detected [ 5 ].
This condition is also called folliculitis keloidalis nuchae. This is among the causes of scarring alopecia [ 4 ].
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In curly hairs, the hair infundibulum is believed to grow backwards and cause a reaction in dermis which in turn triggers scarring. Follicle is surrounded by lymphocytes and plasma cells. Inflammation is observed in the upper part of the follicle. Ruptured follicles cause secondary granuloma formation. Abscess formation and sinus tracts can also be formed. Dense hypertrophic scar and collagenosis is noticeable Figure 5. Exactly a true keloid formation is not seen [ 6 ]. Dystrophic calcification can be seen in scarring acne lesions.
The lesions are formed due to the transition of hair from infundibulum to the surrounding epidermis. Histopathologically mixed type inflammatory cells and foreign-body-type giant cells are seen in the intrafollicular and perifollicular area.
The lesions present as umbilicated erythematous papules and pustules. The lesions are located in the follicle. Comedones are not expected [ 2 ]. The term acne is misnomer. Histopathologically perifollicular lymphocytic infiltrate is seen. This infiltrate makes exocytosis into follicular epithelia and causes dense necrosis in keratinocytes. In advanced lesions, necrosis of the follicles can be confluent and clinically ends up with formation of depressed scars [ 6 ].
There are some acne forms that are induced or developed by drugs, sunlight exposure, impulsive skin picking, or different materials. Acne cosmetica pomade acne : this clinical entity is a temporary follicular occlusion that ends up with acneiform eruption. Acne cosmetica is caused by dense cosmetic usage.
- Acneiform eruption.
- Oxygen Transport to Tissue. Satellite Symposium of the 28th International Congress of Physiological Sciences, Budapest, Hungary, 1980.
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The follicle infundibulum is dilated and thin. Histopathologically in addition to classical acne findings, pseudoepitheliomatous hyperplasia, intraepithelial small abscess and granulomatous inflammation can be seen [ 3 ]. Chemical exposure to mineral oils and dioxin can cause acneiform eruptions predominantly comedones, this is called chloracne. The comedones are shaped as a bottle or column. Follicular keratin stasis and increased melanocytic activity is detected in epidermis and hair infundibulum [ 7 ].
Steroid-induced acne is caused as a result of high dose corticosteroid treatment. In contrast to chloracne comedones are not expected.
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Generally monomorphic pustules are observed [ 8 ]. EGFR inhibitors can cause acneiform drug reaction [ 3 ]. Acne aestivalis Mallorcan acne : presents with papules and pustules, favors head and neck, sun exposure triggers the lesions. Histopathologically folliculitis and necrosis of follicular epithelia is noticeable [ 9 , 10 ]. Morbus Morbihan Morbihan disease : is a clinical form of severe acne which presents with solid facial edema and favors primarily the central face area.
Acne fulminans: characterized by abrupt onset of tender nodules, plaques, and ulcers. Clinically fever, lymphadenopathy, hepatosplenomegaly, weight loss, etc. Acne Excoriee: scratched acneiform lesions seen in young women due to impulsive picking emotion. Acne mechanica: acneiform lesions are observed secondary to hair friction caused by hat, helmet, etc.
Nevus comedonicus acne nevus : is a term used when multiple open comedones are gathered together on a plaque lesion [ 3 ]. This lesion can also be evaluated as a hamartoma made up of small infundibular cysts [ 6 ]. In conclusion, a comprehensive dermatological examination and detailed history taking is indispensable in all clinical entities mentioned above. Flowchart 1 summarizes all the above-mentioned clinical entities.
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Acne vulgaris is the prototype of acneiform lesions and is the inflammatory disease of sweat glands and pilosebaceous units, mostly observed in teenagers and young adults. In contrast to age predilection, race and sex predilection do not exist. The clinical course is severe in male patients [ 2 ].
Acne lesions favor forehead, chin, cheek, chest, shoulder, and back.
Family history may be present. In most patients, the lesions regress in a few years period. The lesions are generally presented as erythematous papules, pustules, blackheads, and whiteheads. In severe cases, tender and painful nodules and cysts can be apparent. Because hair follicle is plugged with keratin, excreted sebum is accumulated in addition to P.
Severe desquamation of follicle epithelia and sebaceous gland epithelia also plays a role in pathogenesis. Acne vulgaris lesions are studied in two groups: noninflammatory blackheads and whiteheads or comedones and inflammatory folliculitis, etc. Acne lesions can end up with postinflammatory hyperpigmentation and scars Figures 6 — 8.
Keloid formation is quite rare. Deeper part of the same lesion in Figures 6 and 7. Acne is diagnosed clinically, and biopsy confirmation is generally not required.
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Histopathologically noninflammatory lesions comedones are a kind of follicular retention cysts. These tiny cysts may consist of cornified cells, hair shafts, sebum, P. The precursors of inflammatory lesions are generally closed comedones or subclinical microcomedones. Open comedones do not trigger the inflammatory process. In comedonal lesions around the affected hair follicle, few inflammatory cells may be present. Comedonal lesions due to retention the follicular wall is quite thin and the follicular content oozes into adjacent dermis which in turn causes accumulation of inflammatory cells in dermis.
This process plays the major role in the formation of inflammatory lesions. When the follicle wall becomes much thinner, the follicle may rupture and lead to pustule Figure 13 and by the time, nodule formation is in deep dermis. Depending on follicular damage and severity of inflammatory response scar formation, dermal necrosis, and confluent abscesses formation can be observed. Perifollicular elastolysis can be noticed in acne vulgaris scars [ 8 ]. In a noninflammatory lesion if the follicular opening does not expand the follicular wall becomes thinner thus follicular rupture becomes inevitable [ 8 ].
Spongiosis is noticeable in follicular epithelia of both inflammatory and noninflammatory lesions. In inflammatory lesions the inflammatory cells attacking follicular epithelia or perifollicular inflammatory cells are composed of mixed type cells polymorphonuclear leucocytes, lymphocytes, histiocytes. Rosacea is a disease characterized by macular erythema and flushing of central face generally affecting adult population.