Patient self-reported outcome scales have recently been used to evaluate total knee arthroplasty (TKA) outcomes. Many follow-up studies have been conducted on patients undergoing TKA; however, they have mostly reported outcomes after unilateral TKA. We believe that a longitudinal study after bilateral TKA will be more useful in evaluating the quality of life (QOL) of such patients. The objective of this study was to longitudinally evaluate QOL using the Japanese Knee Osteoarthritis Measure (JKOM). Objective outcomes were assessed using the Knee Society Score (KSS) and the Timed Up and Go test (TUG) for more than 5 years after bilateral TKA. Furthermore, QOL and objective outcomes were compared between younger (age ≤ 80 years at the final follow-up point) and older (age > 80 years) age groups.Introduction
Objectives
Various methods to manage medial tibial defects in primary total knee arthroplasty (TKA) have been described. According to Vail TP, metal augmentation is usually indicated for defect depth of >10 mm of the medial tibial plateau. The outcomes of metal augmentation have been described as excellent. Nevertheless, we believe that it is mandatory to preserve as much of the bone as possible for future revision surgeries. Therefore, we performed autologous impaction bone grafting even for large bone defects (defect depth of ≥10 mm) in primary TKA. The objectives of this study are to describe our bone grafting technique in detail and to assess the radiological outcomes of the grafted bone. Between 2003 and 2011, 26 TKAs with autologous impaction bone grafting for ≥10 mm medial tibial defects were performed. The preoperative diagnoses were osteoarthritis in 17 knees, rheumatoid arthritis in 2 knees, osteonecrosis of the medial tibial condyle in 6 knees, and Charcot's joint in 1 knee. The average mediolateral width and depth of the medial tibial defects, measured after the horizontal osteotomy of the tibial articular surface, were 17.8 mm (range, 10–25 mm) and 12.0 mm (range, 10–23 mm), respectively. The average patient age at surgery was 73.2 years (range, 56–85 years). The patients were followed up for an average of 55 months (range 27–109 months). Bone grafting technique: Multiple drill holes (white arrow) were made on the floor of the defect (A) and a morselized cancellous bone was impacted using the grip end of a metal hammer (white asterisk) and firm manual pressure to fill the defect. Thus, the firm impaction prevented bone cement from entering the space between the graft and the tibial host bed. An assistant's index finger (black asterisk) was used as a bank (B). The tibial component was fixed on the grafted bone (white asterisk) with bone cement (C). Internal fixation devices were not required, and stem extension was used in only Charcot's joint (defect depth=23 mm). Aftertreatment was the same as that for the usual TKAs without bone defects.Introduction
Methods
In the pubertal growth plate, sex hormones play important roles for the regulation of the proliferation, differentiation, maturation and programmed death of chondrocytes. Many studies have been reported on the regulation of oestrogen in long bone growth, however, some of the mechanisms have remained unclarified to date including its role for cell kinetics in the growth plate chondrocytes. The aim of this study was to clarify the effect of the deficiency of oestrogen on growth plate chondrocytes. We obtained the growth plates of femoral head from the normal and ovariectomized Japanese white rabbits at 10, 15, 20 and 25 weeks. Ovariectomy was performed at 8 weeks. The cell kinetics of chondrocytes as defined by the numbers of proliferating and programmed dying cells was investigated using immunohistological methods. The lengths of the femur were almost same both in the ovariectomised and normal rabbits. The height of the growth plate was larger in the former. The total number of chondrocytes in the ovariectomised rabbits was less than that of normal rabbits of the same age. Immunostaining of proliferating cell nucleous antigen (PCNA) showed a decrease number of proliferating chondrocytes and that of caspase-3 indicated a little increased number of apoptotic chondrocytes. Oestrogen regulates endochondral bone formation through several pathways. It directly binds oestrogen receptor alpha and beta, and the former accelerates longitudinal bone growth whereas the latter represses it. Another pathway is through the GH-IGF-I axis: it closely interacts with GH and IGF-I for the control of longitudinal bone growth. In addition, there might be other mediators including transforming growth factor-beta, other IGFs and still unknown paracrine or auto-crine factors as IHH PTHrP. Our study suggests that in the rabbit growth plate during puberty, oestrogen mainly acts through the GH-IGF-I axis since its defi-ciency declined the proliferating ability of chondrocytes, which led the decrease of the number of chondrocytes.
Endochondral ossification involves a well ordered sequence of cellular events. Chondrocytes change their morphology and functions and are ultimately removed by the process of apoptosis. A variety of apoptotic-related signals have been characterised. These include Fas receptor (FasR)/Fas ligand (FasL), p53 and Bcl family. However, there is little known regarding the activity of these signals in the process of fracture healing. The purpose of this study was to investigate mRNA expression of apoptotic signals using RNase protection assay (RPA) and immunohistochemistry in endochondral bone formation. BALB/C mice aged 8 to 10 weeks were used for this study. First, a transverse fracture was made in the right tibia. Mice were euthanised at 1, 2 and 3 weeks postfracture. The calluses were harvested and studied for the expression of caspase-8, a key enzyme of apoptosis, and apoptosis inducers: tumour necrosis factor-alpha (TNF-α) and its receptor p55, FasL and Fas receptor (FasR), and TNF-related apoptosis-inducing ligand (TRAIL). Four mice at each timepoint were used for immunostaining of fracture callus. Sections were incubated with primary antibody then labelled by avi-din-biotin complex method. Another four to ten tibiae were used for RPA. Fracture callus were harvested and snap frozen in liquid nitrogen. RNA was isolated by TRI reagent and BCP, and mRNAs expression of apoptotic signals were detected. At each timepoint, mRNA of caspase-8, TNF-α, p55, FasL,FasR and TRAIL were detected by RPA. Immunostainings clearly showed that those apoptotic-related proteins were expressed by callus chondrocytes. Cartilaginous callus is replaced by woven bone in endochondral ossification. In this process, chondrocytes should be removed by the process of apoptosis in which death factors are elaborated directly in both an autocrine and paracrine manner.
