Pimple-popping, or Zit-popping, is the act of bursting or popping pimples with one's finger. Pimple-popping can lead to the introduction of bacteria into the pimple, infection, the creation of more pimples, and permanent scarring. Thus, popping is usually deprecated by dermatologists and estheticians and it is recommended to let the pimples run through their life span.

Practicing good hygiene, including regularly washing skin areas with neutral cleansers, can reduce the amount of dead skin cells and other external contaminants on the skin that can contribute to the development of pimples. However, it is not always possible to completely prevent pimples, even with good hygiene practices as a number of externalities such as hormones and genetics are at play.

Prickly heat can be prevented by avoiding activities that induce sweating, using air conditioning to cool the environment, wearing light clothing and in general, avoiding hot and humid weather. Frequent cool showers or cool baths with mild soap can help to prevent heat rash.

Miliaria occurs when the sweat gland ducts get plugged due to dead skin cells or bacteria such as "Staphylococcus epidermidis", a common bacterium that occurs on the skin which is also associated with acne.

The trapped sweat leads to irritation (prickling), itching and to a rash of very small blisters, usually in a localized area of the skin.

One way to treat xerotic eczema is to avoid ing the affected area and to apply anti-itch or moisturizing lotion frequently.

A study published in 2005 found positive results from soaking the affected area in water for twenty minutes and then applying mid- to high-strength corticosteroid ointment.

Hot tub folliculitis (also known as "Pseudomonas aeruginosa" folliculitis) is a common type of folliculitis, a condition which causes inflammation of hair follicles.

This condition is caused by an infection of hair follicles due to the bacterium "Pseudomonas aeruginosa". The bacterium is commonly found in hot tubs, water slides, and such places. Children are more prone to this because they usually stay in the water longer than adults. Hot tub folliculitis appears on the skin in the form of a rash, roughly resembling chicken pox and then develops further to appear as a pimple. Hot tub folliculitis can be extremely painful and/or itchy, and left alone without scratching will go away much more quickly. If the rash is aggravated, it can stay, worsen, and spread, lasting for months. By that time, it is much more difficult to treat. The dots usually go away after about 7 to 10 days but the condition leaves a hyperpigmented lesion that goes away after a few months.

Normally, the rash does not need specific treatment and will go away on its own. Antibiotics may be prescribed in some cases. If the rash continues to appear longer than the 7- to 10-day time period, a physician should be consulted. Folliculitis that is not treated properly could worsen and cause abscesses.

The best form of prevention is to determine whether shaving or waxing irritates the skin and hair worse.When shaving, there are a few precautions that can be taken to prevent ingrown hairs including proper shaving techniques and preparation of the skin before shaving. When shaving, applying the proper amount of lubrication (in the form of shaving cream, gel, or soap) is important to prevent the hair from being forced underneath the surface of the skin. Also the application of too much force with a razor can contribute to hair that is cut shorter than the surrounding dermis. Using a beard trimmer at the lowest setting (1 mm or 0.5 mm) instead of shaving is an effective alternative.

Alternatively, ingrown hair can be prevented by removing the hair permanently, e.g. by laser hair removal or hair removal through electrolysis.

Xerotic eczema (also known as "Eczema craquelé", "Pruritus hiemalis", "Asteatotic eczema", "Winter itch", "Desiccation dermatitis," and "Winter eczema") is a form of eczema that is characterized by changes that occur when skin becomes abnormally dry, itchy, and cracked. Lower legs tend to be especially affected, although it can appear in the underarm area as well.

Xerotic eczema is common in elderly people, though it is not uncommon for people in their 20s. It can appear in red, bumpy, pimple-like irritations. Shaving can cause it to become inflamed.

Symptoms include rash, itching skin, and hair which remains in spite of shaving. The site of the ingrown hair will form a reddish, raised bump, similar in appearance to a pimple.

The transmission of Tinea Barbae to humans occurs through contact of an infected animal to the skin of a human. Infection can occasionally be transmitted through contact of infected animal hair on human skin. Tinea Barbae is very rarely transmitted through human to human contact but is not completely impossible.

Tinea barbæ (also known as "Barber's itch," "Ringworm of the beard," and "Tinea sycosis") is a fungal infection of the hair. Tinea barbae is due to a dermatophytic infection around the bearded area of men. Generally, the infection occurs as a follicular inflammation, or as a cutaneous granulomatous lesion, i.e. a chronic inflammatory reaction. It is one of the causes of Folliculitis. It is most common among agricultural workers, as the transmission is more common from animal-to-human than human-to-human. The most common causes are "Trichophyton mentagrophytes" and "T. verrucosum".

Most people, especially Africans and African Americans, have a positive family history of keloid disorder. Development of keloids among twins also lends credibility to existence of a genetic susceptibility to develop keloids. Marneros et al. (1) reported four sets of identical twins with keloids; Ramakrishnan et al. also described a pair of twins who developed keloids at the same time after vaccination. Case series have reported clinically severe forms of keloids in individuals with a positive family history and black African ethnic origin.

Most skin injury types can contribute to scarring. This includes burns, acne scars, chickenpox scars, ear piercing, scratches, surgical cuts, and vaccination sites.

According to the (US) National Center for Biotechnology Information, keloid scarring is common in young people between the ages of 10 and 20. Studies have shown that those with darker complexions are at a higher risk of keloid scarring as a result of skin trauma. They occur in 15 – 20% of individuals with African, Asian or Latino ancestry, significantly less in those of a Caucasian background and there are no reported cases in patients with albinism.

Keloids tend to have a genetic component, which means one is more likely to have keloids if one or both of their parents has them. However, no single gene has yet been identified which is a causing factor in keloid scarring but several susceptibility loci have been discovered, most notably in Chromosome 15.

Granuloma annulare is a fairly rare, chronic skin condition which presents as reddish bumps on the skin arranged in a circle or ring. It can initially occur at any age and is four times more common in females.

The condition is usually seen in otherwise healthy people. Occasionally, it may be associated with diabetes or thyroid disease. It has also been associated with auto-immune diseases such as systemic lupus erythematosus, rheumatoid arthritis, Lyme disease and Addison's disease. At this time no conclusive connection has been made between patients.

A hickey, hickie or love bite in British English, is a bruise or bruise-like mark caused by the kissing or sucking of the skin, usually on the neck or arm. While biting might be part of giving a hickey, sucking is sufficient to burst small superficial blood vessels under the skin.

The origin of the word is from its earlier meaning of "pimple, skin lesion" (c. 1915); perhaps a sense extension and spelling variation from the earlier word meaning "small gadget, device; any unspecified object" which has a unknown origin (1909).

Hickeys typically last from 5 to 12 days and may be treated in the same way as other bruises. Ways to reduce the appearance of hickeys include icing recent hickeys to reduce swelling, rubbing them with a chilled spoon to remove the bruise, and applying a warm compress to older hickeys to dilate vessels and promote blood flow. They can be covered with a concealer or powder corresponding to the sufferer's skin tone, or a fake tan. Alternatively, articles of clothing such as scarves, snoods, turtle necks, or sleeves may be used to conceal hickeys.

Scabies is endemic in many developing countries, where it tends to be particularly problematic in rural and remote areas. In such settings, community-wide control strategies are required to reduce the rate of disease, as treatment of only individuals is ineffective due to the high rate of reinfection. Large-scale mass drug administration strategies may be required where coordinated interventions aim to treat whole communities in one concerted effort. Although such strategies have shown to be able to reduce the burden of scabies in these kinds of communities, debate remains about the best strategy to adopt, including the choice of drug.

The resources required to implement such large-scale interventions in a cost-effective and sustainable way are significant. Furthermore, since endemic scabies is largely restricted to poor and remote areas, it is a public health issue that has not attracted much attention from policy makers and international donors.

Moxidectin is being evaluated as a treatment for scabies. It is established in veterinary medicine to treat a range of parasites, including sarcoptic mange. Its advantage over ivermectin is its longer half life in humans and, thus, potential duration of action. Tea tree oil appears to be effective in a Petri dish.

Buruli ulcer commonly affects poor people in remote rural areas with limited access to health care. The disease can affect all age groups, although children under the age of 15 years (range 2–14 years) are predominantly affected. There are no sex differences in the distribution of cases among children. Among adults, some studies have reported higher rates among women than males (Debacker "et al." accepted for publication). No racial or socio-economic group is exempt from the disease. Most ulcers occur on the extremities; lesions on the lower extremities are almost twice as common as those on the upper extremities. Ulcers on the head and trunk accounted for less than 8% of cases in one large series.

Cutaneous vasculitis can have various causes including but not limited to medications, bacterial and viral infections or allergens. It is estimated that 45-55% of cases are idiopathic, meaning the cause is unknown. In cases where a cause can be determined, medications and infectious pathogens are most common in adults, while IgA vasculitis (Henoch-Schönlein purpura) frequently affects children. Other etiologies include autoimmune conditions and malignancies, usually hematologic (related to the blood).

The small vessels in the skin affected are located in the superficial dermis and include arterioles (small arteries carrying blood to capillaries), capillaries, and venules (small veins receiving blood from capillaries). In general, immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, including enzymes causing damage to vessel tissue. Evidence of this process can be seen with a sample of removed skin tissue, or biopsy, viewed under a microscope. Neutrophils are seen surrounding blood vessels and their debris within vessel walls, causing fibrinoid necrosis. This finding on histological examination is termed “leukocytoclastic vasculitis”.

Considering the wide range of potential causes leading to cutaneous small vessel vasculitis, there are subtle variations in the underlying pathophysiology for each cause. For example, medications are metabolized to smaller molecules that can attach to proteins in the blood or vessel walls. The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. A similar process occurs with infectious agents, such as bacteria, in which antibodies target microbial components.

Cutaneous small-vessel vasculitis, also known as hypersensitivity vasculitis, cutaneous leukocytoclastic vasculitis, hypersensitivity angiitis, cutaneous leukocytoclastic angiitis, cutaneous necrotizing vasculitis and cutaneous necrotizing venulitis, is inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura. It is the most common vasculitis seen in clinical practice.

"Leukocytoclastic" refers to the damage caused by nuclear debris from infiltrating neutrophils in and around the vessels.

Buruli ulcer has been reported from at least 32 countries around the world, mostly in tropical areas:

- West Africa: Benin, Burkina Faso, Côte d'Ivoire, Ghana, Liberia, Nigeria, Togo, Guinea, Sierra Leone.

- Other African Countries: Angola, Cameroon, Congo, Democratic Republic of Congo, Equatorial Guinea, Gabon, Sudan, Uganda.

- Western Pacific: Australia, Papua New Guinea, Kiribati.

- Americas: French Guiana, Mexico, Peru, Suriname.

- Asia: China, Malaysia, Japan.

In several of these countries, the disease is not considered to be a public health problem, hence the current distribution and the number of cases are not known. Possible reasons include:

- the distribution of the disease is often localized in certain parts of endemic countries;

- Buruli ulcer is not a notifiable disease

- In most places where the disease occurs, patients receive care from private sources such as voluntary mission hospitals and traditional healers. Hence the existence of the disease may not come to the attention of the ministries of health.

It most commonly occurs in Africa: Congo and Cameroon in Central Africa, Côte d'Ivoire, Ghana and Benin in West Africa. Some Southeast Asian countries (Papua New Guinea) and Australia have major foci, and there have been a few patients reported from South America (French Guyana and Surinam) and Mexico. Focal outbreaks have followed flooding, human migrations, and man-made topographic modifications such as dams and resorts. Deforestation and increased basic agricultural activities may significantly contribute to the recent marked increases in the incidence of "M. ulcerans" infections, especially in West Africa, where the disease is rapidly emerging.

Epidermoid cysts commonly result from implantation of epidermis into the dermis, as in trauma or surgery. They can also be caused by a blocked pore adjacent to a body piercing. They are also seen in Gardner's syndrome and Nevoid Basal Cell Carcinoma Syndrome on the head and neck. They can be infected by bacteria and form a pimple-like shape.

An epidermoid cyst is a benign cyst usually found on the skin. The cyst develops out of ectodermal tissue. Histologically, it is made of a thin layer of squamous epithelium.

A single copy of the abnormal gene from one parent is able to cause the disease; this is called autosomal dominance. A mutation in the DLX3 gene has been confirmed as the cause of TDO. The onset of TDO begins with a 4 base pair deletion on chromosome 17q21, causing a mutation, specifically frameshift, and the termination codon to be the cause of the lack of complete maturation of the tooth enamel; this mutation is also responsible for the osseous defects in the bone. DLX-3 is expressed in the placenta and is significantly important during embryonic development in regards to hard bone tissue which is present in the teeth, skull, and long bones such as in the arms and legs. During normal tooth development, DLX 3 shifts from predominant expression in the inner enamel epithelium; the outer layer does not express DLX 3. In TDO cases, the DLX-3 is present on the outer enamel epithelium and leads to the dental abnormalities seen in this disease. Improper expression of DLX-3 causes the tooth enamel to be thinner, which leads to attrition and is most often the cause of dental abscess seen in TDO persons.

During osseous, connective tissue, and dermal cell differentiation, DLX 3 in TDO is also responsible for upper cranial thickness, calvaria, osteosclerosis of the long bones, long narrow head (dolichocephaly), abnormally thin brittle nails, and premature closing of fibrous joints. Consequently, 95% of people with TDO that are 16 years old or younger show skeletal abnormalities before full maturation takes place. Lack of mastoid pneumatization by mastoid cells occurs in 82% of the cases and is rarely prevalent outside of TDO diagnosis. Mastoid pneumatization occurs at about 6 months of ages and acts to minimize pressure fluctuations in the Eustachian tubes of the ear. The mastoid lies posterior to the lower jawbone (mandible) and distal to the ear. The Eustachian tube connects the middle ear to the back of the nose, and acts to create a specific pressure in the ear canal that causes vibrations to the eardrum; if adequate pressure is not attained, muffled, dull hearing results. In addition to the mastoid pneumatization assisting the Eustachian tubes for normal hearing, lack of mastoid pneumatization causes inflammation of the ear, general irritation, and does not allow enough air in to assist with mucus flowing out. It is not completely understood why gene mutations occur, but it is known that genetic mutations that cause disease are acquired from either or both parents at fertilization.