The past decades have seen an expansion in adolescent sports participation, as well as changing injury patterns. 1 In 1972, the United States implemented Title IX of the Education Amendments Act. 2 Subsequently, female participation in organized sports increased, and female athletes now represent one third of U.S. college and Olympic athletes. 3 The overall incidence of back injury in sports has been estimated at 10% to 15%. 4,5 Gender differences are somewhat inconclusive. However, in the general population, women made more orthopedic office visits in one year than men for low back pain. 6 Additionally, the female athlete may be at increased risk for back injuries. 7,8 Certainly, scoliosis and spondylolysis are predominant concerns for the female athlete. 9–12
There are a myriad of factors contributing to spinal deformity and injury in the female athlete. Sport-specific mechanics, anthropomorphic factors, relative weakness of growth cartilage, and hormonal and nutritional factors all create an interactive model for understanding these spinal problems. The clinician should attempt to quantify each of these factors to evaluate and plan management in female athletes.
Back injuries are often sport-specific. Certain female-dominated sports, such as gymnastics, figure skating, and dance, emphasize the extremes of spinal motion. 11–13 Athletes in these sports are at risk for spinal injuries and abnormal curve development. Back pain has been reported in 86% of rhythmic gymnasts. 14 Spondylolysis has been estimated to occur in 32% of gymnasts and 33% of ballet dancers. 15–16 Classical ballet has also been associated with an increased incidence of scoliosis. 9 Repetitive asymmetric forces are felt to contribute to abnormal curve development.
Intrinsic biomechanics affect the ground reactive forces resulting from repetitive motions. Nadler et al. 8 found increased reporting of low back pain in female college athletes engaged in multiple noncontact sports. The low back pain was associated with lower extremity ligamentous laxity and overuse injuries. A malalignment syndrome has been described in women that includes increased hip bitrochanteric width, greater hip varus angulation, increased femoral anteversion, genu valgum, and foot pronation. 17 These factors are often implicated in patellar tracking dysfunction and other lower extremity injuries. However, some of these factors may affect the spine and pelvis in a closed chain pattern. Stress fractures to the hip and pelvic ring are found in a greater proportion of female athletes than male athletes. 18
Factors that increase lumbar lordosis also increase the compression load to the posterior elements and tensile forces to the disc. 19 Tight hip flexors and hamstring are commonly associated with hyperlordosis. 20 Femoral anteversion indirectly increases the lordosis in ballet dancers because of the hip limitation to turnout. The immature dancer will often compensate by increasing lumbar lordosis, which releases the ilioinguinal ligament and opens up the acetabulum, allowing more external rotation. 21
Many of these sports begin with intense training in early childhood, which continues through adolescence. The growth plate represents the weak link in the musculoskeletal system during adolescence. 22 The spine has abundant growth cartilage, which is vulnerable to deforming compressive and tensile forces. Growth cartilage is not gender-specific. However, specific sports that are gender-dominated may produce certain injury patterns. Anteriorly, the vertebral body contains the physeal endplate and ring apophysis. These are attached to the more rigid anulus fibrosus. 23 Compressive forces may result in Schmorl nodes and limbus vertebrae. 24 Tensile forces may result in apophysitis and apophyseal avulsion. Repetitive abnormal forces may contribute to asymmetric growth. 25
In the posterior elements, the spinous process apophysis is subject to tensile and compressive forces. The posterior neural arch has a single ossification center in each pedicle. 26 Incomplete ossification of the pars interarticularis may predispose to a spondylolytic lesion with lumbar hyperextension. 27 This lesion may occur from compression of the inferior articular facet of the superior segment onto the pars and lamina at the level below. 28
HORMONAL AND NUTRITIONAL FACTORS
Bone homeostasis is unique to the female athlete and is influenced by multiple factors, including cyclic loading and hormonal and nutritional balance. Training in the physiologic range results in a positive anabolic response to bone density. However, overtraining may result in a catabolic response. 29 Adolescence and early adulthood are the period in a woman's life when over half of the bone mass is accrued, whereas the maximum bone density is attained between 20 and 30 years of age. 30 Theoretically, athletic participation with compressive loads should enhance bone mineral density. 31 However, the athlete whose caloric intake is lower than her caloric output develops an energy drain, with diminished estrogen production and a subsequent decrease in menstruation. 32 This hypoestrogenic state counteracts some of the beneficial effects of exercise. This is particularly important in sports emphasizing body image, such as figure skating, ballet, and gymnastics. Lower estrogen levels correlate with diminished bone density in all age groups. 33 These athletes may develop premature osteopenia, or osteoporosis and stress fractures. 29 Although these changes are reversible with increased caloric intake, the reversibility is incomplete. 33 Furthermore, replacement of estrogen without an increase in caloric balance will not increase bone density. 34 Increased caloric intake is essential in reversing the process.
Some studies have demonstrated the association of secondary amenorrhea and stress fractures. 9,35,36 Although Nattiv 37 was unable to demonstrate this association in track athletes, she showed an association of lower extremity stress fractures and lower bone density of the lumbar spine. The significance of delayed menarche is still not fully understood. However, several studies have associated delayed onset of menstruation with scoliosis and stress fractures. 9,34
Bone health is also dependent on nutritional factors, including calcium and vitamin D. Female adolescent bone mineralization is directly correlated with calcium intake. 38 Unfortunately, calcium is often deficient in the diet of adolescent girls. 39 Furthermore, stress fractures have also been associated with lower calcium intake in athletes. 40 Vitamin D is essential in the absorption of calcium and the stimulation of bone production. 29
A complete history of specific sport involvement should be collected. Although there is much crossover, sports may be categorized as being predominantly lumbar flexion sports, such as crew and power lifting; as extension sports, such as ballet and gymnastics; or as rotational sports, such as golf and tennis. This may assist in identifying the type of spine injury. A history of sports participation should include the number of hours per week of involvement, as well as the slope of acceleration to that level. Some sports, such as gymnastics, demonstrate a threshold participation time of 15 hours per week to predispose to spinal injuries. 41 Progression should not exceed 10% per week by volume of time. 42
A menstrual history should include the number of cycles over the last year. Cycles exceeding 36 days reflect oligomenorrhea, which is associated with low bone density. 36 Primary amenorrhea is the absence of menarche by the age of 16, and is associated with low bone density and scoliosis. 9 Nutritional and calcium intake are probed. Daily calcium intake should be 1,500 mg per day. 39 Caloric intake is also assessed.
Clinical examination should include assessment of gait and lower extremities. Standing lumbar flexion and extension range is assessed. Forward flexion may elicit scoliosis, kyphosis, lordosis, or pain. Spinal extension induces pain from posterior element injury, such as in spondylolysis. However, this may also irritate a far lateral disk herniation. Single leg lumbar hyperextension assists in localizing the side of spondylitic involvement. Pelvic obliquity and sacroiliac motion is examined. Dural tension tests, such as the straight leg-raising test and a femoral stretch test, may produce only back pain in the young athlete.
Adolescent idiopathic scoliosis is a common abnormality in young women. 10 Scoliosis may be classified as infantile, juvenile, or adolescent idiopathic, depending on the age at presentation. 43 Infantile scoliosis presents before 3 years of age, while juvenile scoliosis presents between 3 and 10 years of age. Adolescent scoliosis presents between the age of 10 and skeletal maturity. The frequency of curves of a small magnitude is equal between genders. However, with increasing curve angle, the female-to-male ratio rises to 4:1. 44,45 The prevalence of adolescent scoliosis is about 2% to 3% in the general population. 44 However, in certain sports, this prevalence has been noted to be as high as 24%. 9,47
A number of sports have been associated with asymmetric torque forces contributing to a functional scoliosis. 46 These activities include swimming, throwing, and serving. 7 Most recently, Tanchev 47 demonstrated a 10-fold increased frequency of scoliosis in rhythmic gymnasts. He correlated the association of a sports scoliosis with the triad of delayed maturity, ligamentous laxity, and asymmetric spinal loading. Warren 9 had previously shown the association of ballet dancing and scoliosis, which was related to delayed menarche and small body habitus. Additionally, intense training prior to puberty has been implicated in sports scoliosis. 48 Finally, a low upper-to-lower body ratio, i.e., the ideal body type in classical ballet, could predispose to scoliosis. 9
Back pain should not be attributed merely to the adolescent scoliosis curve. 49 Its presence should prompt an evaluation for underlying causes, such as a syrinx, disk herniation, spondylolysis, tethered cord, or tumor. 50 Nonetheless, back pain has been shown in adolescent scoliosis, particularly when the curve presentation occurs after age 15 with a Risser grade 2 or higher. 51 Furthermore, back pain has been demonstrated more frequently in the athletic population, and may be unrelated to the scoliosis. 49,52
Idiopathic scoliosis should be differentiated from functional scoliosis secondary to sports involvement or to limb length discrepancy. It has been suggested that minor scoliosis, secondary to sport involvement, may benefit from crosstraining, with counteracting muscular strengthening. 46 Exercise regimens have never been accepted as an isolated management for scoliosis. However, one study demonstrated an ancillary benefit to trunk strengthening, specifically with rotary torso strengthening. 53 At the very least, trunk strengthening and peripelvic flexibility will assist in spinal stabilization for prevention of other mechanical injuries. In general, sports are not contraindicated.
Athletes with scoliosis are treated based on curve magnitude, age, and developmental status. The Risser score is a sign of skeletal maturity, and correlates with curve progression. 54 For instance, a minor curvature of less than 20° has a 22% risk of progression with a Risser grade 0–1, and a 1.6% risk of progression in a mature patient. 55 Several other risk factors relate to curve progression. These factors include the magnitude of the curve at presentation, and the presence of double curves. 56,57 Girls have a greater risk of progression before menarche. 58,55–57
Athletes with a curve of less than 25° are observed with repeat radiographs every 4 to 6 months. The immature athlete with a curve of 25° is treated with a brace, often the Boston brace or Charleston brace. 7 The Boston brace is worn 16 to 23 hours per day. The Charleston brace is worn for 8 hours during nighttime sleeping. The Boston brace is favored in most studies showing less curve progression. 59,60 The athlete may wear the brace during most athletic competition, or may opt to play without the brace for several hours. 60 When the curve reaches 40° to 45°, progression is likely in the immature athlete, and surgical intervention is considered. 56 Surgical intervention should preserve as many free segments as possible. After instrumentation and fusion, contact sports and activities with rapid flexion and extension, such as gymnastics, are contraindicated. 61
SAGITTAL CURVE DEFORMITY
Classic Scheuermann thoracic kyphosis begins in adolescence. Holger Scheuermann first described thoracic kyphosis with at least 5° wedging of three consecutive anterior vertebral bodies. He initially proposed this as having a traumatic etiology. 62 Repetitive ballistic movements at the extremes of spinal motion, and extreme loads in flexion, may result in injury to the vertebral apophysis and at the endplate. 63 Disk deformity may also be responsible. 64 This sagittal deformity is often seen in gymnasts, wrestlers, and water skiers, starting in the prepubertal years. 65,66 Radiographic findings include anterior wedging of the vertebral endplates, Schmorl nodes, and anterior intravertebral disk herniation. 49 This is differentiated from a juvenile postural round back, which is reversible with overhead arm extension.
Wojtys demonstrated increased sagittal plane curvature with thoracic hyperkyphosis and lumbar hyperlordosis in adolescents participating in rigorous sports, exceeding 400 hours per year. 65 Intense physical training, with the immature spine transferring tremendous loads from the upper to the lower extremities, is felt to provide the deforming forces. No gender difference was noted. The athletes most affected were in gymnastics, followed by football, hockey, swimming, and wrestling. 65
Management of these entities includes upper trunk and postural exercises. When the kyphotic curve in Scheuermann reaches 60°, thoracolumbar sacral orthosis (TLSO) bracing is instituted. In contrast, juvenile round back syndrome may be considered for bracing when the curve reaches 70° to 80°. 67
Spondylolysis is a stress fracture of the pars interarticularis with multiple contributing factors. Congenital weakness of the pars may play a role. 27,49 Stewart demonstrated a strong familial component with spondylolysis, identified in about 50% of Alaskan natives. 68 The female athlete often competes in sports associated with extreme motion in both flexion and extension. In addition, associated eating disorders and oligomenorrhea (diminished menstruation) or amenorrhea may contribute to bone fragility in sports such as ballet. 9 Intrinsic biomechanical factors that increase lumbar lordosis are often contributory. 19
Spondylolysis is not always symptomatic. Sarasta 69 reported 13% of spondylolysis in the general population presenting with long-term pain. The nonathletic population with spondylolysis may represent individuals with a congenitally weak pars interarticularis, predisposed to a painless fracture with minimal stress. However, athletes with repetitive stress forces destabilizing the pars are usually symptomatic, and remain so if they pursue continued high-level training.
The athlete that presents with pain on lumbar hyperextension is further evaluated with plain radiographs, including antero-posterior and lateral lumbar spine radiographs. 67 Radiographs will evaluate the general alignment, detect congenital anomalies, and demonstrate an obvious spondylolisthesis. A bone scan with single photon emission computed tomography (SPECT) imaging is then performed. This study has high sensitivity for posterior element stress injury. 70 In this scenario, oblique x-rays are often unnecessary. Saifuddin 71 showed that only 32% of pars fractures fall within the necessary 15° of the oblique beam. If the SPECT scan demonstrates an area of focal uptake, a limited CT isolated to that level is performed with 3 mm cuts to define the fracture. Morita 72 categorized the CT findings of a spondylolysis fracture as early, progressive, or terminal (Fig. 1). With corset bracing, 73% of the early lesions healed, and none of the terminal lesions healed.
Early detection of the fracture facilitates management with bracing and physical therapy. Fracture healing is the ideal goal, but this modality of management may also decrease the likelihood of spondylolisthesis progression. The algorithm for evaluation and management of symptomatic lumbar hyperextension is depicted in Figure 2. If a CT demonstrates a fracture, full-time antilordotic bracing for 4 to 6 months is prescribed, along with physical therapy. However, the athlete is returned to full sports participation after 4 to 6 weeks of relative rest, providing the brace is worn and there is no pain. Many sports, such as soccer, basketball, and volleyball, are well tolerated in the brace. Several sports, such as gymnastics and ballet, allow for minimal participation due to the limitation of spine extension. For the athlete with a negative CT scan or who only demonstrated diffuse posterior element uptake on the bone scan, limited bracing for symptomatic control is prescribed.
The primary goal of bracing is to decrease the lumbar lordosis, rendering the sagittal alignment of the pars more vertical. This increases the potential for compression healing with decreased shear. Immobilization, per se, is a less important goal.
If a spondylolysis fracture is demonstrated on the initial CT scan, a follow-up scan is performed in 4 to 6 months to evaluate healing. A fibrous union that is stable and asymptomatic is an acceptable outcome. In the young athlete with a persistent symptomatic lesion, electrical stimulation may be added, although its efficacy is not established. 73 Patients with a persistent, painful spondylolysis may require surgical stabilization, possibly with repair of the pars defect or, more commonly, in situ fusion. 74 This would limit sports participation for 1 year. 61 Rehabilitation stresses improving strength and flexibility of the spine.
LORDOTIC LOW BACK PAIN
During growth, inflexibility of the spinal ligaments and thoracolumbar fascia may manifest with a lumbar hyperlordosis and a compensatory hyperkyphosis of the thoracic spine. With the increased lumbar lordosis, compression is placed on the posterior elements and may result in a facet joint or spinous process abutment syndrome in extension. 75 During flexion, excessive tensile forces are applied to the spinous process apophysis. Spinous process apophysitis may result, and is manifested with palpable tenderness and often demonstrated on SPECT bone scan.
Emphasis on thoracolumbar and peripelvic flexibility is stressed in physical therapy. Temporary bracing is often helpful in refractory cases. Occasionally, injections of corticosteroids in the mature athlete's facets are performed with fluoroscopic control. Return to sports is variable and limited by pain.
A transitional vertebra is an incomplete segmentation of the lower lumbosacral spine. Plain radiographs often identify a pseudarthrosis from a lumbar extension to the sacral ala or iliac wing. Rapid flexion and extension in gymnastics may cause inflammation to the pseudarthrosis, and is referred to as Bertolotti syndrome. 76,77 This may be mistaken for spondylolysis. With careful review of the bone scan, an inflamed pseudarthrosis may be identified. The pain may also be generated from the disk level above the pseudarthrosis. Spondylolysis may be comorbid with the transitional vertebra.
Temporary rigid bracing is often helpful in diminishing the inflammation. Fluoroscopically directed corticosteroid injections to the pseudarthrosis are helpful in a diagnostic and therapeutic manner. The response often helps determine the origin of pain.
Sacroiliac motion transfers forces between the lower extremities and trunk. The inferior portion is a true joint. 78 Sacroiliac motion is referred to as nutation with backward rotation of the ileum on the sacrum and counter-nutation with forward rotation of the ileum on the sacrum. 79 Ligamentous laxity, limb length discrepancy, or trauma may cause impaired function with unilateral diminished mobility. Sacral stress fractures in the osteopenic female athlete may mimic this entity. Stress fractures of the pelvic ring are more common in female athletes. 29,35 Inflammatory and infectious causes must also be considered. An MRI is very helpful in differentiating these causes.
With sacroiliac inflammation, the sacroiliac belt is helpful initially. Gradual mobilization, along with peripelvic and lumbar stabilization, are addressed. Fluoroscopically directed intraarticular corticosteroids can be quite helpful. Stress fractures are treated with partial weight-bearing until pain free. Impact exercises are held for 4 to 6 weeks.
Atypical Scheuermann kyphosis
Atypical Scheuermann kyphosis demonstrates similar findings at the thoracolumbar juncture as the thoracic Scheuermann. This includes limbus vertebrae, Schmorl nodes, and end plate wedging. However, in this region, the presentation is a flat back with a lumbar hyperlordosis. These athletes will have diffuse lower back pain.
Relative rest while maintaining a cross training regimen is important: a lumbosacral orthosis with 15° of extension can dramatically reduce pain. Therapy regimes include extension exercises. Once the athlete has been pain-free for one month, sport-specific training is begun.
Athletes involved in loaded flexion sports, such as crew, risk disk injury. The spectrum of disk injury includes disk degeneration with dehydration, internal disk derangement, and full disk herniation. An internal disk derangement represents a radial tear of the inner annulus. This contained tear manifests pain during increased disk pressure, such as with forward flexion and prolonged sitting. Athletes with an internal disk derangement are difficult to diagnose. In the older athlete, discography may be required. 80 Conversely, a disk herniation may manifest sciatica or axial pain.
Extension-based lumbar stabilization programs are employed. Temporary bracing with a lumbosacral orthosis is helpful. Epidural corticosteroids are often quite helpful in resolving the inflammation with a disk herniation. Surgical intervention is indicated with a progressive neurologic deficit, a cauda equina syndrome, and refractory pain. Athletes with sciatica are often kept from the aggravating sport activity for 4 to 6 months.
The female athlete with an injury to the spine requires consideration of the unique physiologic and environmental interactions seen in sports. Gender-specific issues include hormonal, nutritional, and anthropomorphic factors. Gender-neutral factors, such as growth cartilage, can be gender-specific problems in sports predominantly engaged in by the female athlete. These sports often involve movement which is ballistic and at the extremes of spinal motion. When these sports interact with underlying hormonal and biomechanical issues, different patterns of spinal injury and deformity may result. Medical management requires intervention in all areas of these interactive factors.
1. Maffulli N, Baxter-Jones ADG. Common skeletal injuries in young athletes. Sports Med 1995; 19:137–149.
2. Title IX, Education Amendments of 1972. Title 20. United States Constitution Sections 1681–1688.
3. Tosi L. Women and the orthopaedic surgeon. Clin Orthop 2000; 372:17–31.
4. Micheli LJ. Back injuries in gymnastics. Clin Sports Med 1985; 4 (1): 85–93.
5. Hubbard DD. Injuries to the spine in children and adolescents. CIRN Orthopedics 1974; 100:56–65.
6. Schappert SM. Office visits to orthopedic surgeons: United States 1995–96. Advance data from vital and health statistics. No. 302. Hyattsville, MD: National Center for Health Statistics 1998.
7. Omey ML, Micheli LJ, Gerbino PG. Idiopathic scoliosis and spondylolysis in the female athlete. Clin Orthop 2000; 372:74–84.
8. Nadler SF, Wu KD, Galski T. Low back pain in college athletes. A prospective study correlating lower extremity overuse or acquired ligamentous laxity with low back pain. Spine 1998; 23 (7):828–33.
9. Warren MP, Brooks-Gunn J, Hamilton LH, et al. Scoliosis and fractures in young ballet dancers: relation delayed menarche and secondary amenorrhea. N Eng J Med 1986; 314:1348–1353.
10. Jackson DW. Spinal injuries in children's sports. In: Micheli LJ, ed. Pediatric and Adolescent Sports Medicine. Boston: Little, Brown and Company, 1984;107–123.
11. Cirillo JV, Jackson DW. Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med 1985; 4:95–110.
12. Micheli LJ. Back injuries in dancers. Clin Sports Med 1983; 2:473–484.
13. Sward L, Hellstrom M, Jacobsonn B, et al. Acute injury
to the vertebral ring apophysis and intervertebral disc in adolescent gymnasts. Spine 1990; 15:144–48.
14. Hutchinson MR. Low back pain in elite rhythmic gymnasts. Med Sci Sports Exerc 1999; 31 (11):1686–8.
15. Sward L, Hellstrom M, Jacobsonn B, et al. Disc degeneration and associated abnormalities of the spine in elite gymnasts: a magnetic resonance imaging study. Spine 1991; 16:437–443.
16. Seitsalo S, Antila H, Karrinaho T. Spondylolysis in ballet dancers. J Dance Med Sci 1997; 1:51–54.
17. Frey C. Foot health and shoewear for women. Clin Orthop 2000; 372:32–44.
18. Arendt EA. Orthopaedic issues for active and athletic women. Clin Sports Med 1994; 13:483–503.
19. Trepman E, Walaszek A, Micheli L. Spinal problems in the dancer. In: Solomon R, Minton S, Solomon J, eds. Preventing Dance Injuries: An Interdisciplinary Perspective. Reston, Va: American Alliance for Health, Physical Education, Recreation and Dance, 1990:103–131.
20. Sammarco G. The dancer's hip. Clin Sports Med 1983; 2:485–498.
21. Brown T, Micheli L. Where artistry meets injury
. Biomechanics 1998; 5 (9):12–22.
22. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg (Am) 1963; 45:587–622.
23. Bick EM, Copel JW. Longitudinal growth of the human vertebrae. J Bone Joint Surg (Am) 1950; 32:803–814.
24. Lundin O, Ekstrom L, Hellstrom M, et al. Injuries in the adolescent spine exposed to mechanical compression. Spine 1998; 23 (23):2574–2579.
25. Mente PL, Stokes IA, Spence H, et al. Progression of vertebral wedging in an asymmetrically loaded rat-tail model. Spine 1997; 22:1290–1296.
26. Sagi H, James G, Jarvis M, Uhthoff H. Histomorphic analysis of the pars interarticularis and its association with isthmic spondylolysis. Spine 1998; 23:1635–1640.
27. Merbs C. Incomplete spondylolysis and healing. Spine 1995; 20 (21):2328–2334.
28. Lane W. A remarkable example of the manner in which pressure changes in the skeleton may reveal the labour-history of the individual. J Anat Physiol 1886; 12:385–406.
29. Arendt EA. Stress fractures and the female athlete. Clin Orthop 2000; 372:131–138.
30. Bonjour JP, Theintz G, Buchs B. Critical years and stages of puberty for spinal and femoral bone mass accumulation during adolescence. J Clin Endocrinol Metab 1991; 73 (3):555–63.
31. Wolman RL. Bone mineral density levels in elite female athletes. Ann Rheum Dis 1990; 49 (12):1013–6.
32. Mansfield MJ, Emans SJ. Anorexia nervosa, athletics, and amenorrhea. Pediatr Clin North Am 1989; 36 (3):533–49.
33. Drinkwater BL, et al. Menstrual history as a detriment to current bone density in the young athlete. JAMA 1990; 263:545–8.
34. Warren MP, Fox RP, Derogates AJ, et al. Osteopenia in hypothalamic amenorrhea: a three year longitudinal study. Proceedings from Endocrine Society, 1994.
35. Bennell KL, Malcom SA, Thomas SA, et al. Risk factors for stress fractures in female track-and-field athletes: a retrospective analysis. Clin J Sports Med 1995; 5:229–35.
36. Drinkwater BL, Nilson K, Chestnut III, CH et al. Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med 1994; 311:277–81.
37. Nattiv A. Which athletes are most at risk for stress fractures. Sports Medicine Digest 2001; 23 (1):1–5.
38. Loyd T, Andon MB, Rollings N, et al. Calcium supplementation and bone mineral density in adolescent girls. JAMA 1993; 270:841–4.
39. National Institutes of Health. Consensus development panel on optimal calcium intake. JAMA
40. Mybergh KH, Bacarach LK, Lewis B, et al. Low bone density is an etiologic factor for stress fractures in athletes. Ann Intern Med 1990; 113:754–9.
41. Goldstein JD, Berger PE, Windler GE. Spine injury
in gymnasts and swimmers: an epidemiologic investigation. Am J Sports Med 1991; 19:463–8.
42. Gerbino PG, Micheli LJ. Back injuries in the young athlete. Clin Sports Med 1995; 14 (3):571–89.
43. Rogala EJ, Drummond DS, Gurr J. Scoliosis: incidence and natural history. A prospective epidemiologic study. J Bone Joint Surg 1978; 60A:173–6.
44. Brooks HL, Azen SP, Gerberg E, et al. Scoliosis: a prospective epidemiologic study. J Bone Joint Surg Am 1975; 57:968–72.
45. Miller NH. Adolescent idiopathic scoliosis: etiology. In: Weinstein SL, ed. The Pediatric Spine. Philadelphia, PA: Lippincott Williams and Wilkins, 2001:347–54.
46. Becker TJ. Scoliosis in swimmers. Clin Sports Med 1986; 5:149–158.
47. Tanchev PI, Dzherov AD, Parushev AD, et al. Scoliosis in rhythmic gymnasts. Spine 2000; 25 (11):1367–72.
48. Warren MP. The effects of exercise on pubertal progression and reproduction in girls. J Clin Endocrinol Metab 1980; 51:1150.
49. Micheli LJ, Mintzer CM. Overuse injuries of the spine. In: Harries M, Williams C, Stanish WD, Micheli LJ, eds. Oxford Textbook of Sports Medicine
2nd ed. Oxford: Oxford University Press, 1998:709–20.
50. Schwend RM, Hennrikus W, Hall JE, et al. Childhood scoliosis: clinical indications for MRL. J Bone Joint Surg 1995; 77A:46–53.
51. Ramirez M, Jonsston CE, Browne RH. The prevalence of back pain in children who have idiopathic scoliosis. J Bone Joint Surg 1997; 79A:364–8.
52. Sward L, Hellstrom M, Jacobbson B, et al. Back pain and the radiologic changes in the thoracolumbar spine of athletes. Spine 1990; 15:124–9.
53. Mooney V, Gulick J, Pozos R. A preliminary report on the effect of measured strength training in adolescent idiopathic scoliosis. J Spinal Disord 2000; 3 (2):102–7.
54. Risser JC. The iliac apophysis: an invaluable sign in the management of scoliosis. Clin Orthop 1958; 11:111–9.
55. Lonstein JE, Carlson JM. The prediction of curve progression in untreated idiopathic scoliosis during growth. J Bone Joint Surg Am 1984; 66:1061–71.
56. Weinstein SL. Adolescent idiopathic scoliosis: natural history. The Pediatric Spine.
Philadelphia, PA: Lippincott Williams and Wilkins, 2001:355–70.
57. Bunnell WP. A study of the natural history of idiopathic scoliosis before skeletal maturity. Spine 1986; 11:773–776.
58. Ascani C, Bartolozzi P, Logroscino CA, et al. Natural history of untreated idiopathic scoliosis after skeletal maturity. Spine 1986; 11:784–789.
59. Emans JB, Kaelin A, Bancel P, et al. The Boston bracing
system for idiopathic scoliosis: follow-up results in 295 patients. Spine 1986; 11:792–801.
60. Green NE. Part-time bracing
of adolescent idiopathic scoliosis. J Bone Joint Surg 1986; 68A:738–42.
61. Micheli LJ. Sports following spinal surgery in the young athlete. Clin Orthop 1985; 198:152–7.
62. Scheuermann HW. Kyphosis dorsalis juvenalis. Ugeskr Laeger 1920; 82:385–389.
63. Ippolito E, Bellocci M, Montonaro A, et al. Juvenile kyphosis: an ultrastructural study. J Pediatr Orthop 1985; 5:315–22.
64. Stokes IA, Aronson DD, Spence H, et al. Mechanical modulation of intervertebral disc thickness in growing rat tails. J Spinal Disord 1998; 11:261–5.
65. Wojts EEM, Ashton-Miller JA, Huston LJ, et al. The association between athletic training time and the sagittal curvature of the immature spine. Am J Sports Med 2000; 28 (4):490–8.
66. Tall RL, DeVault W. Spinal injury
in sport: epidemiologic considerations. Clin Sport Med 1996; 12 (3):441–446.
67. d'Hemecourt PA, Gerbino GG, Micheli LJ. Back injuries in the young athlete. Clin Sport Med 2000; 19 (4):663–79.
68. Stewart T. The age and incidence of neural arch defects in Alaskan natives. J Bone Joint Surg Am 1953; 35:937.
69. Sarasta H. Long term clinical and radiographic follow-up of spondylolysis and spondylolisthesis. J Pediatr Orthop 1987; 7:631–637.
70. Bellah RD, Summerville DA, Treves ST, Micheli LJ. Low back pain in adolescent athletes: detection of stress injury
to the pars intra-articularis with SPECT. Radiol 1991; 180:509–12.
71. Saifuddin A, White J, Tucker S, et al. Orientation of lumbar pars defects: implications for radiological and surgical management. J Bone Joint Surg (Br) 1998; 80 (2):208–211.
72. Morita T, Ikata T, Katoh S, et al. Lumbar spondylolysis in children and adolescents. J Bone and Joint Surg 1995; 77B:620–5.
73. Pettine K, Salib R, Walker S. Electrical stimulation and bracing
for the treatment of spondylolysis: a case report. Spine 1993; 18 (4):436–9.
74. Buck J. Direct repair of the defect in spondylolisthesis. J Bone Joint Surg 1970; 52B:432–437.
75. Borenstein DG, Weisel SW, Boden SD. Mechanical disorders of the lumbosacral spine. In: Borenstein DG, Weisel SW, Boden SD, eds. Low Back Pain: Medical Diagnosis and Comprehensive Management
, 2nd edition. Philadelphia: WB Saunders Co., 1995:183–197.
76. Elster AD. Bertolotti's syndrome revisited. Transitional vertebrae of the lumbar spine. Spine 1989; 14 (12):1373–7.
77. Santavista S, Tallroth K, Ylinen P. Surgical treatment of Bertoletti's Syndrome: follow up of 16 patients. Arch Orthop Trauma Surg 1993; 112:82–7.
78. Bernard T, Cassidy J. The sacroiliac joint syndrome: pathophysiology, diagnosis, and management. In: Frymoyer J, ed. The Adult Spine: Principles and Practice. New York: Raven Press, 1991;2107–2130.
79. Sturesson B, Selvic G, Uden A. Movements of the sacroiliac joints—a roentgen stereophotogrammetric analysis. Spine 1989; 14:162–165.
80. Derby R. The relationship between intradiscal pressure and pain provocation during discography. J Bone Joint Surg (Br) 1995; 19:59–60.
Nicola Maffulli, M.D., Guest Editor