Average 10.1-year follow-up of cementless total knee arthroplasty in patients with rheumatoid arthritis.

BACKGROUND: Total knee arthroplasty (TKA) using a cemented technique has been recommended in patients with rheumatoid arthritis owing to the initial stability of the fixation and long-term durability of the components; however, similar long-term follow-up results have been reported in patients who have undergone cementless TKA. The purpose of this study was to evaluate the radiologic and clinical outcomes of cementless TKA in patients with rheumatoid arthritis. METHODS: We enrolled patients undergoing cementless TKA from March 1990 to February 2000. Clinical and radiologic evaluations were performed using the Knee Society clinical rating system and radiographic evaluation and scoring system. RESULTS: We included the cases of 112 patients who underwent 179 cementless TKA procedures in our analysis. Their mean age was 62.3 years, and the mean follow-up period was 10.1 years. The final survival rate was 0.968 at the 15.5-year follow-up. Regarding radiologic results after surgery, the mean total valgus angle was 6.7°, the mean femoral flexion angle was 97.5° and the mean tibial angle was 89.2° on the anteroposterior radiographs. On the lateral films, the mean femoral flexion angle was 1.6° and the mean tibial angle was 89.2°. At the last follow-up, the mean total valgus angle was 6.5°, the mean femoral flexion angle was 97.4° and the mean tibial angle was 89.1°, as seen on the anteroposterior view. On the lateral views, the mean femoral flexion angle was 1.4° and the mean tibial angle was 89.0°. Regarding the clinical outcome, the mean knee score and function score on the Knee Society clinical rating system were also enhanced from 47.5 and 43.6, respectively, before the operation to 91.2 and 82.3, respectively, at the last follow-up. CONCLUSION: On radiologic and clinical follow-up of cementless TKA for patients with rheumatoid arthritis, there were no serious complications, and the results of the operation were satisfactory with improvement in range of motion and clinical symptoms.

Agreements between different methods of gap balance estimation in cruciate-retaining total knee arthroplasty.

The authors investigated the agreements between three different methods of estimating gap balance in cruciate-retaining (CR) total knee arthroplasty (TKA) with the use of a subvastus approach. One hundred consecutive CR TKAs were prospectively included in this study. After completing soft tissue release and bone cutting for CR TKA, flexion-extension gap balance was assessed using a distractor, spacer blocks, and trial components. Levels of agreement between the estimation techniques used were substantial. All three techniques were reliable in the assessment of gap balance. But, observations made during this study suggest that if more than one estimation technique is applied during CR TKA, the incidence of undetected gap imbalance can be reduced.

Factors affecting flexion gap tightness in cruciate-retaining total knee arthroplasty.

With the exception of flexion gap tightness, which is common in cruciate-retaining (CR) total knee arthroplasty (TKA), the risk factors of flexion gap tightness have not been described. This retrospective study characterized factors that are associated with flexion gap tightness in CR TKA. Data on 203 consecutive knees that underwent CR TKA were reviewed. The prevalence rate of flexion gap tightness was 21.1%. By logistic regression analysis after adjusting for age, preoperative flexion contracture, and referencing method used for femoral sizing, insufficient tibial slope remained a significant independent risk factor of flexion gap tightness. Although excessive tibial slope should be avoided, the findings of the present study demonstrate that the risk of flexion gap tightness can be reduced by increasing the tibial slope in CR TKA.

Proliferation of anterior cruciate ligament cells in vitro by photo-immobilized epidermal growth factor.

The purpose of this study was to explore the early treatment potential of anterior cruciate ligament (ACL) injuries using artificial juxtacrine stimulation by photo-immobilization of a growth factor. A photo-reactive epidermal growth factor complex (EGF-Az) was synthesized by conjugating EGF with N-(4-azidobenzoyloxy) succinimide followed by immobilization onto polystyrene culture plates using UV irradiation. ACL cells from human tissues (1 x 10(5)cells, 100 microl/well) were cultured as follows: control, no EGF; 50 microl native EGF; 50 microl EGF-Az immobilized; and 100 microl EGF-Az immobilized. The ACL cells were cultured long-term and evaluated for possible differences in their responses to EGF. An in vitro wound closure assay was developed to enable examination of cellular proliferation and migration. ACL cell proliferation was most evident in the photo-immobilized EGF culture group and was seen to increase in proportion to the amount of added EGF. In the in vitro wound closure assay, the lesioned area at 72 h after culture initiation was indistinguishable in the photo-immobilized cultures, but remained clearly visible in the controls. We conclude that photo-immobilized EGF induced rapid proliferation of ACL fibroblast cells by artificial juxtacrine stimulation and speculate that similar EGF immobilization onto bioabsorbable material (e.g., polyglycolic acid or polylactic acid) might contribute to a new therapy for the treatment of ACL injuries.

Long-term clinical and radiological outcomes of hybrid total knee arthroplasty.

OBJECTIVES: The purpose of this study was to evaluate the clinical effectiveness and radiological results of hybrid total knee arthroplasty (TKA). METHODS: This study recruited 105 patients (169 cases) who underwent hybrid TKA for osteoarthritis and rheumatoid arthritis from 1999 to 2002. Maxim (Biomet Inc., Warsaw, IN, USA) prosthesis was used, and average follow-up was 8.6 years. Radiologically, femorotibial angle was measured in a standing anteroposterior (AP) view, and a femoral flexion angle and a tibial angle were measured using the Knee Society roentgenographic evaluation and scoring system. Radiolucent lines were detected at the last follow-up. Clinically, range of joint motion and the Knee Society clinical rating system scores were evaluated. RESULTS: The femorotibial angle was improved from varus 4.5° to 6.4° at the last follow-up. The femoral flexion in an AP view at the postoperative and last follow-up was 96.5° and 95.7°, respectively, and the tibial angle was 89.1° and 88.7°, respectively. In lateral view, the femoral flexion was 2.6° and 2.7°, respectively, and the tibial angle was 88.4° and 87.8°, respectively. Total scores of radiolucencies were 4 points or less in all cases, and the average width was 1.1 mm. Flexion contracture was improved from 10.0° to 3.5°, and further flexion was increased from 110.5° to 130.4°. Knee score and function score were also enhanced from 47.6 and 46.8 preoperatively to 89.7 and 88.4 after the operation, respectively. CONCLUSION: Hybrid technique for TKA can be effective clinically and radiologically on longterm follow-up.

Notochordal cells stimulate migration of cartilage end plate chondrocytes of the intervertebral disc in in vitro cell migration assays.

BACKGROUND CONTEXT: It was recently demonstrated that the postnatal transition from a notochordal to a fibrocartilaginous nucleus pulposus (NP) is accomplished exogenously by chondrocytes migrating from hyaline cartilage end plates (CEs) into the ectopic notochordal NP region. Although our previous in vivo studies showed evidences for the migration of CE chondrocyte from hyaline CEs into the notochordal NP, it is unknown whether CE chondrocytes of the intervertebral disc (IVD) really have a motile property. In addition, the effect of notochordal cells on this property has not been elucidated. PURPOSE: The purpose of this in vitro study was to demonstrate whether CE chondrocytes of the IVD are capable of migration, and whether there is any biological link between notochordal cells and CE chondrocytes that may regulate the CE chondrocyte migration. STUDY DESIGN/SETTING: In vitro cell migration assays were performed using rat IVDs. METHODS: Notochordal cells and chondrocytes were obtained from the NP and CE tissues, respectively, and were cultured separately. The different numbers of notochordal cells and the supernatant (conditioned medium) that contained soluble factors produced by notochordal cells were used to demonstrate their effects on the migration of CE chondrocytes. Bovine serum albumin (BSA) and lysophosphatidic acid (LPA) were used as negative and positive controls, respectively. RESULTS: Compared with BSA, LPA, notochordal cells (N=4x, 2x, 1x, and 0.5 x 10(5)), and its conditioned media (unconcentrated and fivefold concentrated) significantly increased migration of CE chondrocytes (p<.05 in all comparisons). Particularly, notochordal cells and its conditioned media increased migration in a number- and concentration-dependent manner, respectively. CONCLUSIONS: This study demonstrates that CE chondrocytes of the IVD are capable of migration and that soluble factors produced by notochordal cells stimulate the migration. These results provide a plausible explanation to the question of why CE chondrocytes of the IVD migrate into the ectopic NP region during the natural transition from the notochordal to fibrocartilaginous NP.

Arthroscopic fixation of anterior cruciate ligament tibial avulsion fractures using bioabsorbable suture anchors.

This article describes a new technique for the arthroscopic reduction and fixation of anterior cruciate ligament (ACL) tibial avulsion fractures using bioabsorbable suture anchors. This described technique requires the use of anterolateral, anteromedial, medial mid-patellar, and lateral mid-patellar portals. A suture hook loaded with No. 2 polydioxanone (PDS) was used to pierce the ACL through the anteromedial or anterolateral portal, and bioabsorbable suture anchors were inserted through the medial and lateral mid-patellar portals. The five patients treated using this technique were evaluated at 1 year postoperatively. All patients showed bony union without anterior laxity or flexion contracture. The described technique provides firm fixation of fracture fragment and can be used in both skeletally immature and mature patients.

Senescence of nucleus pulposus chondrocytes in human intervertebral discs.

STUDY DESIGN: Senescence-related markers were assessed in surgically obtained human nucleus pulposus (NP) specimens. PURPOSE: To demonstrate the mechanism and signaling pathway involved in the senescence of NP chondrocytes. OVERVIEW OF LITERATURE: The population of senescent disc cells has been shown to be increased in degenerated or herniated discs. However, the mechanism and signaling pathway involved in the senescence of NP chondrocytes are unknown. METHODS: We examined cell senescence markers [senescence-associated beta-galactosidase (SA-beta-gal), telomere length, telomerase activity, p53, p21, pRB and p16] and the hydrogen peroxide (H(2)O(2)) content in human NP specimens. RESULTS: The percentage of SA-beta-gal-positive NP chondrocytes increased with age, while the telomere length and telomerase activity declined. However, there was no significant correlation between age and H(2)O(2) content. The NP specimens with grade III or IV degeneration showed significantly higher percentages of SA-beta-gal-positive NP chondrocytes than those with grade II degeneration. Immunohistochemistry showed that senescent NP chondrocytes in all specimens expressed p53, p21, and pRB, while a few NP chondrocytes in only two specimens expressed p16. CONCLUSIONS: The present study demonstrates that, with increasing age and advancing disc degeneration, senescent NP chondrocytes increase or accumulate in the NP. Furthermore, the telomere-based p53, p21, pRB pathway, rather than the stress-based p16, pRB pathway, plays a more important role in the senescence of NP chondrocytes in in vivo conditions. Our results suggest that prevention or reversal of senescence of NP chondrocytes can be a novel mechanism by which to prevent human disc degeneration.

The apoptotic effects of oxidative stress and antiapoptotic effects of caspase inhibitors on rat notochordal cells.

STUDY DESIGN: Western blotting and flow cytometric analyses were performed using rat notochordal cells. OBJECTIVE: To demonstrate the apoptotic effect of oxidative stress and the antiapoptotic effects of caspase inhibitors on rat notochordal cells. SUMMARY OF BACKGROUND DATA: Although oxidative stress causes apoptosis in many cell types, its effect on the apoptosis of notochordal cell and antiapoptotic effects of caspase inhibitors on the oxidative stress-induced apoptosis are unknown. METHODS: Cultured rat notochordal cells were exposed to oxidative stress [500 micromol/L of hydrogen peroxide (H2O2)]. To determine the oxidative stress-induced apoptotic pathways, activations of caspases (-3, -8, and -9) as well as cleavages of Bid and poly (ADP-ribose) polymerase (PARP) were evaluated with Western blotting 6 hours after oxidative stress. To elucidate the antiapoptotic effects of caspase inhibitors on the oxidative stress induced-apoptosis, apoptotic rates of notochordal cells with or without treatment of specific caspase inhibitors (z-IETD-fmk for caspase-8, z-LEHD-fmk for caspase-9, and z-DEVD-fmk for caspase-3) were quantified by flow cytometry. RESULTS: Oxidative stress significantly increased apoptosis of rat notochordal cells (2.1% vs. 4.75%, P = 0.008) and led to activations of initiators of intrinsic (caspases-9) and extrinsic (caspase-8) pathways as well as their common executioner (caspase-3). It also caused cleavages of Bid and PARP. Flow cytometric analysis showed that inhibition of only one of the intrinsic and extrinsic pathways by caspase-9 inhibitor (4.75% vs. 3.56%, P = 0.31) and caspase-8 inhibitor (4.75% vs. 5.24%, P = 0.84) did not significantly suppress the oxidative stress-induced apoptosis. However, inhibition of both pathways by caspase-3 inhibitor significantly reduced the oxidative stress-induced apoptosis (4.75% vs. 2.64%, P = 0.008) to the control level (2.1% vs. 2.64%, P = 0.15). CONCLUSION: Oxidative stress caused apoptosis of rat notochordal cells via both intrinsic and extrinsic (Type I and Type II) pathways. Because caspase inhibitors are being used in clinical trials, inhibition of both pathways using caspase inhibitors might be of future therapeutic importance in oxidative stress-induced apoptosis of notochordal cells. Our results suggest that inhibition of inappropriate or premature oxidative stress-induced apoptosis of notochordal cells may delay the starting point of disc degeneration.

Expressions of membrane-type I matrix metalloproteinase, Ki-67 protein, and type II collagen by chondrocytes migrating from cartilage endplate into nucleus pulposus in rat intervertebral discs: a cartilage endplate-fracture model using an intervertebral disc organ culture.

STUDY DESIGN: Immunohistochemistry was performed in organ-cultured intact and cartilage endplate (CE)-fractured rat intervertebral discs (IVDs). OBJECTIVES: To demonstrate biologic events associated with migration of chondrocytes from hyaline CE into nucleus pulposus (NP). SUMMARY OF BACKGROUND DATA: It was recently revealed that the transition from a notochordal NP to a fibrocartilaginous NP in the rabbit IVD is accomplished exogenously by chondrocytes migrating from CEs into the NP. This observation has not been studied in other animal models, and the biologic events associated with chondrocyte migration have not been elucidated in the literature. METHODS: IVDs including cranial and caudal CEs were obtained from 4-week, 6-month, 12-month, and 18-month old Wistar rats. To accelerate chondrocyte migration, CEs of IVDs were fractured and cultured for 48 hours. IVDs without CE-fracture were used as a control for each age group. Expressions of membrane-type I matrix metalloproteinase (MT1-MMP, as a marker for cell migration and extracellular matrix digestion) and Ki-67 protein (as a proliferation marker) and pericellular deposition of type II collagen (as a marker for fibrocartilaginous matrix) by the chondrocytes migrating from CE into NP were examined immunohistochemically. RESULTS: In the control groups, chondrocyte migration limited only along the periphery of the notochordal NP and no chondrocytes were inside the NP proper. However, all the IVDs in the CE-fracture groups showed direct and more extensive migration of chondrocytes from CEs into the NP proper. The migrating chondrocytes in both control and CE-fracture groups expressed MT1-MMP and Ki-67 protein and deposited type II collagen in the NP. CONCLUSIONS: This report demonstrates the chondrocyte migration from CE into NP in the organ-cultured rat IVDs. This phenomenon is accelerated in the presence of CE fracture. The chondrocytes migrating from CEs into the NP expressed MT1-MMP and Ki-67 protein and deposited type II collagen. These biologic strategies probably enable chondrocytes of the hyaline CE to migrate into the ectopic NP region, replace notochordal cells, and change the notochordal tissue into fibrocartilage. These results suggest that similar biologic mechanisms may be involved in the natural transition from the notochordal NP to the fibrocartilaginous NP in other animal models, including human.

An autocrine or paracrine Fas-mediated counterattack: a potential mechanism for apoptosis of notochordal cells in intact rat nucleus pulposus.

STUDY DESIGN: Immunohistochemistry and in situ nick end-labeling (TUNEL) were performed in rat lumbar intervertebral discs. OBJECTIVES: To demonstrate the mechanism of notochordal cell death in the nucleus pulposus (NP). SUMMARY OF BACKGROUND DATA: With age, notochordal cells gradually disappear in the NP. We hypothesized that this phenomenon might be related to Fas-mediated apoptosis. MATERIALS AND METHODS: Expressions of Fas; Fas ligand (FasL); caspase 3, 8, 9, 10; Ki-67 protein; and TUNEL were examined in 4-week-, 6-month- and 12-month-old rat NPs. Apoptosis (TUNEL-positive) and proliferation potential (Ki-67-positive) indexes of notochordal cells were calculated and compared among age groups. RESULTS: Notochordal cells constitutively expressed both Fas and FasL. Among their downstream initiator (caspase 8, 9, and 10) and executioner (caspase 3) caspases tested, caspase 9 and 3 were expressed. Proliferation potential of the notochordal cells was the highest at 4 weeks (1.96 +/- 1.3%) and decreased to a significantly lower level at 6 (0.81 +/- 0.68%) and 12 months (0.8 +/- 0.37%; P = 0.03 and 0.01, respectively). In contrast, apoptosis of the notochordal cells was the lowest at 4 weeks (3.52 +/- 1.07%) and increased to a significantly higher level at 6 (19.38 +/- 10.99%) and 12 months (21.51 +/- 16.99%; P < 0.001 in both comparisons). CONCLUSIONS: Fas-mediated mitochondrial caspase 9 pathway is constitutively present in the rat notochordal cells. The constitutive expression of Fas, FasL and its downstream caspases, as well as the homogeneity ofnotochordal cell population suggests an autocrine or paracrine Fas-mediated counterattack to be a potential mechanism for apoptosis of rat notochordal cells. A regulated negative balance of notochordal cell proliferation against apoptosis is likely to involve the disappearance of notochordal cells in the rat NP. This information on the mechanism for apoptosis of notochordal cells could be important in the investigation of intervertebral disc development as well as aging and perhaps degeneration.