Amount of torque and duration of stretching affects correction of knee contracture in a rat model of spinal cord injury

Abstract

Background: Joint contractures are a common complication of many neurologic conditions, and stretching often is advocated to prevent and treat these contractures. However, the magnitude and duration of the stretching done in practice usually are guided by subjective clinical impressions.

Questions/purposes: Using an established T8 spinal cord injury rat model of knee contracture, we sought to determine what combination of static or intermittent stretching, varied by magnitude (high or low) and duration (long or short), leads to the best (1) improvement in the limitation in ROM; (2) restoration of the muscular and articular factors leading to contractures; and (3) prevention and treatment of contracture-associated histologic alterations of joint capsule and articular cartilage.

Methods: Using a rat animal model, the spinal cord was transected completely at the level of T8. The rats were randomly assigned to seven treatment groups (n = 4 per group), which were composed of static or intermittent stretching in combination with different amounts of applied torque magnitude and duration. We assessed the effect of stretching by measuring the ROM and evaluating the histologic alteration of the capsule and cartilage.

Results: Contractures improved in all treated groups except for the low-torque and short-duration static stretching conditions. High-torque stretching was effective against shortening of the synovial membrane and adhesions in the posterosuperior regions. Collagen Type II and VEGF in the cartilage were increased by stretching.

Conclusions: High-torque and long-duration static stretching led to greater restoration of ROM than the other torque and duration treatment groups. Stretching was more effective in improving articular components of contractures compared with the muscular components. Stretching in this rat model prevented shortening and adhesion of the joint capsule, and affected biochemical composition, but did not change morphologic features of the cartilage.

Clinical relevance: This animal study tends to support the ideas that static stretching can influence joint ROM and histologic qualities of joint tissues, and that the way stretching is performed influences its efficacy. However, further studies are warranted to determine if our findings are clinically applicable.

Fig. 1

The knee extension angle was measured with a mechanical goniometer. The position of the goniometer and hand are shown.

Fig. 2

Knee extension ROM improved in the treated groups when compared with the untreated spinal cord injury group (S). Error bars = ± 1 SD. * There were significant differences between each treatment group and the untreated spinal cord injury group (p < 0.001). C = control; S = untreated after spinal cord injury; HL = high-torque and long-duration static stretched; HI = high-torque and intermittent stretched; HS = high-torque and short-duration static stretched; LL = low-torque and long-duration static stretched; LI = low-torque and intermittent stretched; LS = low-torque and short-duration static stretched.

Fig. 3A–C

The (A) total and (B) posterosuperior synovial intima lengths in the treated groups were significantly longer than that of the untreated spinal cord injury group (S), but not the (C) posteroinferior length. Error bars = ± 1 SD. * There were significant differences between each treatment group and the untreated spinal cord injury group, p < 0.05. C = control; S = untreated after spinal cord injury; HL = high-torque and long-duration static stretched; HI = high-torque and intermittent stretched; HS = high-torque and short-duration static stretched; LL = low-torque and long-duration static stretched; LI = low-torque and intermittent stretched; LS = low-torque and short-duration static stretched.

Fig. 4A–C

Adhesions in the posterosuperior regions after spinal cord injury were improved by stretch interventions in the (A) control group, (B) untreated spinal cord injury group (arrowheads), and (C) high-torque and long-duration static stretched group (arrows). Bar = 500 μm; (Stain, aldehyde fuchsin-Masson Goldner staining; original magnification, ×40).

Fig. 5A–C

The uncalcified layer of the posterior femoral cartilage region was thinner after spinal cord injury and stretching had no significant effect on cartilage thickness in the (A) control group, (B) untreated spinal cord injury group, and (C) low-torque and long-duration static stretched group. UL = uncalcified layer; CL = calcified layer; Bar = 200 μm; (Stain, toluidine blue staining; original magnification, ×100).

Fig. 6A–C

VEGF immunostaining was seen strongly in the chondrocytes of the spinal cord injury groups and was most increased by the long- and short-duration static stretching with a high torque in the (A) control group, (B) untreated spinal cord injury group, and (C) high-torque and short-duration static stretched group. Bar = 100 μm; (Stain, anti-VEGF antibodies; original magnification, ×200).

Fig. 7A–C

Immunolabeling for collagen Type II was increased by stretch interventions. These findings were pronounced in the high-torque groups, and immunolabeling of the uncalcified layer was seen clearly in the (A) control group, (B) untreated spinal cord injury group, and (C) high-torque and short-duration static stretched group. Bar = 200 μm; (Stain, anti-collagen Type II antibodies; original magnification, ×100).