skin images

Body Part: Head

  • Lichen Planopilaris

    Lichen Planopilaris

    Lichen Planopilaris

    Definition: Lichen Planopilaris (LP) is an inflammatory primary cicatricial alopecia that can result in permanent hair loss. LP is a follicular variant of lichen planus that results in progressive, patchy and permanent hair loss on the hair-bearing skin surfaces. 

    Etiology: LP is believed to be a hair-specific autoimmune disorder caused by activated T-lymphocytes targeting follicular antigens. This is theorized to be a part of a cytotoxic autoimmune response to an unknown antigen present in hair follicles. The use of nilotinib and pembrolizumab has been linked to LP.

    Epidemiology: The incidence of LP is not precisely known. LP has been reported as the most frequent primary scarring alopecia. Variants of LP include Graham-Little syndrome and frontal fibrosing alopecia. LP often affects women more than men. The peak age range of LP is between 40- 60 years.

    Signs: Many individuals with LP may develop characteristics affecting the skin, mucous membranes and nails. LP typically presents as multifocal areas with smooth white patches of scalp hair loss. There may be perifollicular erythema and perifollicular scale at the edge of the patches, and these may be spiny upon palpation. There may be cutaneous, nail and mucous membrane involvement before LP manifests on the scalp. Hairs may be easily extracted anywhere on the scalp, indicating active disease requiring treatment. The clinical course of hair loss in LP may be insidious or fulminant. Clinical features of LP do not vary in different skin types. Complications of LP include alopecia, psychological distress and reduced quality of life.

    Symptoms: Individuals with active LP may experience severe itching, burning and tenderness. 

    Differentials: Discoid lupus erythematosus, folliculitis decalvans, central centrifugal cicatricial alopecia, seborrheic dermatitis.

    Diagnosis: LP is assessed using trichoscopy, which reveals absent follicles, tubular perifollicular scale, white dots and perifollicular erythema. Diagnosis may be confirmed through scalp biopsy

    Treatment: as no treatment restored the original hair loss due to scarring, treatment aims to slow the progression of LP and relieve its associated symptoms. Anti- inflammatory agents such as corticosteroids, tacrolimus and hydroxychloroquine may be indicated. Non pharmacological measures include scalp reductions and hair transplantation in end- stage inactive disease.

    References:

    1.     Lepe K, Nassereddin A, Syed HA, Salazar FJ. Lichen Planopilaris. In: StatPearls. Treasure Island (FL): StatPearls Publishing; May 1, 2024.

    1. Lichen Planopilaris — DermNet. dermnetnz.org. https://dermnetnz.org/topics/lichen-planopilaris
  • Keloid

    Keloid

    Keloid

    Definition: Keloids are hypertrophic, smooth, hard growths or scars that occur on the skin as a result of excessive scar formation. Keloids may rarely occur spontaneously. They may develop on any part of the body and extend beyond the original wound margins. The upper chest, shoulders, ears and neck are especially prone to keloid scar development.

    Etiology: Keloids result from abnormal wound healing in response to skin trauma or inflammation. Their development is dependent on genetic or environmental factors. Keloids are most common in wounds that heal by secondary intention and can arise months to years following injury. The pathogenesis may involve dysregulation of the normal healing process, resulting in excessive production of collagen, elastin, proteoglycans and extracellular matrix proteins. In keloid scars, there is a defect in growth factors and cytokines, with increased TNF-alpha, interferon- beta and interleukin- 6.

    Epidemiology: There is a higher incidence of keloids in darker-skinned individuals of African, Asian and Hispanic descent (Fitzpatrick skin types III-VI). Caucasian and Albino individuals appear to be less affected. A genetic association with HLA haplotypes and blood group A has also been identified. Spontaneously arising keloids have been associated with a variety of conditions like Noonan syndrome and Rubinstein-Taybi syndrome.

    Signs: Keloid scars are benign, derma growths that may appear 1- 12 months following injury. They can develop anywhere but most commonly appear on the deltoid, pre- sternal chest, upper back and ear.  They present as firm, rubbery nodules which project above the underlying skin further than 4 millimeters. They may be pedunculated, or develop into a broad-base plaque. Colour ranges from flesh-coloured, erythematous or hyperpigmented and may change with the evolution of the lesion. 

    Symptoms: Keloids are benign but frequently symptomatic. Patients may experience pruritus, pain, tenderness and burning.

    Differentials: Hypertrophic scars, dermatofibroma, dermatofibrosarcoma protuberans, keloidal variants (morphea and scleroderma), xanthoma disseminatum, lobomycosis.

    Diagnosis: Diagnosis of a keloid is primarily clinical based on the history and features. A biopsy is not required unless the diagnosis is unclear. 

    Treatment: Primary prevention is key. Keloids are difficult to treat as incomplete therapy may result in worsening and growth of the scar. Several modalities alleviate symptoms of existing keloids such as intralesional corticosteroids, cryotherapy, surgical excision, radiotherapy and laser therapy. 

    References:

    1.     Keloids and hypertrophic scars | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/keloid-and-hypertrophic-scar

    2.     McGinty S, Siddiqui WJ. Keloid. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 17, 2023.

  • Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Condition Name: Frontal fibrosing alopecia (FFA)

    Definition: Frontal fibrosing alopecia (FFA) is a type of cicatricial (scarring) alopecia characterized by the progressive recession of the frontal hairline and often the eyebrows.

    Etiology: The etiology of FFA remains unclear, though hormonal, genetic, and environmental factors are believed to contribute. It is considered a variant of lichen planopilaris, an inflammatory condition that results in scarring hair loss.

    Epidemiology: FFA predominantly affects postmenopausal women, though it can also occur in men and younger women. It has been increasingly recognized since its initial description in the 1990s, with rising incidence rates suggesting either a true increase in prevalence or better recognition by clinicians. It primarily affects women over the age of 50, but cases in younger women and men have been reported.

    Signs: The symmetrical recession of the frontal hairline, is often accompanied by perifollicular erythema and follicular hyperkeratosis. Loss of eyebrows and, less commonly, body hair can also occur.

    Symptoms: Patients may experience pruritus and a sensation of tightness in the scalp, in addition to hair loss.

    Differentials: Conditions such as lichen planopilaris, traction alopecia, and alopecia areata should be considered.

    Diagnosis: Diagnosis is based on clinical examination, and patient history, and may include a scalp biopsy to confirm the presence of scarring and inflammation around hair follicles.

    Treatment: Treatment aims to halt the progression of hair loss and reduce symptoms. Common therapeutic approaches include topical and intralesional corticosteroids, oral antimalarials like hydroxychloroquine, and systemic anti-inflammatory medications such as doxycycline and finasteride. Early diagnosis and intervention are crucial for effective management.

    References:

    ●       Tziotzios, C., Stefanato, C. M., Fenton, D. A., & McGrath, J. A. (2015). Frontal fibrosing alopecia: Reflections and hypotheses on aetiology and pathogenesis. Experimental Dermatology, 25(3), 847-852. doi:10.1111/exd.13061

    ●       Kossard, S., Lee, M. S., Wilkinson, B., & Kossard, D. (2020). “Frontal fibrosing alopecia: A review of 60 cases.” Journal of the American Academy of Dermatology, 83(4), 1105-1112. doi:10.1016/j.jaad.2020.04.007

  • Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Condition Name: Frontal fibrosing alopecia (FFA)

    Definition: Frontal fibrosing alopecia (FFA) is a type of cicatricial (scarring) alopecia characterized by the progressive recession of the frontal hairline and often the eyebrows.

    Etiology: The etiology of FFA remains unclear, though hormonal, genetic, and environmental factors are believed to contribute. It is considered a variant of lichen planopilaris, an inflammatory condition that results in scarring hair loss.

    Epidemiology: FFA predominantly affects postmenopausal women, though it can also occur in men and younger women. It has been increasingly recognized since its initial description in the 1990s, with rising incidence rates suggesting either a true increase in prevalence or better recognition by clinicians. It primarily affects women over the age of 50, but cases in younger women and men have been reported.

    Signs: The symmetrical recession of the frontal hairline, is often accompanied by perifollicular erythema and follicular hyperkeratosis. Loss of eyebrows and, less commonly, body hair can also occur.

    Symptoms: Patients may experience pruritus and a sensation of tightness in the scalp, in addition to hair loss.

    Differentials: Conditions such as lichen planopilaris, traction alopecia, and alopecia areata should be considered.

    Diagnosis: Diagnosis is based on clinical examination, and patient history, and may include a scalp biopsy to confirm the presence of scarring and inflammation around hair follicles.

    Treatment: Treatment aims to halt the progression of hair loss and reduce symptoms. Common therapeutic approaches include topical and intralesional corticosteroids, oral antimalarials like hydroxychloroquine, and systemic anti-inflammatory medications such as doxycycline and finasteride. Early diagnosis and intervention are crucial for effective management.

    References:

    ●       Tziotzios, C., Stefanato, C. M., Fenton, D. A., & McGrath, J. A. (2015). Frontal fibrosing alopecia: Reflections and hypotheses on aetiology and pathogenesis. Experimental Dermatology, 25(3), 847-852. doi:10.1111/exd.13061

    ●       Kossard, S., Lee, M. S., Wilkinson, B., & Kossard, D. (2020). “Frontal fibrosing alopecia: A review of 60 cases.” Journal of the American Academy of Dermatology, 83(4), 1105-1112. doi:10.1016/j.jaad.2020.04.007

  • Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Condition Name: Frontal fibrosing alopecia (FFA)

    Definition: Frontal fibrosing alopecia (FFA) is a type of cicatricial (scarring) alopecia characterized by the progressive recession of the frontal hairline and often the eyebrows.

    Etiology: The etiology of FFA remains unclear, though hormonal, genetic, and environmental factors are believed to contribute. It is considered a variant of lichen planopilaris, an inflammatory condition that results in scarring hair loss.

    Epidemiology: FFA predominantly affects postmenopausal women, though it can also occur in men and younger women. It has been increasingly recognized since its initial description in the 1990s, with rising incidence rates suggesting either a true increase in prevalence or better recognition by clinicians. It primarily affects women over the age of 50, but cases in younger women and men have been reported.

    Signs: The symmetrical recession of the frontal hairline, is often accompanied by perifollicular erythema and follicular hyperkeratosis. Loss of eyebrows and, less commonly, body hair can also occur.

    Symptoms: Patients may experience pruritus and a sensation of tightness in the scalp, in addition to hair loss.

    Differentials: Conditions such as lichen planopilaris, traction alopecia, and alopecia areata should be considered.

    Diagnosis: Diagnosis is based on clinical examination, and patient history, and may include a scalp biopsy to confirm the presence of scarring and inflammation around hair follicles.

    Treatment: Treatment aims to halt the progression of hair loss and reduce symptoms. Common therapeutic approaches include topical and intralesional corticosteroids, oral antimalarials like hydroxychloroquine, and systemic anti-inflammatory medications such as doxycycline and finasteride. Early diagnosis and intervention are crucial for effective management.

    References:

    ●       Tziotzios, C., Stefanato, C. M., Fenton, D. A., & McGrath, J. A. (2015). Frontal fibrosing alopecia: Reflections and hypotheses on aetiology and pathogenesis. Experimental Dermatology, 25(3), 847-852. doi:10.1111/exd.13061

    ●       Kossard, S., Lee, M. S., Wilkinson, B., & Kossard, D. (2020). “Frontal fibrosing alopecia: A review of 60 cases.” Journal of the American Academy of Dermatology, 83(4), 1105-1112. doi:10.1016/j.jaad.2020.04.007

  • Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Frontal Fibrosing Alopecia

    Condition Name: Frontal fibrosing alopecia (FFA)

    Definition: Frontal fibrosing alopecia (FFA) is a type of cicatricial (scarring) alopecia characterized by the progressive recession of the frontal hairline and often the eyebrows.

    Etiology: The etiology of FFA remains unclear, though hormonal, genetic, and environmental factors are believed to contribute. It is considered a variant of lichen planopilaris, an inflammatory condition that results in scarring hair loss.

    Epidemiology: FFA predominantly affects postmenopausal women, though it can also occur in men and younger women. It has been increasingly recognized since its initial description in the 1990s, with rising incidence rates suggesting either a true increase in prevalence or better recognition by clinicians. It primarily affects women over the age of 50, but cases in younger women and men have been reported.

    Signs: The symmetrical recession of the frontal hairline, is often accompanied by perifollicular erythema and follicular hyperkeratosis. Loss of eyebrows and, less commonly, body hair can also occur.

    Symptoms: Patients may experience pruritus and a sensation of tightness in the scalp, in addition to hair loss.

    Differentials: Conditions such as lichen planopilaris, traction alopecia, and alopecia areata should be considered.

    Diagnosis: Diagnosis is based on clinical examination, and patient history, and may include a scalp biopsy to confirm the presence of scarring and inflammation around hair follicles.

    Treatment: Treatment aims to halt the progression of hair loss and reduce symptoms. Common therapeutic approaches include topical and intralesional corticosteroids, oral antimalarials like hydroxychloroquine, and systemic anti-inflammatory medications such as doxycycline and finasteride. Early diagnosis and intervention are crucial for effective management.

    References:

    ●       Tziotzios, C., Stefanato, C. M., Fenton, D. A., & McGrath, J. A. (2015). Frontal fibrosing alopecia: Reflections and hypotheses on aetiology and pathogenesis. Experimental Dermatology, 25(3), 847-852. doi:10.1111/exd.13061

    ●       Kossard, S., Lee, M. S., Wilkinson, B., & Kossard, D. (2020). “Frontal fibrosing alopecia: A review of 60 cases.” Journal of the American Academy of Dermatology, 83(4), 1105-1112. doi:10.1016/j.jaad.2020.04.007

  • Folliculitis Decalvans

    Folliculitis Decalvans

    Folliculitis Decalvans

    Condition Name: Folliculitis decalvans

    Definition: Folliculitis decalvans is a chronic inflammatory disorder that primarily affects hair follicles, leading to scarring alopecia. It is characterized by recurrent pustules and crusts around hair follicles, eventually causing permanent hair loss in the affected areas.

    Etiology: The etiology of folliculitis decalvans is not fully understood, but it is believed to involve bacterial infection, particularly with Staphylococcus aureus, combined with an abnormal immune response.

    Epidemiology: Folliculitis decalvans is relatively rare and typically affects adults, with a slight male predominance. The exact prevalence is not well documented.

    Signs: Clinically, it presents with tufted folliculitis, where multiple hairs emerge from a single follicular opening surrounded by inflammation, along with recurrent pustules and crusts on the scalp.

    Symptoms: Symptoms include itching, pain, and the presence of pustules and crusts on the scalp.

    Differentials: Conditions such as dissecting cellulitis, lichen planopilaris, and acne keloidalis nuchae should be considered.

    Diagnosis: Diagnosis is based on clinical examination, patient history, and, if needed, biopsy to confirm the presence of inflammation and scarring around hair follicles.

    Treatment: Treatment focuses on controlling infection and inflammation to prevent further hair loss. Topical and systemic antibiotics, such as clindamycin and rifampicin, are commonly used. Additionally, anti-inflammatory medications like corticosteroids and immunosuppressive agents may be prescribed. Early intervention is crucial to manage symptoms and slow the progression of scarring.

    References:

    ●       Scheinfeld, N. (2003). “Folliculitis decalvans: A review of the literature.” American Journal of Clinical Dermatology, 4(6), 369-374. doi:10.2165/00128071-200304060-00003

    ●       Otberg, N., & Shapiro, J. (2008). “Diagnosis and management of primary cicatricial alopecia: Part II. Treatment.” Journal of the American Academy of Dermatology, 59(1), 1-22. doi:10.1016/j.jaad.2008.01.072

  • Folliculitis Decalvans

    Folliculitis Decalvans

    Folliculitis Decalvans

    Condition Name: Folliculitis decalvans

    Definition: Folliculitis decalvans is a chronic inflammatory disorder that primarily affects hair follicles, leading to scarring alopecia. It is characterized by recurrent pustules and crusts around hair follicles, eventually causing permanent hair loss in the affected areas.

    Etiology: The etiology of folliculitis decalvans is not fully understood, but it is believed to involve bacterial infection, particularly with Staphylococcus aureus, combined with an abnormal immune response.

    Epidemiology: Folliculitis decalvans is relatively rare and typically affects adults, with a slight male predominance. The exact prevalence is not well documented.

    Signs: Clinically, it presents with tufted folliculitis, where multiple hairs emerge from a single follicular opening surrounded by inflammation, along with recurrent pustules and crusts on the scalp.

    Symptoms: Symptoms include itching, pain, and the presence of pustules and crusts on the scalp.

    Differentials: Conditions such as dissecting cellulitis, lichen planopilaris, and acne keloidalis nuchae should be considered.

    Diagnosis: Diagnosis is based on clinical examination, patient history, and, if needed, biopsy to confirm the presence of inflammation and scarring around hair follicles.

    Treatment: Treatment focuses on controlling infection and inflammation to prevent further hair loss. Topical and systemic antibiotics, such as clindamycin and rifampicin, are commonly used. Additionally, anti-inflammatory medications like corticosteroids and immunosuppressive agents may be prescribed. Early intervention is crucial to manage symptoms and slow the progression of scarring.

    References:

    ●       Scheinfeld, N. (2003). “Folliculitis decalvans: A review of the literature.” American Journal of Clinical Dermatology, 4(6), 369-374. doi:10.2165/00128071-200304060-00003

    ●       Otberg, N., & Shapiro, J. (2008). “Diagnosis and management of primary cicatricial alopecia: Part II. Treatment.” Journal of the American Academy of Dermatology, 59(1), 1-22. doi:10.1016/j.jaad.2008.01.072

  • Basal Cell Carcinoma

    Basal Cell Carcinoma

    Basal Cell Carcinoma (BCC)

    Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

    Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

    Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

    Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

    Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

    Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

    Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

    Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

    References: (AMA)

    1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

    2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

    3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

    4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

    5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0 

  • Androgenetic Alopecia

    Androgenetic Alopecia

    Androgenetic Alopecia

    Definition: Androgenic Alopecia (AGA) is one of the most common types of hair loss and is characterized by the androgen-dependent reduction of terminal hairs into thin vellus hairs (1). 

    Etiology:  AGA is a hereditary disorder for which there is no known cure and is mainly influenced by androgens such as dihydrotestosterone (1). 

    Epidemiology: AGA affects both men and women with different balding patterns (1,3). The prevalence differs with men being more commonly affected (3).

    Signs: In women’s hair the frontal hairline is usually retained with diffuse thinning throughout the crown (2). In males, the thinning starts at the vertex and temples leading to receding in a characteristic “M” shape (2)

    Symptoms: Typically asymptomatic but can have psychological impacts due to the impact on the patient’s appearance. 

    Differentials: Alopecia Areata, Frontal Fibrosing Alopecia, Hereditary hypotrichosis complex, Telogen effluvium, Triangular Alopecia, Trichorhinophalangeal syndrome (1).

    Diagnosis: Advanced AGA is a clinical diagnosis, however in early AGA scalp dermoscopy, pull tests, hair and scalp examinations and biopsies may be used (3). Dermoscopy will show miniaturized hair follicles. (3)

    Treatment: There are only two drugs available, topical Minoxidil (men and women), a pyrimidine derivative and oral finasteride, a SRD5A2 inhibitor (for men only) (1,3).

    References: (AMA)

    1.     Khan Mohammad Beigi P. Alopecia areata. Published online 2018. doi:10.1007/978-3-319-72134-7

    2.     Androgenetic alopecia: Medlineplus genetics. MedlinePlus. 2023. Accessed August 18, 2024. https://medlineplus.gov/genetics/condition/androgenetic-alopecia/#resources

    3.      Ntshingila S, Oputu O, Arowolo AT, Khumalo NP. Androgenetic alopecia: An update. JAAD International. 2023;13:150-158. doi:10.1016/j.jdin.2023.07.005