Background: Conventional magnetic resonance pulse sequence echo times (TEs) produces no signal of cortical bone. In this pilot study we wished to explore the value of a novel pulse sequence with an ultrashort echo time (UTE), which is able to detect signal from cortical bone and periosteum (Ref.). The signal obtained using an UTE sequence from cortical bone reflects the soft tissue component of cortical bone including its vasculature. We hypothesized that conditions, which alter the soft tissue component and vascularity of bone, show a change in signal. We have examined the lower limb in patients and volunteers of different age and at different time points following fracture of the tibia.

Subjects and Methods: Seven volunteers (aged 29 – 85 years) and eight patients with acute fractures of the tibia (aged 18 – 56 years) were examined at different time points (2 days – 16 weeks) following fracture, in three of the patients serial scans were obtained. Three patients were examined years following bone injury: one patient with a hypertrophic mal-union at 5 years, one patient with polio 14 years following a tibial osteotomy and one patient 28 years following a tibial fracture. Ultra-short echo time pulse sequences (TE = 0.07 or 0.08 ms) were used with and without preceding fat suppression and / or long T2 component suppression pulses. Intravenous gadolinium (0.3 mmol/kg) was administered to one volunteer and three of the patients. Mean signal intensity (AU) was plotted against time following contrast enhancement. T1 and T2* values for cortical bone were determined and T1 was plotted against age.

Results A signal was obtained of cortical bone, periosteum and callus in all subjects. The injection of contrast enhanced the signal in all of these tissues. Distribution curves of gadolinium in cortical bone showed enhanced signal intensity following fracture. The signal was dependent on the type and severity of fracture and the time following fracture. There was a marked increase in signal in a hypertrophic mal-union 5 years following fracture and a moderate increase in signal was still detectable 28 years following fracture. Osteoporosis associated with polio reduced volume and signal of bone. T1 echo times ranged from 140 – 260 ms and increased significantly with age (P < 0.01). T2* ranged from 0.42 – 0.50 ms. Fat suppression and long T2 suppression increased the conspicuity of the periosteum.

Conclusion: Magnetic resonance imaging using UTE sequences is able to detect a signal from cortical bone for the first time. Cortical bone, callus and adult periosteum show a distinct signal following fracture with a characteristic time course. Measurements reflect the organic matrix rather than the inorganic crystals of bone. The T1 of cortical bone is very short and changes with age. The distribution curve of gadolinium can be established in cortical bone and is understood to reflect changes in blood flow. We present a pilot study to introduce a new MRI sequence, which at present a research tool, has potential for selected clinical application.

Fifty-three ununited fractures with a median time since injury of 28 months were treated by electrical stimulation using pulsing electromagnetic fields. Union was achieved in 38 cases (71.7 per cent) in a median time of six months. For ununited fractures of the tibia the success rate was higher at 86.7 per cent. Previous or active sepsis, the presence of plates or nails, the age of the patient or the time since the injury did not affect the results. Analysis of the failures suggests that inadequate immobilisation, a fracture gap of more than five millimetres or the presence of a screw in the fracture gap was responsible. In four patients no cause of failure could be determined.

A patient with Rubinstein-Taybi syndrome complicated by tetraplegia secondary to cervical spondylolisthesis is reported. The abnormalities presenting in this condition are reviewed.

Eleven patients with arthrogryposis multiplex congenita neurologica have been reviewed. Distinct patterns of deformity and muscle activity were identified which have been correlated with specific levels of segmental neurological motor deficit without sensory loss. The clinical picture was consistent with localised lesions of the anterior horn cell cell columns. This finding agreed with the recorded pathological lesions. Orthopaedic treatment should take account of the paralytic nature of the deformities.