Slippage mechanism of pediatric spondylolysis: biomechanical study using immature calf spines.

STUDY DESIGN: This study analyzed the skeletal-age-dependent strength of the lumbar growth plate to resist anterior shearing forces using the MTS system in the immature calf spine with pars defects. OBJECTIVE: To clarify the pathomechanism of the skeletal-age-dependent incidence of slippage in pediatric patients with pars defects by comparing the strength of the lumbar growth plate among three skeletal age groups. SUMMARY OF BACKGROUND DATA: Isthmic spondylolisthesis occurs and progresses more frequently during the growth period, whereas it is rare afterward. However, little evidence has been demonstrated to elucidate the etiology. METHODS: For this study, 15 lumbar functional spine units were divided into three groups according to their skeletal ages. Five were from neonates (Group 1), five from calves approximately 2 months old (Group 2), and five from calves about 24 months old (Group 3). An anterior shearing force was applied to each specimen until failure, after bilateral pars defects were created. Failure load (newtons) and displacement at failure (millimeters) were calculated from the load-displacement curve. The site of failure was confirmed by plain radiograph. RESULTS: All 15 functional spine units failed at the growth plate. The failure load was 242.79 +/- 46.05 N in Group 1, 986.40 +/- 124.16 N in Group 2, and 2024.54 +/- 245.53 N in Group 3. Statistically significant differences were found among the three groups (P < 0.05). The displacement at failure was 7.52 +/- 1.84 mm in Group 1, 11.10 +/- 2.30 mm in Group 2, and 8.15 +/- 2.66 mm in Group 3. There were no significant differences among the groups. CONCLUSIONS: The results indicate that the strength of the growth plate, the weakest link in this model, against anterior shearing forces depends on the skeletal maturity, and that the biomechanical weakness of the growth plate plays an important role in the slippage mechanism.

Development of spondylolytic olisthesis in adolescents.

BACKGROUND CONTEXT: Although it has been well documented that slippage in patients with spondylolysis is most prevalent during the growth period, the exact time when slippage initiates and halts during the growth period is still unknown. Moreover, the contribution of spinal deformities, such as wedging of the vertebral body to the slippage, remains controversial. PURPOSE: To clarify when slippage in pediatric spondylolysis initiates and halts. STUDY DESIGN: Retrospective study. PATIENT SAMPLE: We radiographically examined 46 athletes under 18 years of age with spondylolysis at the fifth lumbar vertebra (L5). The mean age at the first consultation was 13.3 years. The average follow-up period was 6.0 years. OUTCOME MEASURES: Longitudinal observation of slippage at L5 on radiogram in correlation with the maturity of the lumbar spine. METHODS: From a lateral radiogram of each patient, percent slippage, lumbar index (LI), and skeletal age of the affected vertebra were measured. Changes in the percent slippage over time were investigated, and the correlation between the percent slippage and LI was analyzed. RESULTS: From the cartilaginous stage to the apophyseal stage, the slippage increased in 80.0% of the patients (16 of 20). From the cartilaginous stage to the epiphyseal stage, slippage increased in 11.1% of the patients (3 of 27). None of the patients (0 of 22) showed an increase after the epiphyseal stage. In 20 patients in whom slippage increased during the follow-up period, the percent slippage at the final consultation and the LI at the first consultation showed no significant correlation; however, the percent slippage and the LI at the final consultation were significantly (p<.01) correlated. CONCLUSION: In conclusion, slippage was more prevalent in individuals of a younger skeletal age whose lumbar spine was immature, and it halted during the epiphyseal stage when the growth period was over and the vertebra matured. Furthermore, the results suggest that wedge deformity of an affected vertebra might be the result rather than the cause of slippage.

Relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine ulcerative colitis.

OBJECTIVE: The possible role of fecal bile acids in colorectal carcinogenesis in ulcerative colitis has been reported. In this study, we investigated the relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine colitis induced by dextran sulfate sodium. METHODS: Colorectal neoplasia in experimental colitis was induced by dextran sulfate sodium subsequent to a single azoxymethane pretreatment. Fecal bile acids were analyzed by gas-liquid chromatography. RESULTS: Multiple high-grade dysplasias (intramucosal adenocarcinoma) and inflammatory changes were seen in all mice administered dextran sulfate sodium and azoxymethane. Inflammatory changes were also observed in all mice given dextran sulfate sodium only, while neither tumor nor inflammatory changes were detected in any of the control mice. Significant increases in cholic acid were observed in the mice of the colorectal tumor and experimental colitis groups during the experimental period, while in the control mice, no significant changes in fecal bile acids were observed. CONCLUSION: It is suggested that fecal cholic acid and colitis may be intimately related to the development of colorectal neoplasia in this experimental model of murine colitis as well as in ulcerative colitis.

Promotion of colorectal neoplasia in experimental murine ulcerative colitis.

BACKGROUND: The mechanisms underlying the frequent development of colorectal carcinomas in patients with ulcerative colitis are still unknown. AIMS: To evaluate whether mucosal necrosis and regeneration act as enhancing or promoting factors in colorectal tumorigenesis, development of multiple colorectal tumours was studied in a murine model of ulcerative colitis with azoxymethane pretreatment. METHODS: Periods of chronic ulcerative colitis in mice were induced by three repeated administrations of 3% dextran sulphate sodium subsequent to a single azoxymethane pretreatment, to give conditions similar to the clinically observed active and remission phases. RESULTS: In the chronic colitis group with carcinogen exposure, multiple mucosal tumours (10.5/mouse) developed in the colorectum. This occurred primarily on the left side of the large intestine or transverse colon, the sites of the most severe colitic injury. The observed lesions were high grade dysplasias and invasive adenocarcinomas. Increased cell proliferation was evidenced by high uptake of bromodeoxyuridine, and increased activities of thymidylate synthetase and thymidine kinase. No tumours were induced in the control groups with azoxymethane pretreatment or chronic colitis alone. CONCLUSIONS: Repeated mucosal erosion with necrosis and regeneration is critical for the development of colorectal tumours in this experimental colitis system.