Figure 1 - uploaded by Hideki Moriyama
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Diagrams of eight articular cartilage regions in femoral condyle and tibial plateau of the right knee joint. Femoral articular surface ( a ). Tibial articular surface ( b ). Cartilage regions were defined according to their positions in embedded joints where the knee joint was positioned at an angle of 125 1 . The anterior femoral (FA) and anterior tibial (TA) regions were defined as the regions of articular cartilage located between the inner edges of the anterior and posterior meniscal horns. The edge of the posterior femoral (FP) region was located 20 m m beyond the outer edge of the posterior meniscal horn, and the posterior tibial (TP) cartilage was located adjacent to the posterior horn of the meniscus. Knee flexion contractures develop in our models with SCI, as we have reported previously. 5–7 Therefore, the FA cartilage corresponds to unapposed regions (no contact between cartilage surfaces) of the flexed knee. The FP, TA and TP regions are located at apposed regions (where the articular cartilages of two bones contact each other). 9
Source publication
Experimental, controlled trial, animal study.Objective:To assess morphologic changes in different cartilage plates after spinal cord injury and identify the localization of these alterations.
Saitama, Japan.
A total of 16 Wistar rats were used. Eight rats underwent a spinal cord injury and eight rats had no intervention as control. The cartilage al...
Context in source publication
Context 1
... histology Determination of measurement sites. Femoral and tibial cartilage alterations at the medial and lateral mid-condylar level were determined at the eight regions with the methods of O'Connor ( Figure 1). 12 In addition, the superficial cartilage was defined as the area from the cartilage surface down to a depth of 30 mm and the deep cartilage was from the tidemark up to a depth of 30 mm. 11 Cartilage thickness. ...
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Background
Mechanical loading during exercise has been shown to promote tissue remodeling. Safe and accessible exercise may be beneficial to populations at risk of diminished bone and joint health. We examined the effect of drop height and instruction on knee loading during a drop-landing task and proposed a task that makes use of drop heights that...
Citations
... We have previously established SCI rat models with knee contractures [4] and proposed that both muscular and articular factors contribute almost equally to the overall progression of the contractures after 14 days of SCI [5]. Subsequently, we have shown that the intra-articular alterations after SCI exhibit the specific changes that differed from those observed in animal models with immobilized joints [6][7][8]. However, what causes the SCI-specific characteristics of joint contractures has not been previously investigated, and whether hypertonia plays a part in contracture development after SCI remains controversial. ...
... Surgical procedures and postoperative care conformed to those in our previous studies [4][5][6][7][8]. Rats in the SCI and BTX groups were anesthetized by an intraperitoneal administration of 40 mg/kg of sodium pentobarbital and subcutaneously injected with 0.02 mg/kg buprenorphine to give relief of pain. ...
Study design:
Experimental animal study.
Objectives:
Spastic hypertonia is originally believed to cause contractures from clinical observations. Botulinum toxin is effective for the treatment of spasticity and is widely used in patients who have joints with contractures. Using an established rat model with knee contractures after spinal cord injuries, we aimed to verify whether hypertonia contributes to contracture development, and the botulinum toxin improves structural changes in muscles and joint components responsible for contractures.
Setting:
University laboratory in Japan.
Methods:
To evaluate the effect of hypertonia on contracture development, the rats received botulinum toxin injections after spinal cord injuries. Knee extension motion was measured with a goniometer applying a standardized torque under anesthesia, and the contribution by muscle or non-muscle structures to contractures were calculated by measuring joint motion before and after the myotomies. We quantitatively measured the muscle atrophy, muscle fibrosis, and synovial intima length.
Results:
Botulinum toxin injections significantly improved contractures, whereas did not completely prevent contracture development. Botulinum toxin was effective in improving the muscular factor, but little difference in the articular factor. Spinal cord injuries induced muscle atrophy, and botulinum toxin significantly accelerated muscle atrophy and fibrosis. The synovial intima length decreased significantly after spinal cord injuries, and botulinum toxin did not improve this shortening.
Conclusions:
This animal study provides new evidence that hypertonia is not the sole cause rather is the partial contributor of contractures after spinal cord injuries. Furthermore, botulinum toxin has adverse effects in the muscle.
... However, contractures after central nervous system injury are mediated by not only structural adaptation of soft tissues, but also neural factors including paralysis [3,25]. We developed a rat model of contracture after spinal cord injury as a representative animal model of central nervous system injury [28,[30][31][32][33], and reported that high-torque and long-duration static stretching led to restoration of the loss of ROM and prevented shortening and adhesions of the joint capsule [29]. ...
... The rats in the control group had no intervention, whereas the others underwent spinal cord transection at the level of T8. Surgical procedures and postoperative care confirmed results of previous studies [28][29][30][31][32][33]. We provided no treatment for 2 weeks postinjury to develop spasticity and contracture [32] and started intervention at postoperative Day 15. ...
Background
Contractures are a prevalent and potentially severe complication in patients with neurologic disorders. Although heat, cold, and stretching are commonly used for treatment of contractures and/or spasticity (the cause of many contractures), the sequential effects of these modalities remain unclear. Questions/purposesUsing an established rat model with spinal cord injury with knee flexion contracture, we sought to determine what combination of heat or cold before stretching is the most effective for treatment of contractures derived from spastic paralyses and investigated which treatment leads to the best (1) improvement in the loss of ROM; (2) restoration of deterioration in the muscular and articular factors responsible for contractures; and (3) amelioration of histopathologic features such as muscular fibrosis in biceps femoris and shortening of the joint capsule. Methods
Forty-two adolescent male Wistar rats were used. After spasticity developed at 2 weeks postinjury, each animal with spinal cord injury underwent the treatment protocol daily for 1 week. Knee extension ROM was measured with a goniometer by two examiners blinded to each other’s scores. The muscular and articular factors contributing to contractures were calculated by measuring ROM before and after the myotomies. We quantitatively measured the muscular fibrosis and the synovial intima length, and observed the distribution of collagen of skeletal muscle. The results were confirmed by a blinded observer. ResultsThe ROM of heat alone (34° ± 1°) and cold alone (34° ± 2°) rats were not different with the numbers available from that of rats with spinal cord injury (35° ± 2°) (p = 0.92 and 0.89, respectively). Stretching after heat (24° ± 1°) was more effective than stretching alone (27° ± 3°) at increasing ROM (p < 0.001). Contrastingly, there was no difference between stretching after cold (25° ± 1°) and stretching alone (p = 0.352). Stretching after heat was the most effective for percentage improvement of muscular (29%) and articular (50%) factors of contractures. Although quantification of muscular fibrosis in the rats with spinal cord injury (11% ± 1%) was higher than that of controls (9% ± 0.4%) (p = 0.01), no difference was found between spinal cord injury and each treatment protocol. The total synovial intima length of rats with spinal cord injury (5.9 ± 0.2 mm) became shorter than those of the controls (7.6 ± 0.2 mm) (p < 0.001), and those of stretching alone (6.9 ± 0.4 mm), stretching after heat (7.1 ± 0.3 mm), and stretching after cold (6.7 ± 0.4 mm) increased compared with rats with spinal cord injury (p = 0.01, p = 0.001, and p = 0.04, respectively). The staining intensity and pattern of collagen showed no difference among the treatment protocols. Conclusions
This animal study implies that heat or cold alone is ineffective, and that stretching is helpful for the correction of contractures after spinal cord injury. In addition, we provide evidence that heat is more beneficial than cold to increase the effectiveness of stretching. Clinical RelevanceOur findings tend to support the idea that stretching after heat can improve the loss of ROM and histopathologic features of joint tissues. However, further studies are warranted to determine if our findings are clinically applicable.
... We therefore developed a unique animal model of contractures using rats with spinal cord injuries, with the goal of having this model be representative of animals with central nervous system injuries [25,26]. Previous studies have shown that the articular component (bone, cartilage, synovial membrane, capsule, and ligaments) plays a larger role in pathogenesis of contractures after spinal cord injury than does the muscular component (muscle, tendon, and fascia) [22][23][24]26]. The two major pathologic changes in joint contractures are joint capsule stiffness and cartilage degeneration [5,[22][23][24]34]. ...
... Previous studies have shown that the articular component (bone, cartilage, synovial membrane, capsule, and ligaments) plays a larger role in pathogenesis of contractures after spinal cord injury than does the muscular component (muscle, tendon, and fascia) [22][23][24]26]. The two major pathologic changes in joint contractures are joint capsule stiffness and cartilage degeneration [5,[22][23][24]34]. ...
... In total, 32 male Wistar rats (CLEA Japan Inc, Tokyo, Japan; age, 10 weeks; weight, 240-268 g) were used for this study. Surgical procedures and postoperative care conformed to our previous studies [22][23][24][25][26]. Twenty-eight of the 32 rats were anesthetized by intraperitoneal administration of 40 mg/kg sodium pentobarbital. ...
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.
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.
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.
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.
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.
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.
... Spinal cord injury (SCI) is one of the most common causes of long-term unloading and immobilization, whereby changes in the periarticular connective tissue, contractures, periarticular osteoporosis, joint space narrowing and articular cartilage degeneration have been described (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). ...
Objective:
To assess femoral cartilage thickness in patients with spinal cord injury (SCI).
Subjects:
Forty-six patients with SCI (35 men, 11 women; mean age: 33.6 years (standard deviation 8.1) and 46 age-, sex- and body mass index (BMI)-matched healthy subjects were enrolled.
Methods:
Patients were evaluated with the American Spinal Injury Association (ASIA) Impairment Scale, Modified Ashworth Scale, Walking Index for Spinal Cord Injury, and Functional Independence Measurement. Mid-point ultrasonographic femoral cartilage thickness measurements were taken from the right lateral condyle, right intercondylar area, right medial condyle, left medial condyle, left intercondylar area and left lateral condyle.
Results:
Ultrasonographic measurements revealed significantly thicker values in the intercondylar areas (bilaterally) and the medial condyle (left knee) of patients with SCI compared with those of controls. When the subgroups were compared with their paired healthy controls, measurements pertaining to the motor complete group were found to be significantly thicker in the intercondylar areas (bilaterally) and the medial condyle (left knee). Cartilage thickness values correlated negatively with the duration of immobilization (for bilateral intercondylar areas), and with BMI and ASIA level (for bilateral lateral condyles).
Conclusion:
Femoral cartilage thicknesses were found to change after SCI, and to have a negative correlation with disease duration and severity. Future studies including histological evaluations may elucidate whether such changes are favourable for the knee joints of patients with spinal cord injury.
... Chondrocyte apoptosis has been reported following hind-limb unloading and microgravity exposure in rats [24,25]. Additionally, reduced chondrocyte numbers have been reported in the articular cartilage at the knee in rodents with SCI [26,27]. Collectively, these findings suggest that mechanical loading is required for chondrogenesis. ...
Spinal cord injury is associated with rapid bone loss and arrested long bone growth due to mechanisms that are poorly understood. In this study, we sought to determine the effects of severe T10 contusion spinal cord injury on the sublesional bone microenvironment in adolescent rats. A severe lower thoracic (vertebral T10) spinal cord injury was generated by weight drop (10 g×50 mm). Severely injured and body weight-matched uninjured male Sprague-Dawley rats were studied. At 3 and 5 days post-injury, we performed histological analysis of the distal femoral metaphysis, TUNEL assay, immunohistochemistry, real-time PCR, and western blot analysis compared to uninjured controls. We observed severe hindlimb functional deficits typical of this model. We detected uncoupled remodeling with increased osteoclast activity in the absence of osteoblast activity. We detected osteoblast, osteocyte, and chondrocyte apoptosis with suppressed osteoblast and chondrocyte proliferation and growth plate arrest due to spinal cord injury. We also detected altered gene expression in both whole bone extracts and bone marrow monocytes following spinal cord injury. We conclude that spinal cord injury results in altered gene expression of key regulators of osteoblast and chondrocyte activity. This leads to premature cellular apoptosis, suppressed cellular proliferation, growth plate arrest, and uncoupled bone remodeling in sublesional bone with unopposed osteoclastic resorption.
Background:
Joint contractures are a major complication in patients with spinal cord injuries. Positioning, stretching, and physical therapy are advocated to prevent and treat contractures; however, many patients still develop them. Joint motion (exercise) is crucial to correct contractures. Transcutaneous carbon dioxide (CO2) therapy was developed recently, and its effect is similar to that of exercise. This therapy may be an alternative or complementary approach to exercise.
Question/purposes:
Using an established model of spinal cord injury in rats with knee flexion contractures, we sought to clarify whether transcutaneous CO2 altered (1) contracture, as measured by ROM; (2) muscular and articular factors contributing to the loss of ROM; (3) fibrosis and fibrosis-related gene expression in muscle; and (4) the morphology of and fibrosis-related protein expression in the joint capsule.
Methods:
Thirty-six Wistar rats were divided into three equal groups: caged control, those untreated after spinal cord injury, and those treated with CO2 after spinal cord injury. The rats were treated with CO2 from either the first day (prevention) or 15th day (treatment) after spinal cord injury for 2 or 4 weeks. The hindlimbs of rats in the treated group were exposed to CO2 gas for 20 minutes once daily. Knee extension ROM was measured with a goniometer and was measured again after myotomy. We calculated the muscular and articular factors responsible for contractures by subtracting the post-myotomy ROM from that before myotomy. We also quantified histologic muscle fibrosis and evaluated fibrosis-related genes (collagen Type 1, α1 and transforming growth factor beta) in the biceps femoris muscle with real-time polymerase chain reaction. The synovial intima's length was measured, and the distribution of fibrosis-related proteins (Type | collagen and transforming growth factor beta) in the joint capsule was observed with immunohistochemistry. Knee flexion contractures developed in rats after spinal cord injuries at all timepoints.
Results:
CO2 therapy improved limited-extension ROM in the prevention group at 2 weeks (22° ± 2°) and 4 weeks (29° ± 1°) and in the treatment group at 2 weeks (31° ± 1°) compared with untreated rats after spinal cord injuries (35° ± 2°, mean difference, 13°; 39° ± 1°, mean difference, 9°; and 38° ± 1°, mean difference, 7°, respectively) (95% CI, 10.50-14.86, 8.10-10.19, and 4.73-9.01, respectively; all p < 0.001). Muscular factors decreased in treated rats in the prevention group at 2 weeks (8° ± 2°) and 4 weeks (14°± 1°) and in the treatment group at 2 weeks (14 ± 1°) compared with untreated rats (15° ± 1°, 4.85-9.42; 16° ± 1°, 1.24-3.86; and 17° ± 2°, 1.16-5.34, respectively; all p < 0.05). The therapy improved articular factors in the prevention group at 2 weeks (4° ± 1°) and 4 weeks (6° ± 1°) and in the treatment group at 2 weeks (8° ± 1°) compared with untreated rats (10° ± 1°, 4.05-7.05; 12° ± 1°, 5.18-8.02; and 11° ± 2°, 1.73-5.50, respectively; all p < 0.05). CO2 therapy decreased muscle fibrosis in the prevention group at 2 weeks (p < 0.001). The expression of collagen Type 1, α1 mRNA in the biceps femoris decreased in treated rats in the prevention group at 2 and 4 weeks compared with untreated rat (p = 0.002 and p = 0.008, respectively), although there was little difference in the expression of transforming growth factor beta (p > 0.05). CO2 therapy did not improve shortening of the synovial intima at all timepoints (all p > 0.05). CO2 therapy decreased transforming growth factor beta immunolabeling in joint capsules in the rats in the prevention group at 2 weeks. The staining intensity and Type | collagen pattern showed no differences among all groups at all timepoints.
Conclusion:
CO2 therapy may be useful for preventing and treating contractures after spinal cord injuries. CO2 therapy particularly appears to be more effective as a prevention and treatment strategy in early-stage contractures before irreversible degeneration occurs, as shown in a rat model.
Clinical relevance:
Our findings support the idea that CO2 therapy may be able to improve the loss of ROM after spinal cord injury.
The impact of aging on joints can have a profound effect on an individual's functioning. Our objectives were to assess the histological and mechanical properties of the knee joint capsule and articular cartilage with aging, and to examine the effects of exercise on age-related changes in the knee joint. 2-year-old Wistar rats were divided into a sedentary control group and an exercise-trained group. 10-week-old animals were used to investigate the changes with aging. The joint capsule and cartilage were evaluated with histological, histomorphometric, immunohistochemical, and mechanical analyses. Severe degenerative changes in articular cartilage were observed with aging, whereas exercise apparently did not have a significant effect. The articular cartilage of aged rats was characterized by damage to the cartilage surface, cell clustering, and an abnormal cartilage matrix. Histomorphometric analysis further revealed changes in cartilage thickness as well as a decreased number of chondrocytes. Aging led to stiffness of the articular cartilage and reduced the ability to dissipate the load and distribute the strain generated within the joint. Joint stiffness with aging was independent of capsular stiffness and synovitis was not a characteristic feature of the aging joint. This study confirms that aging alone eventually leads to joint degeneration in a rat model. The lack of recovery in aging joint changes may be due to several factors, such as the duration of the intervention and the regeneration ability of the cartilage.
