The main concern in the patient with idiopathic scoliosis relates to curve progression and resulting cosmetic deformity. The risk of curve progression is correlated primarily to periods of rapid skeletal growth.7,10,11,14,17,44,45 Factors that are related to growth potential, such as patient age at the time of diagnosis, status of menarche, and Risser sign, proved to be important predictors of the progression of scoliosis.7,18,31,42 In addition to future skeletal growth, curve magnitude and curve shape have proven to be predictors of progression of idiopathic scoliosis. Large initial curves, thoracic curves, and double curves were more likely to progress.7,31,42 In addition, with curves greater than 40° Cobb angle, there may be considerable risk of continuous small progression after skeletal maturity has been reached.4,20,24,36,58
Bracing currently is the accepted nonoperative treatment to prevent curve progression in mild to moderate scoliosis during the growth period. A prospective multicenter study on brace effectiveness, performed by the Scoliosis Research Society, reported brace treatment has a significant effect on curve progression of idiopathic scoliosis.38 However, others doubted the effectiveness of braces.13,19,21,35 Corresponding to the natural history of untreated curves, Lonstein and Winter32 found a relationship between the final outcome of brace treatment and curve factors and factors that predict future skeletal growth.
In biomechanical theories about the pathomechanism of scoliosis, spinal growth is thought to be the driving force responsible for curve progression.37,45,54 However, factors that predict potential remaining skeletal growth do not always predict spinal growth correctly.8,29,43 A simple method of determining spinal growth is the increase of sitting or standing height. Anderson et al1 documented the pattern of trunk growth versus chronologic and bone age derived from serial measurements of sitting height of healthy girls and boys. These curves offer a good indication of the amount of spinal growth at different maturation levels. In addition, periods of maximum growth, based on periodically determined standing heights, have been shown to correlate with curve progression.10,11,17 However an increase of the standing height includes the growth of the spine and the growth of the head, pelvis, and lower extremities. In addition, the simultaneous occurrence of spinal growth and progression of the scoliotic curve will influence the trunk height increase.
Only a few studies have concentrated on the correlation between direct radiologic measurements of spinal growth and the progression of the scoliotic curve.11,62 The current study evaluated the velocity of spinal growth, measured as the length of the scoliotic spine on serial longitudinal radiographs, and its relationship to the progression of the scoliotic curve. Progression is evaluated in terms of Cobb angle, lateral deviation, and axial rotation increase in the period before brace therapy and during the time the brace was worn.
MATERIALS AND METHODS
Patient Group
The retrospective longitudinal study was based on measurements made on conventional standing anteroposterior (AP) radiographs of 60 patients (54 girls and six boys) with adolescent idiopathic scoliosis. In all patients, a Boston brace was prescribed during the followup period. This brace treatment was indicated in skeletally immature patients with a Cobb angle between 20° and 45°. Patients who underwent surgical procedures performed during the followup period were excluded from the study.
Radiographs of the patients from their first clinic visit until skeletal growth was completed were used for the study. The mean age of the patients at diagnosis was 11.1 years (standard deviation, 2.01 years). A single thoracic curve was found in 36 patients, and a double curve with a right thoracic and left lumbar pattern was found in 24 patients. All had a major thoracic curve with the apex between T6 and T12. The mean Cobb angle on the first radiographs of the thoracic curves was 25.9° (standard deviation, 8.69°). Subsequent radiographs were taken at 4- to 6-month intervals with the patients in the standing position using the same standardized method.
Radiographic Measurements
For the radiographic measurements, six landmarks per vertebra on each AP radiograph were identified and marked with a fine white ink pen (point size, 0.4 mm). These landmarks were positioned at the corners of the vertebral bodies and the inner edges of both pedicles from T1 to L4. L4 was chosen as the last vertebra because L5 often is barely visible in standing AP radiographs because of its large lordotic tilt. The corners of the vertebrae were determined by means of tangent lines through the upper and lower end plates and both lateral sides of the vertebrae. The landmarks were scanned with a MX5 CCD camera (Adimec, Eindhoven) and digitized with the Bioscan OPTIMAS (V4.1, Bioscan Inc, Washington, VA) software package (Fig 1) . Subsequently, the landmarks were saved as Cartesian coordinates in a computer file.
Fig 1: Positions of the digitized landmarks on the corners of the vertebral bodies and the inner edges of both pedicles on the AP radiograph.
The accuracy of identifying the anatomic landmarks was assessed in 20 radiographs taken at random during the study. The original markings and tangent lines were erased completely, and the radiographs were marked again by the same operator and again digitized. The average variability (standard deviation) of the digitized landmarks was 0.42 mm for the horizontal coordinates and 0.75 mm for the vertical coordinates.
With the two-dimensional coordinates of the landmarks, the midpoints of the vertebral bodies and the lateral tilt of the upper and lower end plates of each vertebra were calculated by a computer algorithm. The computed Cobb angle consisted of the angle between the upper end plate of the upper, most tilted vertebra and the lower end plate of the lowest, most tilted vertebra in the scoliotic curve, and thus an equivalent of the Cobb angle measured clinically. The lateral deviation for each vertebra was measured as the distance between the calculated midpoint of the vertebral bodies and the line passing through the centers of the upper end plate of T1 and the lower end plate of L4. The axial rotation was determined with a method adapted from Stokes et al,53 which uses the coordinates of both pedicles and midpoint of the vertebra.
The length of the scoliotic spine was determined through the distance of the line through the mid-points of all vertebrae and discs between the upper end plate of T1 and the lower end plate of L4 (Fig 2) .
Fig 2: The computed line through the midpoints of all vertebrae and discs between the upper end plate of T1 and the lower end plate of L4 on the AP radiograph.
All measured dimensions on the AP radiographs have been corrected for the magnification. The magnification factor was based on the focus film distance of 290 cm and the estimated distance between the vertebral body and the film according to the method developed by Schultz et al.48 The mean distance from the vertebral body centers to the plumb line on the patient's back, determined on lateral radiographs of 20 patients with adolescent idiopathic scoliosis, was 8.1 cm (standard deviation, 0.84). Using this distance, including the distance of the position frame to the film cassette (6.5 cm), a mean magnification factor of 1.05 was calculated.
The spinal length between T1 and L4, measured on two consecutive radiographs, was used to calculate the growth velocity in millimeters per year. With these data, a spinal growth velocity curve was determined for each patient during the followup period. Subsequently, the followup period was divided into three phases: a phase of rapid spinal growth, a phase of moderate growth, and a phase of little or no spinal growth. On the basis of the mean spinal growth velocity values of all 54 female patients in the study, these three phases were quantified.
In the various growth phases, the mean increase of the Cobb angle, the mean increase of the lateral deviation, and the mean increase of the axial rotation were determined. A distinction was made between curve progression rate before brace treatment and curve progression during brace treatment. The increase of the curve quantities was based on measurements on at least three consecutive radiographs and a period of 8 months. Curve increase calculated from two radiographs in a shorter interval introduced too much error and was not used in the study. The Cobb angle and axial rotation increase were expressed in degrees per year and the lateral deviation increase in millimeters per year.
Statistical Analyses
From the individual serial growth velocity values of the female patients, the median, fifth, 25th, 75th, and 95th percentiles of the spinal growth velocity at consecutive chronologic ages were determined. Growth curves were determined by fitting the percentiles by a third-grade polynomial using the MS EXCEL (V7.0a, Microsoft Corp, Redmond, OR) software package.
SPSS (V6.1, SPSS Inc, Chicago, IL) software was used to determine whether significant differences exist between the progression rate in the three growth phases (Kruskal Wallis H test; p < 0.05) and whether brace treatment has a significant effect on curve progression rate in the various growth phases (Mann Whitney U test; p < 0.05).
RESULTS
Spinal Growth Velocity
The median, fifth, 25th, 75th, and 95th percentiles of the spinal growth velocity of the female patients fitted with a third grade polynomial (r2 = 0.93) are presented Figure 3 . The maximum spinal growth velocity of the female patients was found to be between the ages of 11.5 and 12.5 years. The mean maximum growth velocity was 18.3 mm per year, which extended from approximately 10 to 30 mm per year.
Fig 3: The median, 95th, 75th, 25th, and fifth percentiles of the spinal growth velocity at consecutive chronologic ages of the 54 female patients. The different percentiles of the growth velocity were fitted with a third grade polynomial (r2 = 0.93).
In the growth charts of the sitting height and of the upper and lower extremities, Anderson et al1 also presented curves with the amount of remaining growth at different ages. The charts of the remaining sitting height are used for estimation of the approximate amount of growth, which might be arrested through spondylodesis at specific ages. However, the remaining increase of the sitting height includes the growth of the spine and the growth of the head and pelvis. The remaining growth of T1-L4 versus age, derived from the growth velocity rates of the 54 female patients in the current study, is presented in Figure 4 .
Fig 4: The median, 95th, 75th, 25th, and fifth percentiles of the remaining spinal growth at consecutive chronologic ages of the 54 female patients. The different percentiles of the growth velocity were fitted with a third grade polynomial (r2 = 0.99).
Growth curves as presented for female patients with scoliosis were not determined for the male patients because of their small number. For the six male patients in the current study the maximum growth velocity was found at a mean chronologic age of 15 years (standard deviation, 0.5). The mean maximum spinal growth velocity was 26.1 mm per year (standard deviation, 9.3).
As mentioned, the followup period of each patient was divided into three phases: a phase of very rapid spinal growth, a phase of moderate growth, and a phase of little or no growth. On the basis of the spinal growth velocity curve of the female patients, the period of the most rapid growth was defined as the period in which spinal growth exceeded 20 mm per year, the period with moderate growth as the period with a growth velocity between 10 and 20 mm per year, and the period with the least rapid growth as the period in which the growth velocity did not exceed 10 mm per year.
Progression Rate
The mean progression rate of the Cobb angle, lateral deviation, and axial rotation of the thoracic curve of all patients in the three growth phases is presented in Table 1 . A distinction has been made between the progression rate in the period before brace treatment and the progression rate during brace treatment. In 20 patients the progression rate could be determined on the basis of at least three radiographs in the phase of rapid growth (≥ 20 mm per year). In four of these patients a progression rate could be determined in the period before and after brace treatment. A significantly smaller mean progression rate of the Cobb angle was observed in the group that was treated with a brace than in the group that had not yet been treated with a brace. This brace effect could not be seen in the progression rate of the lateral deviation and axial rotation.
TABLE 1: The Mean Progression Rate of the Thoracic Curve of all Patients, in the Period Before Brace Treatment, and During Brace Treatment, in the Three Growth Phases
In 39 patients the progression rate could be determined in a period with moderate spinal growth (≥ 10 mm per year, < 20 mm per year). In two patients a progression rate could be determined before and after brace treatment. The same pattern could be seen for the progression rate in the period of rapid spinal growth: a significantly smaller progression rate of the Cobb angle when a brace was worn, but no significant influence of the brace on the progression rate of the lateral deviation and axial rotation.
In 35 patients, the progression rate could be determined in the phase of little growth (< 10 mm per year). All patients wore a brace in this phase. The mean progression rate in this phase was found to be significantly smaller compared with the mean progression rate in the phases with moderate and a large spinal growth velocity. This observation was valid for the Cobb angle, the lateral deviation, and the axial rotation increase.
No significant difference could be observed between mean progression rate in the periods with moderate and large spinal growth velocities.
DISCUSSION
Biomechanical factors have a basic influence on the sequence of events that result in the progression of idiopathic scoliosis. Because of the strong correlation of factors that predict potential remaining skeletal growth and curve progression, it is thought that growth of the spinal column plays a major role in this process. In the current study, spinal growth was measured with the length increase of the scoliotic spine (T1-L4 segment) on longitudinal standing AP radiographs. A significantly greater average progression rate of the scoliotic thoracic curve was found in the periods with rapid to moderate growth (≥ 10 mm per year) than in the periods with small or no growth (< 10 mm per year). The difference in progression rates concerned the increase of the Cobb angle and the increase of the lateral deviation and axial rotation.
Despite curve progression during the growth periods, the brace treatment had a significant effect on the Cobb angle increase. However, this brace effect could not be seen for the progression rate of the lateral deviation and axial rotation. These results are in agreement with recent studies concerning the three-dimensional analysis of the short-term effects of the Boston brace system.3,27 In these studies, it was shown that although the brace reduced the Cobb angle in the frontal plane, it induced no significant effect on the lateral deviation and axial rotation of the scoliotic spine. This indicates that the long-term effect of brace treatment should be subjected to critical evaluation. Not only the Cobb angle should be evaluated, as most studies on brace effectiveness have done, but also the axial rotation and displacements of the apical vertebrae in the various planes.
In the current study, longitudinal series of AP radiographs were used for evaluation. For the measurements of the displacements and rotations, six landmarks per vertebra were identified and digitized. The reliability of identifying the landmarks on the AP radiographs was comparable to the reliability reported in a previous study.26 The progression was related to the growth of the T1-L4 segment, which was measured using the length of the spinal column on the AP radiograph. This means the curve in the frontal plane was included in calculating the length, but the sagittal curve (the thoracic kyphosis and lumbar lordosis) was not. Despite this limitation, the periods of rapid spinal growth were well observed. This suggests that only small or no changes occur in the sagittal curve and that the length measurements of the spine are influenced minimally.
Growth charts were derived from the measured individual growth velocity values of the patients of the study. The mean maximum spinal growth velocity of the T1-L4 segment of the female patients was 18.3 mm per year (range, 12.0-30.1 mm per year) and was found between the ages of 11.5 and 12.5 years. These chronologic ages of maximum growth almost coincide with the reported ages of maximum skeletal growth of healthy girls.6,55 In boys, the age of maximum growth was found most frequently 2 years later. Spinal growth was not correlated with the Risser sign because according to the authors the apophyses of the iliac crest insufficiently was visible on the spinal radiographs for assessment of the accurate stage. In addition, it has been reported that the Risser sign is less accurate than is chronologic age as a predictor of skeletal age and should not be used as a substitute for hand and wrist radiographs.29 However, other authors contradict this.1,49
Growth may be regarded as a complex process that depends on hereditary, geographic factors, nutritional factors, health factors, and other things. Thus, many differences in growth patterns between individuals may be seen. The variation in growth pattern in the female patients with scoliosis in this study is presented by percentiles in the growth charts. At the age of 10 years an average length increase of 10 cm of the T1-L4 segment is expected, which varies from 4.5 cm to 17 cm. After the 18th year, longitudinal growth of the spinal column barely can be seen. In addition, after the age of 16.5 years, the growth speed barely exceeds 10 mm per year (95th percentile), the growth speed under which only small progression should be expected on the basis of the data of the current study. However, this growth speed also may be reached at the age of 12 years (fifth percentile).
Numerous studies on growth differences between healthy girls and girls with scoliosis have been done. Unfortunately, the results of these studies are not consistent. Willner60,61 observed a taller mean standing height in girls with scoliosis compared with healthy controls. These findings were supported by other cross-sectional studies.9,23,28,33,39,40,41,50 Loncar-Dusek et al30 showed a higher peak height velocity for children with scoliosis. In addition, Goldberg et al22 and Ylikoski et al63 reported that girls with adolescent idiopathic scoliosis have an earlier growth spurt and earlier attainment of adult height than do healthy controls. These results contrast markedly with other reports that found no difference in growth pattern or height between patients with idiopathic scoliosis and controls.16,56,57 However, one should keep in mind that most of the studies mentioned were done on the basis of length measurements of the sitting height, without correction for the error introduced by the scoliotic deformity.
The current knowledge on natural history of scoliosis indicates there are numerous patients with minor degrees of curvature. Some of these patients can be expected to have curvatures that will increase, requiring brace treatment.5,8,31,36,47 Most of the scoliotic curves that are treated with a brace will stabilize. However, in some cases, the curve increases to such an extent that a spondylodesis becomes necessary. The variation in growth speed per individual, as seen in the current study, may be an explanation for the variation of expression of idiopathic scoliosis, besides other factors, such as the type of curve.
There is growing interest in a two-stage hypothesis: It is postulated that the natural history of idiopathic scoliosis involves an initial stage in which a small curve develops because of a small defect in the neuromuscular control system and a second stage during adolescent growth in which the scoliotic curve is exacerbated by biomechanical factors. It was reported that the expected spinal growth at the moment in which the initial curve is diagnosed is crucially important to additional development of scoliosis.31
Various theories exist regarding the biomechanical mechanism responsible for scoliosis progression during spinal growth. Roaf45 hypothesized that a vicious circle might be the basis of the progression of the scoliotic deformity. It was suggested that asymmetric growth of the apical vertebral bodies because of chronic axial asymmetric loading on the physes according to the Hueter-Volkmann law may result in scoliosis progression. Stokes et al54 quantified the relationship between the degree of asymmetric loading and the degree of asymmetric growth in a rat tail model and confirmed that vertebral wedging results from asymmetric growth in the physes.
Others have stressed the importance of the posterior musculoligamentous structures of the spinal column in the pathomechanism of scoliosis.2,34,37,46 Various physical models and cadaver models were described in which the posterior column functioned as a tension column with a strong tendency to shorten.2,12,25,37,52 It was postulated that the tethering tendency of the musculoligamentous structures of the posterior column compared with the rapid growth of the anterior spinal column will result in curve progression and the complex geometry of scoliosis.37,46,52 It also was suggested that with serious progressive scoliosis, the supportive musculoligamentous structures fail to stabilize the growing spine because of a deficiency in the neuromuscular control system.15,51
The results of the current study show that periods with moderate to rapid spinal growth, measured on successive radiographs, correlate with progression of scoliosis. In addition, it is possible to predict future spinal growth at different chronologic ages using the presented growth charts. However, the growth charts and progression rates are the result of statistical procedures, and thus express a general tendency. The growth curve of a patient will not always follow the average growth curve but sometimes may show slight jumps from one percentile to the other. In addition, the growth charts are from a Dutch population with scoliosis and cannot be extrapolated directly to the population with scoliosis from another continent. In addition, the individual progression rates will be determined by the size and the type of the curve and by the type of brace and the brace compliance.
However, it is clear the length of the spine measured on subsequent radiographs is an excellent parameter for determining spinal growth and thus an excellent predictor of scoliosis progression. The current advance of digital radiographs makes it possible to easily quantify various geometric variables of the scoliotic curve. In addition to the various three-dimensional parameters that are used for the evaluation of brace treatment and surgical treatment, the length of the spine is an important variable for the clinician to determine the growth of the patient with scoliosis.
Acknowledgments
The authors thank W.J. Sluiter, PhD, for statistical advice and G. Nijenbanning, MSc, PhD, for discussion.
References
1. Anderson M, Hwang SC, Green WT: Growth of the normal trunk in boys and girls during the second decade of life; related to age, maturity, and ossification of the iliac epiphyses. J Bone Joint Surg 47A:1554-1564, 1965.
2. Arkin AM: The mechanism of rotation in combination with lateral deviation in the normal spine. J Bone Joint Surg 32A:180-188, 1950.
3. Aubin CE, Dansereau J, de Guise JA, Labelle H: Rib cage-spine coupling patterns involved in brace treatment of adolescent idiopathic scoliosis. Spine 22:629-635, 1997.
4. Bjerkreim I, Hassan I. Progression in untreated idiopathic scoliosis after end of growth. Acta Orthop Scand 53:897-900, 1982.
5. Brooks HL, Azen SP, Gerberg E, Brooks R, Chan L: Scoliosis: A prospective epidemiological study. J Bone Joint Surg 57A:968-972, 1975.
6. Buckler JM, Wild J: Longitudinal study of height and weight at adolescence. Arch Dis Child 62:1224-1232, 1987.
7. Bunnell WP: The natural history of idiopathic scoliosis before skeletal maturity. Spine 11:773-776, 1986.
8. Bunnell WP: The natural history of idiopathic scoliosis. Clin Orthop 229:20-25, 1988.
9. Buric M, Momcilovic B: Growth pattern and skeletal age in school girls with idiopathic scoliosis. Clin Orthop 170:238-242, 1982.
10. Burwell RG: The Relationship Between Scoliosis and Growth. In Zorab PA (ed). Scoliosis and Growth. Edinburgh, Churchill Livingstone 131-150, 1971.
11. Calvo IJ: Observations on the growth of the female adolescent spine and its relation to scoliosis. Clin Orthop 10:40-47, 1957.
12. Deacon P, Archer IA, Dickson RA: The anatomy of spinal deformity: A biomechanical analysis. Orthopedics 10:897-903, 1987.
13. Dickson RA: Conservative treatment for idiopathic scoliosis. J Bone Joint Surg 67B:176-181, 1985.
14. Dickson RA, Deacon P: Spinal growth. J Bone Joint Surg 69B:690-692, 1987.
15. Dobosiewicz K: Neurophysiological mechanism of the unloading reflex as a prognostic factor in the early stages of idiopathic adolescent scoliosis. Eur Spine J 6:93-97, 1997.
16. Drummond DS, Rogala EJ: Growth and maturation of adolescents with idiopathic scoliosis. Spine 5:507-511, 1980.
17. Duval-Beaupere G: Pathogenic Relationship Between Scoliosis and Growth. In Zorab PA (ed). Scoliosis and Growth. Edinburgh, Churchill Livingstone 58-61, 1971.
18. Duval-Beaupere G, Lamireau T: Scoliosis at less than 30 degrees. Properties of the evolutivity (risk of progression). Spine 10:421-424, 1985.
19. Edgar MA: To brace or not to brace? J Bone Joint Surg 67B:173-174, 1985.
20. Edgar MA: The natural history of unfused scoliosis. Orthopedics 10:931-939, 1987.
21. Focarile FA, Bonaldi A, Giarolo MA, et al: Effectiveness of nonsurgical treatment for idiopathic scoliosis. Overview of available evidence. Spine 16:395-401, 1991.
22. Goldberg CJ, Dowling FE, Fogarty EE: Adolescent idiopathic scoliosis: Early menarche, normal growth. Spine 18:529-535, 1993.
23. Hagglund G, Karlberg J, Willner S: Growth in girls with adolescent idiopathic scoliosis. Spine 17:108-111, 1992.
24. Howell FR, Mahood JK, Dickson RA: Growth beyond skeletal maturity. Spine 17:437-440, 1992.
25. Jarvis JG, Ashman RB, Johnston CE, Herring JA: The posterior tether in scoliosis. Clin Orthop 227:126-134, 1987.
26. Labelle H, Dansereau J, Bellefleur C, Jequier JC: Variability of geometric measurements from three-dimensional reconstructions of scoliotic spines and rib cages. Eur Spine J 4:88-94, 1995.
27. Labelle H, Dansereau J, Bellefleur C, Poitras B: Three-dimensional effect of the Boston brace on the thoracic spine and rib cage. Spine 21:59-64, 1996.
28. Leong JC, Low WD, Mok CK, Kung LS, Yau AC: Linear growth in southern Chinese female patients with adolescent idiopathic scoliosis. Spine 7:471-475, 1982.
29. Little DG, Sussman MD: The Risser sign: A critical analysis. J Pediatr Orthop 14:569-675, 1994.
30. Loncar-Dusek M, Pecina M, Prebeg Z: A longitudinal study of growth velocity and development of secondary gender characteristics versus onset of idiopathic scoliosis. Clin Orthop 270:278-282, 1991.
31. Lonstein JE, Carlson JM: The prediction of curve progression in untreated idiopathic scoliosis during growth. J Bone Joint Surg 66A:1061-1071, 1984.
32. Lonstein JE, Winter RB: The Milwaukee brace for the treatment of adolescent idiopathic scoliosis. A review of one thousand and twenty patients. J Bone Joint Surg 76:1207-1221, 1994.
33. Low WD, Mok CK, Leong JC, Yau AC, Lisowski FP: The development of southern Chinese girls with adolescent idiopathic scoliosis. Spine 3:152-156, 1978.
34. Meyer GH: Die Mechanik der Skoliose. Archiv Pathol Anat 35:224-253, 1866.
35. Miller JA, Nachemson AL, Schultz AB: Effectiveness of braces in mild idiopathic scoliosis. Spine 9:632-635, 1984.
36. Montgomery F, Willner S: The natural history of idiopathic scoliosis. A study of the incidence of treatment. Spine 13:401-404, 1988.
37. Murray DW, Bulstrode CJ: The development of idiopathic scoliosis. Eur Spine J 5:251-257, 1996.
38. Nachemson AL, Peterson LE: Effectiveness of treatment with a brace in girls who have adolescent idiopathic scoliosis. A prospective, controlled study based on data from the Brace Study of the Scoliosis Research Society. J Bone Joint Surg 77A:815-822, 1995.
39. Nicolopoulos KS, Burwell RG, Webb JK: Stature and its components in adolescent idiopathic scoliosis. Cephalo-caudal disproportion in the trunk of girls. J Bone Joint Surg 67B:594-601, 1985.
40. Nordwall A, Willner S: A study of skeletal age and height in girls with idiopathic scoliosis. Clin Orthop 110:6-10, 1975.
41. Normelli H, Sevastik J, Ljung G, Aaro S, Jonsson-Soderstrom AM: Anthropometric data relating to normal and scoliotic Scandinavian girls. Spine 10:123-126, 1985.
42. Peterson LE, Nachemson AL: Prediction of progression of the curve in girls who have adolescent idiopathic scoliosis of moderate severity. Logistic regression analysis based on data from The Brace Study of the Scoliosis Research Society. J Bone Joint Surg 77A:823-827, 1995.
43. Risser JC: The iliac apophysis: An invaluable sign in the management of scoliosis. Clin Orthop 11:111-118, 1958.
44. Risser JC, Ferguson AB: Scoliosis: Its prognosis. J Bone Joint Surg 18A:667-670, 1936.
45. Roaf R: Vertebral growth and its mechanical control. J Bone Joint Surg 42B:40-59, 1960.
46. Roaf R: The basic anatomy of scoliosis. J Bone Joint Surg 48B:786-792, 1966.
47. Rogala EJ, Drummond DS, Gurr J: Scoliosis: Incidence and natural history. A prospective epidemiological study. J Bone Joint Surg 60A:173-176, 1978.
48. Schultz AB, Sorensen SE, Andersson GB: Measurement of spine morphology in children, ages 10-16. Spine 9:70-73, 1984.
49. Scoles PV, Salvagno R, Villalba K, Riew D. Relationship of iliac crest maturation to skeletal and chronologic age. J Pediatr Orthop 8:639-644, 1988.
50. Shohat M, Shohat T, Nitzan M, et al: Growth and ethnicity in scoliosis. Acta Orthop Scand 59:310-313, 1988.
51. Smith RM, Dickson RA: Experimental structural scoliosis. J Bone Joint Surg 69B:576-581, 1987.
52. Somerville EW: Rotational lordosis: The development of the single curve. J Bone Joint Surg 34B:421-427, 1952.
53. Stokes IAF, Bigalow LC, Moreland MS: Measurement of axial rotation of vertebrae in scoliosis. Spine 11:213-218, 1986.
54. Stokes IAF, Spence H, Aronsson DD, Kilmer N: Mechanical modulation of vertebral body growth. Implications for scoliosis progression. Spine 21:1162-1167, 1996.
55. Tanner JM, Davies PS: Clinical longitudinal standards for height and height velocity for North American children. J Pediatr 107:317-329, 1985.
56. Taylor JR, Slinger BS: Scoliosis screening and growth in Western Australian students. Med J Aust 17:475-478, 1980.
57. Veldhuizen AG, Baas P, Webb PJ: Observations on the growth of the adolescent spine. J Bone Joint Surg 68B:724-728, 1986.
58. Weinstein SL: Idiopathic scoliosis. Natural history. Spine 11:780-783, 1986.
59. Wever DJ, Veldhuizen AG, Klein JP, et al: A biomechanical analysis of the vertebral and rib deformities in structural scoliosis. Eur Spine J 8:252-260, 1999.
60. Willner S: Growth in height of children with scoliosis. Acta Orthop Scand 45:854-866, 1974.
61. Willner S: A study of growth in girls with adolescent idiopathic structural scoliosis. Clin Orthop 101:129-135, 1974.
62. Ylikoski M: Spinal growth and progression of adolescent idiopathic scoliosis. Eur Spine J 1:236-239, 1993.
63. Ylikoski M, Peltonen J, Poussa M: Biological factors and predictability of bracing in adolescent idiopathic scoliosis. J Pediatr Orthop 9:680-683, 1989.