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What Do We Know About Adolescent Idiopathic Scoliosis?

Posted on: 02/23/2011
Another 10 years has gone by and scientists still haven't unraveled all the mysteries surrounding the diagnosis of adolescent idiopathic scoliosis (AIS). AIS describes a condition of spinal curvature (scoliosis) among teens (adolescent) of unknown cause (idiopathic). Girls are affected more often boys, especially beginning during the pre-adolescent stage of life.

Efforts have been made to find a leading factor such as hormonal, genetic, environmental, lifestyle, biomechanical, or nervous system dysfunction. With all the new information available now on motor control, some scientists are taking a second look at that area as a possible avenue of understanding.

Is there a link between diet and exercise? Too much sugar? Not enough calcium? At best, experts agree it might just be multifactorial with more than one cause linked together. Right now, treatment is still based on symptoms instead of cause, so the search for etiology (cause) is still on.

At this point, there remain more questions than answers. We will give you a sampling of both as it stands now. For example, experts in this field still don't know why humans are the only ones to develop scoliosis or if adolescent idiopathic scoliosis (AIS) is different from other types of scoliosis. Some curves get worse while others do not. In today's modern lingo, "What's up with that?"

What causes the curves to start in the first place? Is the same mechanism responsible for worsening of the curve? Which part of the spinal anatomy is affected first: is it the bone itself or the muscles pulling on the bone? Or are all segments (disc, bone, muscle, cartilage) affected equally and at the same time?

What do we know to be true about this condition? Twin studies support a genetic link but gene studies show many different genes are involved. It may be possible to identify subgroups based on specific genes involved but that's only a theory at this point. Problems in the nervous system also seem to play a part in this condition. More advanced MRIs have helped scientists pinpoint specific areas of the brain (vestibular system, pontine and hindbrain regions) where the pathology may begin.

The role of vision, balance, neuron-motor timing, and failure of postural mechanisms in spinal deformity is also under investigation. Another big area of study is skeletal and spinal cord growth -- speed of growth, coordination between soft tissue and bone, and symmetry of growth have been observed and discussed.

The body of the vertebrae (spinal bones) grows faster than the bony parts along the back of the spinal segment. That process of uneven growth is referred to as relative anterior spinal overgrowth or RASO. The RASO growth pattern results in tension and tightening of the spinal cord and spinal nerve roots (called tethering).

Rib deformities, altered blood supply to the chest wall, and differences in arm length from one side to the other have all been considered as possible causes of adolescent idiopathic scoliosis (AIS). And that's not the end of the research list. Studies have also been done looking at the effect of hormones such as growth hormone, melatonin (sleep wake cycles linked with growth and bone density), leptin (helps with energy), and calmodulin (regulates muscles).

In summary, whether there is one pathway or multiple mechanisms leading to the development of adolescent idiopathic scoliosis (AIS) remains unknown. All efforts to study this condition and unveil its origins have resulted in the conclusion that it is a multifactorial problem that requires an integrative model to understand it fully.

Clearly, there is a pattern of abnormal skeletal growth with possible genetic links and biologic as well as biomechanical factors. Research is needed to continue finding successful ways to treat this condition based on an accurate understanding of the underlying cause.

References:
Wei Jun Wang, PhD, et al. Top Theories for the Etiopathogenesis of Adolescent Idiopathic Scoliosis. In The Journal of Pediatric Orthopaedics. January/February 2011. Vol. 31. No. 1. Supplement. Pp. S14-S27.

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