We evaluated changes in bone mineral density (BMD) after tibial fractures, both at the site of fracture and at adjacent sites, using dual-energy X-ray absorptiometry. Five patients were studied prospectively for six months after fractures of the midshaft treated by intramedullary nailing or the application of an external fixator. We also reviewed 21 adult and 10 children who had sustained fractures of the tibia at least five years previously, comparing BMD in the injured limb with that in the non-injured limb and in a control group of 10 normal subjects. We found a significant fall in BMD distal to a tibial fracture; this was evident at one month, fell to approximately 50% of normal at three months and persisted at six months. We found no significant improvement with weight-bearing. Review at 5 to 11 years after adult midshaft fractures showed persistent bone loss in the distal tibia (46.5 +/- 9.8% of control values), but persisting sclerosis at old fracture sites (172 +/- 38% of control values). In contrast, we found no significant differences in BMD between the injured and control limb after fractures sustained in childhood either at the fracture site or in the distal segment. We conclude that, in adults, tibial fractures are associated with definite and persistent post-traumatic loss of distal BMD.

We studied the quantity and rate of formation of new bone during lengthening of 17 limb segments in 10 patients using dual-energy X-ray absorptiometry (DEXA), ultrasonography and radiography. Whereas new bone was detected by both DEXA and ultrasonography within 1 to 2 weeks of distraction, it was not visible on the radiographs until 4 to 8 weeks. Limb alignment and gap measurement were accurately assessed by DEXA without the need for standard radiographs or scanograms. With ultrasound the distraction gap appeared as an echolucent window which narrowed progressively producing a hyper-reflecting line after which further consolidation could not be assessed. As measured by DEXA the density of the new bone at this stage was approximately 45% of control values and did not represent normal cortication. Whereas ultrasound could be used to identify defects in mineralisation and to determine when to dynamise the fixator system, DEXA could measure the quantity and rate of formation of bone throughout lengthening.

We measured the extent and rate of new bone formation over an 18-month period before, during and after the lengthening of ten leg segments in six patients aged between 8 and 18 years, using dual-energy X-ray absorptiometry (DEXA). New bone formation could be identified within one week of the start of distraction. As lengthening proceeded, the bone density of the gap fell, reaching minimum values at the time of maximal distraction. Consolidation of the regenerating bone was started 1 to 2 weeks later in the tibia, and 2.5 to 3.0 weeks later in the femur. The rate of mineral accretion in new bone was significantly greater in the tibia than in the femur (16 +/- 1.86%/month, and 11 +/- 1.1%/month respectively; mean +/- SEM). There was significant osteoporosis distal to the osteotomy, more in the tibia than in the femur, particularly on the side of the fixator. The bone mineral density of the distal segment remained low at the time of fixator removal (44.2 +/- 5.58% and 61.0 +/- 4.2% of the control values at the tibia and femur respectively) and was only partially reversed by subsequent weight-bearing. We conclude that dual-energy X-ray absorptiometry provides an objective and quantitative assessment of new bone formation during leg lengthening. The technique also allows the measurement of the distraction gap and the assessment of leg alignment from the high-resolution images. Its use may decrease the requirements for conventional radiography.

We report the results of a prospective study of the incidence of algodystrophy following Colles' fracture in 60 patients, using sensitive or quantitative techniques for the assessment of each feature of the syndrome. Nine weeks after fracture, 24 patients had evidence of vasomotor instability, 23 had significant tenderness of the fingers and 23 had lost finger movement. These three abnormalities were significantly associated (p less than 0.001). Swelling was also significantly associated with these three variables. There was no statistical association between the occurrence of algodystrophy and the patient's age or sex, the severity of the fracture, the number of reductions performed or the adequacy of the reduction. We conclude that algodystrophy constitutes a precisely definable and quantifiable syndrome which is more common than has been suspected.

We studied nine patients with Paget's disease affecting the skull or facial bones, who were subsequently treated with either dichloromethylene diphosphonate (clodronate) or ethylene-1-hydroxy-1,1-diphosphonate (etidronate). Long-term treatment induced a clinical and biochemical improvement in eight, and this was associated with a reduction in maxillary or skull volume as assessed by quantitative stereophotogrammetry. The one patient whose disease was resistant to treatment with diphosphonate, showed no change in maxillary shape. These studies suggest that the long-term control of disease activity attained with diphosphonates, results in the improvement of skeletal deformity.

We report 40 cases in one family of an autosomal dominant bone dysplasia, which, though similar in some aspects to Paget's disease, seems unique in some features and in its natural history. The disease shows both general and focal skeletal changes, the latter being mainly in the limbs with an onset from the second decade. Progressive osteoclastic resorption is accompanied by medullary expansion which leads to pain, severe deformity and a tendency to pathological fracture. The serum alkaline phosphatase and urinary hydroxyproline are variably elevated, while other biochemical indices are normal. Most patients had an associated deafness of early onset and loss of dentition. No previous description of this disease has been found in the literature.

The medical treatment of eight patients with paraparesis associated with Paget's disease of the vertebrae is described. Treatment, for 3 to 87 months, with calcitonin or with diphosphonates produced marked clinical improvement in seven of these patients. From this series and a review of 19 additional case reports it is concluded that favourable clinical response is seen in about 90 per cent of patients, and that this may occur very rapidly. Results are as good or better than those obtained by surgical decompression. It seems possible that paraparesis in some cases may be due to diversion of blood supply from the spinal cord to the highly vascular Pagetic bone giving rise to a vascular "steal" syndrome. It is suggested that medical treatment should be used more widely to avoid or delay the need for operation and reduce the risks of recurrence. These patients, however treated, require lifelong follow-up because relapses are common.