It is believed the healthy marrow will provide cells from which osteoclasts will develop. If complications occur in children, patients can be treated with vitamin D. Gamma interferon has also been shown to be effective, and it can be associated to vitamin D. Erythropoetin has been used to treat any associated anemia. Corticosteroids may alleviate both the anemia and stimulate bone resorption. Fractures and osteomyelitis can be treated as usual. Treatment for osteopetrosis depends on the specific symptoms present and the severity in each person. Therefore, treatment options must be evaluated on an individual basis. Nutritional support is important to improve growth and it also enhances responsiveness to other treatment options. A calcium-deficient diet has been beneficial for some affected people.Treatment is necessary for the infantile form:
Vitamin D (calcitriol) appears to stimulate dormant osteoclasts, which stimulates bone resorption
Gamma interferon can have long-term benefits. It improves white blood cell function (leading to fewer infections), decreases bone volume, and increases bone marrow volume. Erythropoietin can be used for anemia, and corticosteroids can be used for anemia and to stimulate bone resorption.Bone marrow transplantation (BMT) improves some cases of severe, infantile osteopetrosis associated with bone marrow failure, and offers the best chance of longer-term survival for individuals with this type.In pediatric (childhood) osteopetrosis, surgery is sometimes needed because of fractures. Adult osteopetrosis typically does not require treatment, but complications of the condition may require intervention. Surgery may be needed for aesthetic or functional reasons (such as multiple fractures, deformity, and loss of function), or for severe degenerative joint disease.
Kindler syndrome (also known as "bullous acrokeratotic poikiloderma of Kindler and Weary",)  is a rare congenital disease of the skin caused by a mutation in the KIND1 gene. Symptoms and signs
Infants and young children with Kindler syndrome have a tendency to blister with minor trauma and are prone to sunburns. As individuals with Kindler syndrome age, they tend to have fewer problems with blistering and photosensitivity. However, pigment changes and thinning of the skin become more prominent. Kindler syndrome can affect various mucous tissues such as the mouth and eyes, which can lead to other health problems. Genetics
Kindler syndrome is an autosomal recessive genodermatosis. The KIND1 gene mutated in Kindler syndrome codes for the protein kindlin-1, which is thought to be active in the interactions between actin and the extracellular matrix (focal adhesion plaques). Kindler syndrome was first described in 1954 by Theresa Kindler. Diagnosis
Clinical and genetic tests are used to confirm diagnosis. Management
Treatment may involve several different types of practitioner to address the various manifestations that may occur. This multidisciplinary team  will also be involved in preventing secondary complications. See also
Rothmund–Thomson syndrome
Epidermolysis bullosa
List of cutaneous conditions

References


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