We studied the effect of vitamin C on fracture healing in the elderly. A total of 80 elderly Osteogenic Disorder Shionogi rats were divided into four groups with different rates of vitamin C intake. A closed bilateral fracture was made in the middle third of the femur of each rat. Five weeks after fracture the femora were analysed by mechanical and histological testing. The groups with the lower vitamin C intake demonstrated a lower mechanical resistance of the healing callus and a lower histological grade. The vitamin C levels in blood during healing correlated with the torque resistance of the callus formed (r = 0.525). Therefore, the supplementary vitamin C improved the mechanical resistance of the fracture callus in elderly rats. If these results are similar in humans, vitamin C supplementation should be recommended during fracture healing in the elderly

Ischaemia-reperfusion injury (IRI) is caused by endothelial and subendothelial damage by neutrophil-derived oxidants. Vitamin C is an antioxidant which attenuates endothelial injury after IRI. Our aim was to evaluate the effect of oral vitamin C in the prevention of IRI in skeletal muscle. We used a model of cross-clamping (3 hours) and reperfusion (1 hour) of the cremaster muscle in rats. Muscle function was assessed electrophysiologically by electrical field stimulation. Infiltration by neutrophils was determined by the activity of tissue myeloperoxidase (MPO) and tissue oedema by the wet-to-dry ratio. Neutrophil respiratory burst activity was measured in control animals and groups pretreated with vitamin C. IRI significantly decreased muscle function and increased muscle neutrophil MPO activity and muscle oedema. Pretreatment with vitamin C preserved muscle function and reduced tissue oedema and neutrophil infiltration. Neutrophil respiratory burst activity was reduced in the group treated with vitamin C compared with the control group. We conclude that pretreatment with oral vitamin C protects against acute muscle IRI, possibly by attenuating neutrophil respiratory burst activity

Compartment syndrome is a unique form of ischaemia of skeletal muscle which occurs despite patency of the large vessels. Decompression allows the influx of activated leucocytes which cause further injury. Vitamin C is a powerful antioxidant which concentrates preferentially in leucocytes and attenuates reperfusion-induced muscle injury. We have evaluated the use of pretreatment with oral vitamin C in the prevention of injury caused by compartment syndrome in a rat cremasteric muscle model. Acute and delayed effects of pretreatment with vitamin C were assessed at one and 24 hours after decompression of compartment syndrome. Muscle function was assessed electrophysiologically. Vascular, cellular and tissue inflammation was assessed by staining of intercellular adhesion molecule-1 (ICAM-1) and by determination of the activity of myeloperoxidase (MPO) in neutrophils and tissue oedema. Compartment syndrome impaired skeletal muscle function and increased the expression of ICAM-1, activity of MPO and muscle weight increased significantly. Pretreatment with vitamin C preserved muscle function and reduced the expression of ICAM-1, infiltration of the neutrophils and oedema

We explored the role of iron overload, deficiency of vitamin C and alcohol abuse in the aetiology of cervical and intertrochanteric fractures of the neck of the femur as a result of minor trauma. We studied prospectively 72 patients (45 men, 27 women). Levels of serum iron markers, vitamin C and alcohol markers were measured. Consumption of alcohol was estimated using questionnaires. The findings were compared with those of an age- and gender-matched control group. The mean age of the men was 59.5 years and of the women 66.9 years, with a male predominance. In the men, iron overload, as shown by high levels of serum ferritin (p < 0.001) and deficiency of vitamin C (p < 0.03), as well as abuse of both Western and the traditional type of alcohol, appear to be important aetiological factors. In women, alcohol abuse was also common, but iron markers and levels of vitamin C did not differ significantly from the control group

The December 2014 Trauma Roundup. 360 . looks at: infection and temporising external fixation; Vitamin C in distal radial fractures; DRAFFT: Cheap and cheerful Kirschner wires win out; femoral neck fractures not as stable as they might be; displaced sacral fractures give high morbidity and mortality; sanders and calcaneal fractures: a 20-year experience; bleeding and pelvic fractures; optimising timing for acetabular fractures; and tibial plateau fractures

Relating the results of our investigations to the knowledge hitherto acquired about the etiology of osteoporosis (which I have already referred to), I am inclined to interpret the pathogenesis of osteoporosis in the following way: 1) Primary osteoblastic deficiency: congenital (Lobstein); involutive (senile osteoporosis?); 2) Reduced osteoblastic activity from absence of trophic stimuli: (inactivity, ovarian agenesia, eunuchoidism, menopause); 3) Reduced osteoblastic activity from inhibitory stimuli: (cortisone, adrenocorticotrophic hormone (A.C.T.H.), stress, Cushing's disease, thyrotoxicosis); 4) Normal osteoblastic activity but insufficiency of constructive material: (malnutrition, disturbances of the digestive system, insufficiency of vitamin C, diabetes, thyrotoxicosis, cortisone, A.C.T.H., stress, Cushing's disease). Osteoporosis may therefore be the consequence either of a congenital osteoblastic deficiency, such as that found in cases of osteogenesis imperfecta, or of reduced osteoblastic activity due to absence of trophic stimuli such as mechanical stress and the sex hormones, or of reduced activity of the bone cells due to anti-anabolic substances which inhibit them, such as cortisone and its derivatives and the thyroid hormone in strong doses, or lastly of reduced availability of construction material due to its introduction in reduced quantities (starvation, dysfunction of the digestive system) or due to hindering of synthesis (deficiency of vitamin C, diabetes, cortisone and its derivatives) or due to an excessive degree of destruction (thyrotoxicosis). In the case of anti-anabolic hormones from the adrenal cortex, the mechanism may thus be twofold: inhibition of the osteoblasts and deprivation of the osteoblasts of glucoprotein material due to a general anomaly of metabolism. This may perhaps explain the most serious forms of bone atrophy which are usually observable in cases of hyperfunction of the adrenal cortex. Senile osteoporosis should, in my opinion, be included in the first of our groups because it cannot be said to be brought about by any of the causes usually cited for osteoporosis– such as deficiency of sex hormones, excess of hormones from the adrenal cortex, deficiency of calcium, etc.–and in all probability it will depend on a progressive involution of the osteoblasts brought about by old age. Senile involution is an expression of the descending phase of life's parabola and it involves all the organs and all the parenchymatous tissues in the human body, but it does not cause a parallel reduction of functions and activities on all of them equally. The skeletal system is one of the first to feel these reductions, because in old age life necessarily becomes less intense. Consequently in the economy of the ageing subject the generally reduced level of metabolism brings about a sort of selection in the nourishment of the different organs and systems, and sometimes almost a dismantling of some of these in an attempt to fall in with the new and reduced level of activities of some of the parenchymatous tissues, activities which may be incomplete or even transferred elsewhere. We believe that the moment which originally determines the beginning of senile osteoporosis coincides with the involutional process of cellular metabolism that strikes at all parenchymatous tissue during old age–striking, in the case of osteoporosis, hardest of all at the bony tissues. There is, indeed, no doubt that certain essential processes of cellular metabolism do alter with age, and that the reduction in the activity of the gonads does have considerable importance. In any case, just as adolescence and old age cannot be explained only in terms of gonadal activity, so the involution of the skeleton cannot be due merely to the involution of the gonads. How should one then interpret the well known benefit afforded by administration of sex hormones in cases of osteoporosis? Probably the action of oestrogens and androgens is, in this case, of a pharmacological nature, and comparable, for instance, to the action of digitalis on the cardiac muscle. It will be remembered how digitalis acts almost exclusively on myofibrils which have become inadequate, and has little or no effect on a normal myocardium. Similarly, the sex hormones would seem to exert a stimulating action on osteoblasts that are on the way to involution, while they exert little or no action on normal osteoblasts. In support of this we have the findings of Urist and other workers, who demonstrated that the administration of sex hormones produces calcium and nitrogen retention only in osteoporotics, while in non-osteoporotic subjects of the same age it produces no effect. On the other hand, the action of the sex hormones might act in cases of senile osteoporosis by returning the changed level of protein metabolism to normal. From the data in the literature and from the results of our own investigations, I conclude that osteoporosis in general, and senile osteoporosis in particular, are first and foremost the result of a disturbance in the metabolism of bone, and that the metabolic disturbance is closely and exclusively related to the degree of activity and the state of activity of the cells in the bone. Lastly, I believe that senile osteoporosis should not be considered an actual disease but rather as one limited aspect of the normal descending parabola which affects to a greater or less degree all the tissues of the body

Aims

Accumulated evidence indicates that local cell origins may ingrain differences in the phenotypic activity of human osteoblasts. We hypothesized that these differences may also exist in osteoblasts harvested from the same bone type at periarticular sites, including those adjacent to the fixation sites for total joint implant components.

This paper reviews the current literature concerning the main clinical factors which can impair the healing of fractures and makes recommendations on avoiding or minimising these in order to optimise the outcome for patients. The clinical implications are described.

A total of seven patients (six men and one woman) with a defect in the Achilles tendon and overlying soft tissue underwent reconstruction using either a composite radial forearm flap (n = 3) or an anterolateral thigh flap (n = 4). The Achilles tendons were reconstructed using chimeric palmaris longus (n = 2) or tensor fascia lata (n = 2) flaps or transfer of the flexor hallucis longus tendon (n = 3). Surgical parameters such as the rate of complications and the time between the initial repair and flap surgery were analysed. Function was measured objectively by recording the circumference of the calf, the isometric strength of the plantar flexors and the range of movement of the ankle. The Achilles tendon Total Rupture Score (ATRS) questionnaire was used as a patient-reported outcome measure. Most patients had undergone several previous operations to the Achilles tendon prior to flap surgery. The mean time to flap surgery was 14.3 months (2.1 to 40.7).

At a mean follow-up of 32.3 months (12.1 to 59.6) the circumference of the calf on the operated lower limb was reduced by a mean of 1.9 cm (sd 0.74) compared with the contralateral limb (p = 0.042). The mean strength of the plantar flexors on the operated lower limb was reduced to 88.9% of that of the contralateral limb (p = 0.043). There was no significant difference in the range of movement between the two sides (p = 0.317). The mean ATRS score was 72 points (sd 20.0). One patient who had an initial successful reconstruction developed a skin defect of the composite flap 12 months after free flap surgery and this resulted in recurrent infections, culminating in transtibial amputation 44 months after reconstruction.

These otherwise indicate that reconstruction of the Achilles tendon combined with flap cover results in a successful and functional reconstruction.

Cite this article: Bone Joint J 2015;97-B:215–20.

The October 2013 Research Roundup³⁶⁰ looks at: Orthopaedics: a dangerous profession?; Freezing and biomarkers for bone turnover; Herniation or degeneration first?; MARS MRI and metallosis; Programmed cell death in partial thickness cuff tears; Lead glasses for trauma surgery?; Smoking inhibits bone healing; Optimising polyethylene microstructure.

We studied prospectively the regional inflammatory response to a unilateral distal radial fracture in 114 patients at eight to nine weeks after injury and again at one year. Our aim was to identify patients at risk for a delayed recovery and particularly those likely to develop complex regional pain syndrome. In order to quantify clinically the inflammatory response, a regional inflammatory score was developed. In addition, blood samples were collected from the antecubital veins of both arms for comparative biochemical and blood-gas analysis.

The severity of the inflammatory response was related to the type of treatment (Kruskal-Wallis test, p = 0.002). A highly significantly-positive correlation was found between the regional inflammatory score and the length of time to full recovery (r² = 0.92, p = 0.01, linear regession). A regional inflammatory score of 5 points with a sensitivity of 100% but a specificity of only 16% also identified patients at risk of complex regional pain syndrome. None of the biochemical parameters studied correlated with regional inflammatory score or predicted the development of complex regional pain syndrome.

Our study suggests that patients with a distal radial fracture and a regional inflammatory score of 5 points or more at eight to nine weeks after injury should be considered for specific anti-inflammatory treatment.

The aim of this retrospective multicentre study was to report the continued occurrence of compartment syndrome secondary to paediatric supracondylar humeral fractures in the period 1995 to 2005. The inclusion criteria were children with a closed, low-energy supracondylar fracture with no associated fractures or vascular compromise, who subsequently developed compartment syndrome. There were 11 patients (seven girls and four boys) identified from eight hospitals in three countries. Ten patients with severe elbow swelling documented at presentation had a mean delay before surgery of 22 hours (6 to 64). One patient without severe swelling documented at presentation suffered arterial entrapment following reduction, with a subsequent compartment syndrome requiring fasciotomy 25 hours after the index procedure.

This series is noteworthy, as all patients had low-energy injuries and presented with an intact radial pulse. Significant swelling at presentation and delay in fracture reduction may be important warning signs for the development of a compartment syndrome in children with supracondylar fractures of the humerus.