Treatment
Medications are used to address certain behavioral problems; therapy for children with PDD should be specialized according to the childs specific needs.Some children with PDD benefit from specialized classrooms in which the class size is small and instruction is given on a one-to-one basis. Others function well in standard special education classes or regular classes with support. Early intervention, including appropriate and specialized educational programs and support services, play a critical role in improving the outcome of individuals with PDD. See also
Infantile neuroaxonal dystrophy
Multiple complex developmental disorder
Multisystem developmental disorder
Overactive disorder associated with mental retardation and stereotyped movements

References
External links
CDCs "Learn the Signs. Act Early." campaign - Information for parents on early childhood development and developmental disabilities
NINFS Pervasive Developmental Disorders Information Page
The symptoms of this disease usually begin during middle age of an adult patient and can include bone pain, and hypomineralization.Some patients suffer from calcium pyrophosphate dihydrate crystal depositions with occasional attacks of arthritis (pseudogout), which appears to be the result of elevated endogenous inorganic pyrophosphate (PPi) levels. These patients may also suffer articular cartilage degeneration and pyrophosphate arthropathy. Radiographs reveal pseudofractures in the lateral cortices of the proximal femora and stress fractures, and patients may experience osteopenia, chondrocalcinosis, features of pyrophosphate arthropathy, and calcific periarthritis. Odontohypophosphatasia
Odontohypophosphatasia is present when dental disease is the only clinical abnormality, and radiographic and/or histologic studies reveal no evidence of rickets or osteomalacia. Although hereditary leukocyte abnormalities and other disorders usually account for this condition, odontohypophosphatasia may explain some “early-onset periodontitis” cases. Causes
Hypophosphatasia is associated with a molecular defect in the gene encoding tissue non-specific alkaline phosphatase (TNSALP). TNSALP is an enzyme that is tethered to the outer surface of osteoblasts and chondrocytes. TNSALP hydrolyzes several substances, including mineralization-inhibiting inorganic pyrophosphate (PPi) and pyridoxal 5’-phosphate (PLP), a major form of vitamin B. A relationship describing physiologic regulation of mineralization has been termed the Stenciling Principle of mineralization, whereby enzyme-substrate pairs imprint mineralization patterns locally into the extracellular matrix (most notably described for bone) by degrading mineralization inhibitors (e.g. TNAP/TNSALP/ALPL enzyme degrading the pyrophosphate inhibition of mineralization, and PHEX enzyme degrading the osteopontin inhibition of mineralization). The Stenciling Principle for mineralization is particularly relevant to the osteomalacia and odontomalacia observed in hypophosphatasia (HPP) and X-linked hypophosphatemia (XLH).6.