2011 SOSORT Guidelines: Orthopaedic & Rehab Treatment of AIS
ScoliosisJournal posted an article regarding; 2011 SOSORT guidelines: Orthopaedic and Rehabilitation Treatment of Idiopathic Scoliosis during growth.
Authors: Stefano Negrini, Angelo G Aulisa, Lorenzo Aulisa, Alin B Circo, Jean C de Mauroy, Jacek Durmala, Theodoros B Grivas, Patrick Knott, Tomasz Kotwicki, Toru Maruyama, Silvia Minozzi, Joseph P O'Brien, Dimitris Papadopoulos, Manuel Rigo, Charles H Rivard, Michele Romano, James H Wynne, Monica Villagrasa, Hans-Rudolf Weiss and Fabio Zaina
The International Scientific Society on Scoliosis Orthopaedic and Rehabilitation Treatment (SOSORT), that produced its first Guidelines in 2005, felt the need to revise them and increase their scientific quality. The aim is to offer to all professionals and their patients an evidence-based updated review of the actual evidence on conservative treatment of idiopathic scoliosis (CTIS).
Methods
All types of professionals (specialty physicians, and allied health professionals) engaged in CTIS have been involved together with a methodologist and a patient representative. A review of all the relevant literature and of the existing Guidelines have been performed. Documents, recommendations, and practical approach flow charts have been developed according to a Delphi procedure. A methodological and practical review has been made, and a final Consensus Session was held during the 2011 Barcelona SOSORT Meeting.
Epidemiology
In approximately 20% of cases, scoliosis is secondary to another pathological process. The remaining 80% are cases of idiopathic scoliosis. Adolescent idiopathic scoliosis (AIS) with a Cobb angle above 10° occurs in the general population in a wide range from 0.93 to 12% : two to three percent is the value the most often found in the literature, and it has been suggested that epidemiology changes according to latitude.
Approximately 10% of these diagnosed cases require conservative treatment and approximately 0.1-0.3% require operative correction of the deformity. Progression of AIS is much more frequently seen in females. When the Cobb angle is 10 to 20°, the ratio of affected girls to boys is similar (1.3:1), increasing to 5.4:1 for Cobb angles between 20 and 30°, and 7:1 for angle values above 30°. If the scoliosis angle at completion of growth exceeds a"critical threshold" (most authors assume it to be between 30° and 50°), there is a higher risk of health problems in adult life, decreased quality of life, cosmetic deformity and visible disability, pain and progressive functional limitations.
Etiology
The etiopathogenesis of scoliosis has not been elucidated. The causes of scoliosis are being sought in congenital or acquired disorders of vertebral structure. Patients with this type of deformity are usually noted to suffer from such co-existent abnormalities as asymmetrical structure of the brain stem, sensory and balance impairment, disorders of blood platelet and collagen function. The role of genetic factors in the development of spinal axial disorders is also emphasised and is confirmed by the tendency of scoliosis to run in families, with researchers suggesting a hereditary disorder of oestrogen receptor structure and function.
Numerous authors indicate that the causes of scoliosis are systemic disorders of, among others, mucopolysaccharide and lipoprotein synthesis. In the 1990s a group of researchers under the guidance of Dubousset proposed that scoliosis develops as a result of melatonin synthesis disorder. They produced spinal curvatures in chickens via pinealectomy and later ameliorated the melatonin deficiency to find decreased incidence of scoliosis in the animals. Machida reported reduced serum melatonin levels in girls with rapidly progressive idiopathic scoliosis. His finding has been questioned by other authors, who found no differences between melatonin levels in scoliotic girls and those in a healthy control group. Currently, melatonin is attributed only a limited role in scoliosis pathogenesis. The possible role of melatonin in scoliosis etiology is also discussed in connection to age at menarche in different geographic latitudes.
According to more recent studies, calmodulin may disturb melatonin levels. Kindsfater assessed calmodulin levels in order to determine the risk of curve progression. Basing on this hypothesis, melatonin plays a secondary role in the spontaneous induction of scoliosis. It is a consequence of interaction with calmodulin, a protein that has receptors for calcium ions and is thus able to influence the contractility of skeletal muscles; it can also be found in blood platelets (its level in platelets was higher in patients with scoliotic progression rates of more than 10° over 12 months). Other authors have evaluated the possibility that gene variants of IL-6 and MMPs might be associated with scoliosis and suggests that MMP-3 and IL-6 promoter polymorphisms constitute important factors for the genetic predisposition to scoliosis. Association Between IL-6.
All in all, the etiology of scoliosis has not been fully elucidated. Based on the variety of opinions on idiopathic scoliosis development, we can assume a multifactorial origin. The opinions presented above are supplementary rather than mutually exclusive. At the same time they explain the complex determinants of and relationships between disorders of spinal development in children and adolescents.
Natural History
Idiopathic scoliosis (IS) may develop at any time during childhood and adolescence. It is most common in periods of growth spurt-between the ages of 6 and 24 months, 5 and 8 years and 11 and 14 years of life. The rate of development of spinal curvature changes the most rapidly at the beginning of puberty. According to the Tanner scale, which assesses tertiary sex characteristics, this period corresponds to stage S2 and P2 in girls, and T2 and P2 in boys. The pubertal growth spurt begins with accelerated longitudinal growth of limbs, which causes a temporary disproportion of the body (long limbs and short trunk). Then longitudinal growth is seen in the axial skeleton. It is the period of the most marked progression of IS. After approx. 2/3 of the period of pubescent growth spurt, girls experience menarche, which indicates a slow, gradual decrease in the risk of scoliosis progression:
There is a much lower potential for progression of idiopathic scoliosis after the spinal growth is complete. In adulthood, IS may intensify as a result of progressive osseous deformities and collapsing of the spine. This phenomenon is reported especially in scoliosis that is more severe than 50°, while the risk of progression starts to increase as the curve grows above 30°; less severe idiopathic scoliosis curves often remain stable. Nevertheless, the natural history of adult scoliosis is not well known to date, and it is still possible the progression can have some peak periods. A "de novo" scoliosis has been recognized as a possible form in adulthood.
To download the PDF on the SOSORT guidelines for 2011 you can do so from the ScoliosisJournal websiteb
Authors: Stefano Negrini, Angelo G Aulisa, Lorenzo Aulisa, Alin B Circo, Jean C de Mauroy, Jacek Durmala, Theodoros B Grivas, Patrick Knott, Tomasz Kotwicki, Toru Maruyama, Silvia Minozzi, Joseph P O'Brien, Dimitris Papadopoulos, Manuel Rigo, Charles H Rivard, Michele Romano, James H Wynne, Monica Villagrasa, Hans-Rudolf Weiss and Fabio Zaina
The International Scientific Society on Scoliosis Orthopaedic and Rehabilitation Treatment (SOSORT), that produced its first Guidelines in 2005, felt the need to revise them and increase their scientific quality. The aim is to offer to all professionals and their patients an evidence-based updated review of the actual evidence on conservative treatment of idiopathic scoliosis (CTIS).
Methods
All types of professionals (specialty physicians, and allied health professionals) engaged in CTIS have been involved together with a methodologist and a patient representative. A review of all the relevant literature and of the existing Guidelines have been performed. Documents, recommendations, and practical approach flow charts have been developed according to a Delphi procedure. A methodological and practical review has been made, and a final Consensus Session was held during the 2011 Barcelona SOSORT Meeting.
Epidemiology
In approximately 20% of cases, scoliosis is secondary to another pathological process. The remaining 80% are cases of idiopathic scoliosis. Adolescent idiopathic scoliosis (AIS) with a Cobb angle above 10° occurs in the general population in a wide range from 0.93 to 12% : two to three percent is the value the most often found in the literature, and it has been suggested that epidemiology changes according to latitude.
Approximately 10% of these diagnosed cases require conservative treatment and approximately 0.1-0.3% require operative correction of the deformity. Progression of AIS is much more frequently seen in females. When the Cobb angle is 10 to 20°, the ratio of affected girls to boys is similar (1.3:1), increasing to 5.4:1 for Cobb angles between 20 and 30°, and 7:1 for angle values above 30°. If the scoliosis angle at completion of growth exceeds a"critical threshold" (most authors assume it to be between 30° and 50°), there is a higher risk of health problems in adult life, decreased quality of life, cosmetic deformity and visible disability, pain and progressive functional limitations.
Etiology
The etiopathogenesis of scoliosis has not been elucidated. The causes of scoliosis are being sought in congenital or acquired disorders of vertebral structure. Patients with this type of deformity are usually noted to suffer from such co-existent abnormalities as asymmetrical structure of the brain stem, sensory and balance impairment, disorders of blood platelet and collagen function. The role of genetic factors in the development of spinal axial disorders is also emphasised and is confirmed by the tendency of scoliosis to run in families, with researchers suggesting a hereditary disorder of oestrogen receptor structure and function.
Numerous authors indicate that the causes of scoliosis are systemic disorders of, among others, mucopolysaccharide and lipoprotein synthesis. In the 1990s a group of researchers under the guidance of Dubousset proposed that scoliosis develops as a result of melatonin synthesis disorder. They produced spinal curvatures in chickens via pinealectomy and later ameliorated the melatonin deficiency to find decreased incidence of scoliosis in the animals. Machida reported reduced serum melatonin levels in girls with rapidly progressive idiopathic scoliosis. His finding has been questioned by other authors, who found no differences between melatonin levels in scoliotic girls and those in a healthy control group. Currently, melatonin is attributed only a limited role in scoliosis pathogenesis. The possible role of melatonin in scoliosis etiology is also discussed in connection to age at menarche in different geographic latitudes.
According to more recent studies, calmodulin may disturb melatonin levels. Kindsfater assessed calmodulin levels in order to determine the risk of curve progression. Basing on this hypothesis, melatonin plays a secondary role in the spontaneous induction of scoliosis. It is a consequence of interaction with calmodulin, a protein that has receptors for calcium ions and is thus able to influence the contractility of skeletal muscles; it can also be found in blood platelets (its level in platelets was higher in patients with scoliotic progression rates of more than 10° over 12 months). Other authors have evaluated the possibility that gene variants of IL-6 and MMPs might be associated with scoliosis and suggests that MMP-3 and IL-6 promoter polymorphisms constitute important factors for the genetic predisposition to scoliosis. Association Between IL-6.
All in all, the etiology of scoliosis has not been fully elucidated. Based on the variety of opinions on idiopathic scoliosis development, we can assume a multifactorial origin. The opinions presented above are supplementary rather than mutually exclusive. At the same time they explain the complex determinants of and relationships between disorders of spinal development in children and adolescents.
Natural History
Idiopathic scoliosis (IS) may develop at any time during childhood and adolescence. It is most common in periods of growth spurt-between the ages of 6 and 24 months, 5 and 8 years and 11 and 14 years of life. The rate of development of spinal curvature changes the most rapidly at the beginning of puberty. According to the Tanner scale, which assesses tertiary sex characteristics, this period corresponds to stage S2 and P2 in girls, and T2 and P2 in boys. The pubertal growth spurt begins with accelerated longitudinal growth of limbs, which causes a temporary disproportion of the body (long limbs and short trunk). Then longitudinal growth is seen in the axial skeleton. It is the period of the most marked progression of IS. After approx. 2/3 of the period of pubescent growth spurt, girls experience menarche, which indicates a slow, gradual decrease in the risk of scoliosis progression:
There is a much lower potential for progression of idiopathic scoliosis after the spinal growth is complete. In adulthood, IS may intensify as a result of progressive osseous deformities and collapsing of the spine. This phenomenon is reported especially in scoliosis that is more severe than 50°, while the risk of progression starts to increase as the curve grows above 30°; less severe idiopathic scoliosis curves often remain stable. Nevertheless, the natural history of adult scoliosis is not well known to date, and it is still possible the progression can have some peak periods. A "de novo" scoliosis has been recognized as a possible form in adulthood.
To download the PDF on the SOSORT guidelines for 2011 you can do so from the ScoliosisJournal websiteb
