We measured the serum concentration of C-reactive protein (CRP) by a high-sensitive method in patients with lumbar disc herniation. There were 48 patients in the study group and 53 normal controls. The level and type of herniation were evaluated. The clinical data including the neurological findings, the angle of straight leg raising and post-operative recovery as measured by the Japanese Orthopaedic Association (JOA) score, were recorded. The high-sensitive CRP (hs-CRP) was measured by an ultrasensitive latex-enhanced immunoassay. The mean hs-CRP concentration was 0.056 ± 0.076 mg/dl in the patient group and 0.017 ± 0.021 mg/dl in the control group. The difference was statistically significant (p = 0.006). There was no other correlation between the hs-CRP concentration and the level and type of herniation, or the pre-operative clinical data. A positive correlation was found between the concentration of hs-CRP before operation and the JOA score after. Those with a higher concentration of hs-CRP before operation showed a poorer recovery after. The significantly high concentration of serum hs-CRP might indicate a systemic inflammatory response to impingement of the nerve root caused by disc herniation and might be a predictor of recovery after operation.

We recorded compound muscle action potentials (CMAPs) from the diaphragm in 15 normal volunteers, nine patients with lesions of the lower cervical cord (C5 to C8), one completely quadriplegic patient (C6) and seven patients with lesions at a higher cervical level (C1 to C4). Transcranial magnetic stimulation and electrical stimulation of the phrenic nerve were carried out.

When the centre of the coil was placed on the interauricular line at a point 3 cm lateral to the vertex on the scalp, the CMAPs from the diaphragm had the largest amplitude and the shortest latency. There was no difference in the mean latency of the CMAPs recorded by transcranial magnetic stimulation in the normal volunteers and in the patients with lesions of the lower cervical cord. In the quadriplegic patient, the latency of the CMAPs was not delayed, but was prolonged in the patients with lesions at a higher level. Those evoked by electrical stimulation of the phrenic nerve were not prolonged in the patients with higher lesions.

Our findings suggest that the prolongation of the latency by transcranial magnetic stimulation reflects dysfunction of the higher cervical cord. The combination of transcranial magnetic stimulation and electrical stimulation of the phrenic nerve can detect the precise level of the lesion in the motor tract to the diaphragm.

Recent studies of the fibroblast growth factor receptor 3 (FGFR3) gene have established that achondroplasia and hypochondroplasia are allelic disorders of different mutations.

To determine whether the genotype could be distinguished on the basis of the phenotype, we analysed height, arm span, and skeletal radiographs from 23 patients with achondroplasia and the G380R mutation of FGFR3 and eight with hypochondroplasia and the N540K mutation. Both conditions share the classical pathological features of micromelic short stature, reduced or unchanged interpedicular distances in the lumbar spine, disproportionately long fibulae, and squared and shortened pelvic ilia. These were significantly more severe in the G380R patients than in the N540K patients.

Our findings have shown a firm statistical correlation between the genotype and the phenotype, although there were a few exceptional cases in which there was phenotypic overlap between the two conditions.

Nine children sustained a second fracture of the distal humerus after union of an ipsilateral supracondylar fracture which had healed with cubitus varus. There were eight boys and one girl with a mean age of five years (1 to 8) at the time of the second fracture which occurred at a mean of 1.5 years after the first. In all patients, the second fracture was an epiphyseal injury of the distal humerus, either associated with a fracture of the lateral metaphysis below the site of the previous supracondylar fracture, or a fracture-separation of the entire distal humeral epiphysis. This suggests that the physis and epiphysis tend to be more subject to injury than the metaphysis of the distal humerus in children who have had a previous supracondylar fracture with varus malunion.

We developed a rat model of limb lengthening to study the basic mechanism of distraction osteogenesis, using a small monolateral external fixator. In 11-week-old male rats we performed a subperiosteal osteotomy in the midshaft of the femur with distraction at 0.25 mm every 12 hours from seven days after operation.

Radiological and histological examinations showed a growth zone of constant thickness in the middle of the lengthened segment, with formation of new bone at its proximal and distal ends.

Osteogenic cells were arranged longitudinally along the tension vector showing the origin and the fate of individual cells in a single section. Typical endochondral bone formation was prominent in the early stage of distraction, but intramembraneous bone formation became the predominant mechanism of ossification at later stages. We also showed a third mechanism of ossification, ‘transchondroid bone formation’. Chondroid bone, a tissue intermediate between bone and cartilage, was formed directly by chondrocyte-like cells, with transition from fibrous tissue to bone occurring gradually and consecutively without capillary invasion.

In situ hybridisation using digoxigenin-11-UTP-labelled complementary RNAs showed that the chondroid bone cells temporarily expressed type-II collagen mRNA. They did not show the classical morphological characteristics of chondrocytes, but were assumed to be young chondrocytes undergoing further differentiation into bone-forming cells.

We found at least three different modes of ossification during bone lengthening by distraction osteogenesis. We believe that this is the first report of such a rat model, and have shown the validity of in situ hybridisation techniques for the study of the cellular and molecular mechanisms involved in distraction osteogenesis.

In an attempt to repair articular cartilage, allograft articular chondrocytes embedded in collagen gel, were transplanted into full-thickness defects in rabbit articular cartilage. Twenty-four weeks after the transplantation, the defects were filled with hyaline cartilage, specifically synthesising Type II collagen. These chondrocytes were autoradiographically proven to have originated from the transplanted grafts. Assessed histologically the success rate was about 80%, a marked improvement over the results reported in previous studies on chondrocyte transplantation without collagen gel. By contrast, the defects without chondrocyte transplantation healed with fibrocartilage. Immunological enhancement induced by transplanted allogenic chondrocytes or collagen was not significant at eight weeks after treatment, so far as shown by both direct and indirect blastformation reactions. Thus, allogenic transplantation of isolated chondrocytes embedded in collagen gel appears to be one of the most promising methods for the restoration of articular cartilage.

We describe the use of allogeneic human tendon as an intra-articular replacement for the anterior cruciate ligament. Depending on the type and degree of functional instability we recommend the addition, in some cases, of supplementary extra-articular procedures. We have reviewed 31 patients at least two years after operation and have found that 30 of them had been able to return to full sporting activities. The indications for operation and the techniques are discussed and the use of allogeneic tendon is recommended.