Oral retinoids have proven effective in treating this disorder. Depending on the side effects they may improve the quality of life. Examples are etretinate, acitretin, isotretinoin

Recent research has focused on changing the mixture of keratins produced in the skin. There are 54 known keratin genes—of which 28 belong to the type I intermediate filament genes and 26 to type II—which work as heterodimers. Many of these genes share substantial structural and functional similarity, but they are specialized to cell type and/or conditions under which they are normally produced. If the balance of production could be shifted away from the mutated, dysfunctional keratin gene toward an intact keratin gene, symptoms could be reduced. For example, sulforaphane, a compound found in broccoli, was found to reduce blistering in a mouse model to the point where affected pups could not be identified visually, when injected into pregnant mice (5 µmol/day = 0.9 mg) and applied topically to newborns (1 µmol/day = 0.2 mg in jojoba oil).

As of 2008 clinical research at the University of Minnesota has included a bone marrow transplant to a 2-year-old child who is one of 2 brothers with EB. The procedure was successful, strongly suggesting that a cure may have been found. A second transplant has also been performed on the child's older brother, and a third transplant is scheduled for a California baby. The clinical trial will ultimately include transplants to 30 subjects. However, the severe immunosuppression that bone marrow transplantation requires causes a significant risk of serious infections in patients with large scale blisters and skin erosions. Indeed, at least four patients have died in the course of either preparation for or institution of bone marrow transplantation for epidermolysis bullosa, out of only a small group of patients treated so far.

A pilot study performed in 2015 suggests that systemic granulocyte-colony stimulating factor (G-CSF) may promote increased wound healing in patients with dystrophic epidermolysis bullosa. In this study seven patients with dystrophic epidermolysis bullosa were treated daily with subcutaneous G-CSF for six days and then re-evaluated on the seventh day. After six days of treatment with G-CSF, the size of the open lesions were reduced by a median of 75.5% and the number of blisters and erosions on the patients were reduced by a median of 36.6%.

Initial treatment involves addressing any existing infections that may have occurred due to the broken state of the skin. Existing wounds are treated with warm compresses, non-adherent (non-stick) dressing, and topical antibiotic ointment. Immunosuppressive agents are administered in attempt to decrease blistering; this is not often effective. The first medication given aiming to heal the wounds are high dose corticosteroids. This is followed by steroid sparing agents which may reduce steroid intake and therefore lessen the side effects. Skin lesions are more likely to respond to this line of treatment than mucosal lesions. However, a high level of caution is advised in patients with a confirmed malignancy, where immunosuppression is vital and dictates treatment options. If the initial therapy fails to control the symptoms of PNP, and the condition of the patient deteriorates, a more aggressive approach may be necessary.

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.

There is no cure for IBS but in the future gene therapy may offer a cure.

Treatments for IBS generally attempt to improve the appearance of the skin and the comfort of the sufferer. This is done by exfoliating and increasing the moisture of the skin. Common treatments include:

- Emollients: moisturisers, petroleum jelly or other emolients are used, often several times a day, to increase the moisture of the skin.

- Baths: long baths (possibly including salt) several times a week are used to soften the skin and allow exfoliation.

- Exfoliating creams: creams containing keratolytics such as urea, salicylic acid and lactic acid may be useful.

- Antiseptic washes: antiseptics may be used to kill bacteria in the skin and prevent odour.

- Retenoids: very severe cases may use oral retinoids to control symptoms but these have many serious side effects including, in the case of IBS, increased blistering.

Azathioprine is a steroid-sparing agent used in combination with Prednisone. It functions by inhibiting RNA and DNA synthesis.

The Epidermolysis Bullosa Activity and Scarring index (EBDASI) is a scoring system that objectively quantifies the severity of epidermolysis bullosa. The EBDASI is a tool for clinicians and patients to monitor the severity of the disease. It has also been designed to evaluate the response to new therapies for the treatment of EB. The EBDASI was developed and validated by Professor Dedee Murrell and her team of students and fellows at the St George Hospital, University of New South Wales, in Sydney, Australia. It was presented at the International Investigative Dermatology congress in Edinburgh in 2013 and a paper-based version was published in the "Journal of the American Academy of Dermatology" in 2014.

Until gene therapy solutions finally become reality, EHK sufferers must treat their fragile skin carefully. Most have learned that taking regular extended baths allows patients to care for their fragile skin and keep it manageable. Baths that include sea salt seem to improve the process of softening and removing the thickened skin.

Ointments like Petroleum Jelly, Aveeno, and other barrier type ointment help hold the moisture in the skin after a bath.

Currently, there are no treatments available for JEB. However, the disorder can be prevented through good breeding management. Horses that are carriers of JEB should not be incorporated into breeding programs. Although, if breeders are insistent on breeding a carrier, precautions need to be taken to ensure that the other mate is not a carrier as well. Genetic testing for the disorder is highly recommended among breeding programs for the Draft horse and Saddlebred breeds to determine their carrier status.

Treatments include class I topical steroids (clobetasol, halobetasol, etc.) which in some studies have proven to be equally effective as systemic, or pill, therapy and somewhat safer. However, in difficult-to-manage or widespread cases, systemic prednisone and powerful steroid-free immunosuppressant medications, such as methotrexate, azathioprine or mycophenolate mofetil, may be appropriate. Antibiotics such as tetracycline or erythromycin may also control the disease, particularly in patients who cannot use corticosteroids. The anti-CD20 monoclonal antibody rituximab has been found to be effective in treating some otherwise refractory cases of bullous pemphigoid.

IgA-mediated pemphigoid can often be difficult to treat even with usually effective medications such as rituximab.

In 2015, an Italian team of scientists, led by Michele De Luca at the University of Modena, successfully treated a seven-year-old Syrian boy who had lost 80% of his skin. The boy's family had fled Syria for Germany in 2013. Upon seeking treatment in Germany, he had lost the epidermis from almost his entire body, with only his head and a patch on his left leg remaining. The group of Italian scientists had previously pioneered a technique to regenerate healthy skin in the laboratory. They used this treatment on the boy by taking a sample from his remaining healthy skin and then genetically modifying the skin cells, using a virus to deliver a healthy version of the LAMB3 gene into the nuclei. The patient underwent two operations in autumn 2015, where the new epidermis was attached. The graft had integrated into the lower layers of skin within a month, curing the boy. The introduction of genetic changes could increase the chances of skin cancer in other patients, but if the treatment is deemed safe in the long term, scientists believe the approach could be used to treat other skin disorders.

Epidermolysis bullosa acquisita is a chronic subepidermal blistering disease associated with autoimmunity to type VII collagen within anchoring fibril structures that are located at the dermoepidermal junction.

Epidermolysis bullosa dystrophica or dystrophic EB (DEB) is an inherited disease affecting the skin and other organs.

"Butterfly child" is the colloquial name for a child born with the disease, as their skin is seen to be as delicate and fragile as that of a butterfly.

One of the biggest risks factors faced by the affected foals is susceptibility to secondary infection. Within three to eight days after birth, the foal may die from infection or is euthanized for welfare reasons.

Junctional epidermolysis bullosa is a skin condition characterized by blister formation within the lamina lucida of the basement membrane zone.

Lethal acantholytic epidermolysis bullosa is a fatal genetic skin disorder caused by mutations in DSP

This is rare and is usually due to mutations in the R-spondin 4 (RSPO4) gene which is located on the short arm of chromosome 20 (20p13). Clinically it is manifest by the absence (anonychia) or hypoplasia (hyponuchia) of finger- and/or toenails.

The deficiency in anchoring fibrils impairs the adherence between the epidermis and the underlying dermis. The skin of DEB patients is thus highly susceptible to severe blistering.Collagen VII is also associated with the epithelium of the esophageal lining, and DEB patients may suffer from chronic scarring, webbing, and obstruction of the esophagus. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infectionsThe chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

The chronic inflammatory state seen in recessive dystrophic epidermolysis bullosa (RDEB) may cause Small fiber peripheral neuropathy (SFN).; RDEB patients have reported the sensation of pain in line with neuropathic pain qualities.

Anonychia is the absence of nails, an anomaly, which may be the result of a congenital ectodermal defect, ichthyosis, severe infection, severe allergic contact dermatitis, self-inflicted trauma, Raynaud phenomenon, lichen planus, epidermolysis bullosa, or severe exfoliative diseases.

Epidermolysis bullosa simplex may be divided into multiple types:

Epidermolysis bullosa simplex (EBS),is a disorder resulting from mutations in the genes encoding keratin 5 or keratin 14.

Blister formation of EBS occurs at the dermoepidermal junction. Sometimes EBS is called "epidermolytic".

Bart syndrome is a genetic disorder characterized by the association of congenital localized absence of skin, epidermolysis bullosa, lesions of the mouth mucosa, and dystrophic nails.

Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the palms and soles.

Autosomal recessive and dominant, X-linked, and acquired forms have all been described.

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.

Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.