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Osteogenesis Imperfecta (OI)

Osteogenesis imperfecta (OI) is a genetic disorder characterized by brittle bones that break easily, often from little or no apparent cause. There are four primary forms of the disorder with extreme variation in severity from one individual to another.

How Common Is It?
What Causes It?
What Are the Symptoms?
How Is It Diagnosed?
Best Treatment Options
What Should You Do Next?

How Common Is Osteogenesis Imperfecta?

While the number of people affected with OI in the United States is unknown, the best estimate suggests a minimum of 20,000 and possibly as many as 50,000.

A parent with a history of OI has a 50% chance of passing the gene, and therefore the disease, on to his or her children.

What Causes Osteogenesis?

What Are the Symptoms of Osteogenesis Imperfecta?

There are 4 major subtypes of OI. The symptoms of AO can vary significantly depending on the subtype and even within the same subtype.

Type I (Mild)

Type II (Most Severe)

Type III (Severe and progressive)

Type IV (Intermediate)

Collagen problems in OI:

Type 1:

Type 2:

Type 3:

Type 4:

Consequence of collagen mutation in Osteogenesis Imperfecta:

1) The defective collagen rods form an abnormal mold into which bone is mineralized, resulting in weakened bones.

2) The badly formed collagen rods are more susceptible to the body's normal process that detects and destroys broken molecules. Thus, the amount of bone, however imperfect, is reduced further by osteoclasts (cells that break down bone) that remove the defective collagen rods.

3) The third and perhaps most important reason for the brittle bone in OI is that the cells that form bone -- the osteoblasts -- are themselves affected by the nearby presence of bad collagen molecules. Osteoblasts have great difficulty making abnormal collagen fibers and transferring them outside the cell. Thus, the cells are filled with vast quantities of imperfect collagen fibers that cannot be moved outside. Consequently, these cells become very inefficient in the way they make additional bone proteins and are very slow to divide and make new bone cells. However, the body demands that the bone cells make more bone, particularly during childhood, when new bone is needed to carry the increased stature and weight of a growing child. Unfortunately, the only bone that it can make still contains the defective fibers, so the strength is never improved. This spiral of ineffective bone formation is never-ending.


How Is Osteogenesis Imperfecta Diagnosed?

What Is the Best Treatment for FMS?

Conventional Treatment for Osteogenesis Imperfecta

Natural Treatment for Osteogenesis Imperfecta


What Should You Do Next?

The doctors at The Connecticut Center for Health are quite experienced in how to treat osteogenesis imperfecta.

If you would like to learn more about natural medicine approaches to osteogenesis imperfecta, contact one of our clinics for a free consultation or an appointment.

Return to Natural Solutions for any Health Problem

  1. Batch, J. A., J. J. Couper, et al. (2003). "Use of bisphosphonate therapy for osteoporosis in childhood and adolescence." J Paediatr Child Health 39(2): 88-92.
  2. Braunwald, E. (2001). Harrison's principles of internal medicine. New York, McGraw-Hill Medical Publishing Division.
  3. Castells, S., C. Colbert, et al. (1979). "Therapy of osteogenesis imperfecta with synthetic salmon calcitonin." J Pediatr 95(5 Pt 1): 807-11.
  4. Cetta, G., L. Lenzi, et al. (1977). "Osteogenesis imperfecta: morphological, histochemical and biochemical aspects. Modifications induced by (+)-catechin." Connect Tissue Res 5(1): 51-8.
  5. Iwamoto, J., K. Matsu, et al. (2003). "Effects of treatment with etidronate and alfacalcidol for osteogenesis imperfecta type I: a case report." J Orthop Sci 8(2): 243-7.
  6. Jones, C. J., C. Cummings, et al. (1984). "A clinical and ultrastructural study of osteogenesis imperfecta after flavonoid (Catergen) therapy." S Afr Med J 66(24): 907-10.
  7. Kurz, D. and E. J. Eyring (1974). "Effects of vitamin C on osteogenesis imperfecta." Pediatrics 54(1): 56-61.
  8. Marini, J. C., E. Hopkins, et al. (2003). "Positive linear growth and bone responses to growth hormone treatment in children with types III and IV osteogenesis imperfecta: high predictive value of the carboxyterminal propeptide of type I procollagen." J Bone Miner Res 18(2): 237-43.