Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

Patient presents with the following signs.

1. Hyperkeratotic papules present over the seborrheic area of the body.

2. V - shaped nicking present at the tip of the nails.

3. Red and white longitudinal nail lines.

A 1992 study of 163 affected persons found that most patients had no other medical problems and most manage to lead a relatively normal life.

Melasma is usually diagnosed visually or with assistance of a Wood's lamp (340 - 400 nm wavelength). Under Wood's lamp, excess melanin in the epidermis can be distinguished from that of the dermis.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Erythromelanosis follicularis faciei et colli is an erythematous pigmentary disease involving the follicles, characterized by a reddish-brown, sharply demarcated, symmetrical discoloration involving the preauricular and maxillary regions.

Warty dyskeratoma must be differentiated from vulvar dysplasia, Bowenoid papulosis, squamous carcinoma, condyloma, and other viral-induced squamous lesions.

There seems to be beneficial responses to clindamycin therapy as the lesions regress. This leads to the hypothesis that microorganisms may be playing a role in the initial stages of Kyrle disease.

A family with Kyrle disease were examined which their skin lesions were benign. However, when three of the young adult members were closely examined, they had posterior subcapsular cataracts and two of those three developed multiple tiny yellow-brown anterior stromal corneal opacities. In order to determine if there is any correlation between Kyrle disease and the ocular observations, more cases of Kyrle disease are to be analyzed.

All in all, since Kyrle disease is relatively rare, more cases need to be studied and analyzed in order to understand the underlying pathogenesis and to improve the management of the disease.

Warty dyskeratoma, also known as an Isolated dyskeratosis follicularis, is a benign epidermal proliferation with distinctive histologic findings that may mimic invasive squamous cell carcinoma and commonly manifests as an umbilicated (Having a central mark or depression resembling a navel) lesion with a keratotic plug, WD have some histopathologic similarities to viral warts but it's not caused by HPV and the majority of these lesions display overall histopathologic features consistent with a follicular adnexal neoplasm. usually limited to the head, neck, scalp or face and vulva. Lesions are generally and sporadic and may be associated with a follicular unit. Oral involvement, particularly the hard palate, and genital involvement have been reported. it can also be thought of as one of the manifestations of focal acantholytic dyskeratosis, an epidermal reaction pattern that can be seen in several disorders, including Darier's disease and Grover's disease. But the main Difference between Darier disease and Warty dyskeratoma, is that Darier disease inherited dermatosis (autosomal dominant) consisting of multiple keratotic papules on the face, trunk, and extremities, while WD occurs as an isolated, noninherited, single keratotic nodule mainly confined to the head and neck as mentioned earlier.

Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic disease.

Epidermolytic palmoplantar keratoderma has been associated with keratin 9 and keratin 16.

Nonepidermolytic palmoplantar keratoderma has been associated with keratin 1 and keratin 16.

Keratosis pilaris atrophicans faciei (also known as "Folliculitis rubra," "Keratosis pilaris rubra atrophicans faciei," "Lichen pilare," "Lichen pilaire ou xerodermie pilaire symetrique de la face," "Ulerythema ophryogenes," and "Xerodermie pilaire symetrique de la face") begins in infancy as follicular papules with perifollicular erythema. Initially, the lesions are restricted to the lateral eyebrows, but with time spread to involve the cheeks and forehead, and may also be associated with keratosis pilaris on the extremities and buttocks.

Atrophodermia vermiculata presents with erythematous follicular papules on the cheeks in childhood and, with time, the lesions develop into pit-like depressions.

DPR is comparable to Naegeli syndrome, both of which are caused by a specific defect in the keratin 14 protein.

Atrophodermia vermiculata is also known as "Acne vermoulante", "Acne vermoulanti", "Atrophoderma reticulata symmetrica faciei", "Atrophoderma reticulatum", "Atrophoderma vermiculata", "Atrophoderma vermiculatum", "Atrophodermia reticulata symmetrica faciei", "Atrophodermia ulerythematosa", "Atrophodermie vermiculée des joues avec kératoses folliculaires", "Folliculitis ulerythema reticulata", "Folliculitis ulerythematous reticulata", "Folliculitis ulerythemosa", "Honeycomb atrophy", "Ulerythema acneforme" and "Ulerythema acneiforme"

Symptoms include lack of sweat glands, thin hair, brittle nails, mottled skin, and lack of fingerprints.

Keratosis follicularis spinulosa decalvans (also known as "Siemens-1 syndrome") is a rare X-linked disorder described by Siemens in 1926, a disease that begins in infancy with keratosis pilaris localized on the face, then evolves to more diffuse involvement.

An association with SAT1 has been suggested.

Keratosis pilaris atropicans includes many forms of keratosis pilaris with cicatricial alopecia. Variants include keratosis pilaris atrophicans faciei, atrophoderma vermiculatum, keratosis follicularis spinulosa decalvans, and ichthyosis follicularis.

Ulerythema means "scar plus redness," and may be used to refer to several different cutaneous conditions, including atrophoderma vermiculatum and keratosis pilaris atrophicans faciei.

The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone replacement therapy.

Treatments are often ineffective as it comes back with continued exposure to the sun. Assessment by a dermatologist will help guide treatment. This may include use of a Woods lamp to determine depth of the melasma pigment. Treatments to hasten the fading of the discolored patches include:

- Topical depigmenting agents, such as hydroquinone (HQ) either in over-the-counter (2%) or prescription (4%) strength. HQ is a chemical that inhibits tyrosinase, an enzyme involved in the production of melanin.

- Tretinoin, an acid that increases skin cell (keratinocyte) turnover. This treatment cannot be used during pregnancy.

- Azelaic acid (20%), thought to decrease the activity of melanocytes.

- Tranexamic acid by mouth has shown to provide rapid and sustained lightening in melasma by decreasing melanogenesis in epidermal melanocytes.

- Cysteamine hydrochloride (5%) over-the-counter. Mechanism of action seems to involve inhibition of melanin synthesis pathway

- Flutamide (1%)

- Chemical peels

- Microdermabrasion to dermabrasion (light to deep)

- Galvanic or ultrasound facials with a combination of a topical crème/gel. Either in an aesthetician's office or as a home massager unit.

- Laser but not IPL (IPL can make the melasma darker)

Evidence-based reviews found that the most effective therapy for melasma includes a combination on topical agents.

In all of these treatments the effects are gradual and a strict avoidance of sunlight is required. The use of broad-spectrum sunscreens with physical blockers, such as titanium dioxide and zinc dioxide is preferred over that with only chemical blockers. This is because UV-A, UV-B and visible lights are all capable of stimulating pigment production.

Patients should avoid other precipitants including hormonal triggers.

Cosmetic camouflage can also be used to hide melasma.

PCNA and Ki67 immunoreactivity happens in case of fibroma and peripheral granuloma.

Advice often given includes:

- Avoid sharing clothing, sports equipment, towels, or sheets.

- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.

- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.

- Avoid touching pets with bald spots, as they are often carriers of the fungus.

Alopecia mucinosa (also known as "Follicular mucinosis," "Mucinosis follicularis,", "Pinkus’ follicular mucinosis," and "Pinkus’ follicular mucinosis–benign primary form") is a skin disorder that generally presents, but not exclusively, as erythematous plaques or flat patches without hair primarily on the scalp and face. This can also present on the body as a follicular mucinosis and may represent a systemic disease.

Dissecting cellulitis of the scalp, also known as dissecting scalp cellulitis, dissecting folliculitis of the scalp, perifolliculitis capitis abscedens et suffodiens of Hoffman, perifolliculitis abscedens et suffodiens, or folliculitis abscedens et suffodiens, is an inflammatory condition of the scalp that can lead to scarring alopecia, which begins with deep inflammatory nodules, primarily over occiput, that progresses to coalescing regions of boggy scalp. Boggy tissue has a high fluid level that results in a spongy feeling.

Isotretinoin proves to be the medicine of choice for the treatment of the disease.

The differential diagnosis is quite extensive and includes

- Buschke–Fischer–Brauer disease

- Curth–Macklin ichthyosis

- Gamborg Nielsen syndrome

- Greither disease

- Haber syndrome

- Hereditary punctate palmoplantar keratoderma

- Jadassohn–Lewandowsky syndrome

- Keratosis follicularis spinulosa decalvans

- Keratosis linearis with ichthyosis congenital and sclerosing keratoderma syndrome

- Meleda disease

- Mucosa hyperkeratosis syndrome

- Naegeli–Franceschetti–Jadassohn syndrome

- Naxos disease

- Olmsted syndrome

- Palmoplantar keratoderma and leukokeratosis anogenitalis

- Pandysautonomia

- Papillomatosis of Gougerot and Carteaud

- Papillon–Lefèvre syndrome

- Punctate porokeratotic keratoderma

- Richner–Hanhart syndrome

- Schöpf–Schulz–Passarge syndrome

- Unna Thost disease

- Vohwinkel syndrome

- Wong's dermatomyositis