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Journal of Physiotherapy & Physical Rehabilitation

Journal of Physiotherapy & Physical Rehabilitation

ISSN: 2573-0312

Open Access
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The majority of patients with imperfect osteogenesis (OI) have mutations in the COL1A1 or COL1A2 gene, which has consequences for the composition of the bone matrix and bone architecture. The mutations result in over-modified collagen molecules, thinner collagen fibers, and hyper-mineralization of bone tissue in the bone matrix. Trabecular bone in OI is characterized by lower trabecular number and connectivity as well as lower trabecular thickness and volumetric bone mass. Cortical bone shows a decrease in cortical thickness with less mechanical anisotropy and an increased percentage of pores due to the increase in osteocytic vacancies and vascular porosity.

Most OI patients have mutations at different locations in the COL1 gene. The severity of the disease in OI is probably partly determined by the nature of the primary collagen defect and its location relative to the C-terminus of the collagen protein. Overall bone biomechanics results in a relatively weak and fragile structure. As this is a result of all of the above factors as well as their interactions, there is considerable variation between patients and it is difficult to accurately predict bone strength in the individual patient with OI.

Current OI treatment focuses on adequate levels of vitamin D and interventions in the bone renewal cycle with bisphosphonates. Bisphosphonates increase bone mineral density, but there is limited evidence of improvement in clinical status. The effects of new drugs such as antibodies to RANKL and sclerostin are currently being studied.

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Citations: 378

Journal of Physiotherapy & Physical Rehabilitation received 378 citations as per Google Scholar report

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