The acute childhood diseases haematogenous staphylococcal osteomyelitis and septic arthritis were studied concurrently using avian models which closely resemble the human diseases. Ultrastructural studies during the initial stages of bone and joint infection showed that adherence of bacteria to cartilage, bacterial proliferation, cartilage destruction and subsequent bacterial spread along the vascular channels within cartilage were common to both disease processes. Histological studies revealed that transphyseal blood vessels were present in the growing chickens and were a likely explanation for the frequency of the concurrence of acute osteomyelitis and adjacent joint infection following intravenous injection of bacteria. Transphyseal vessels provide a direct connection between the growth plate (physis) and epiphyseal cartilage supplying a route for bacteria to spread from an osteomyelitic focus in the metaphysis to the epiphysis and subsequently to the joint lumen

Aims. Venous tumour thrombus (VTT) is a rare finding in osteosarcoma. Despite the high rate of VTT in osteosarcoma of the pelvis, there are very few descriptions of VTT associated with extrapelvic primary osteosarcoma. We therefore sought to describe the prevalence and presenting features of VTT in osteosarcoma of both the pelvis and the limbs. Methods. Records from a single institution were retrospectively reviewed for 308 patients with osteosarcoma of the pelvis or limb treated between January 2000 and December 2022. Primary lesions were located in an upper limb (n = 40), lower limb (n = 198), or pelvis (n = 70). Preoperative imaging and operative reports were reviewed to identify patients with thrombi in proximity to their primary lesion. Imaging and histopathology were used to determine presence of tumour within the thrombus. Results. Tumours abutted the blood vessels in 131 patients (43%) and encased the vessels in 30 (10%). Any form of venous thrombus was identified in 31 patients (10%). Overall, 21 of these thrombi were determined to be involved with the tumour based on imaging (n = 9) or histopathology (n = 12). The rate of VTT was 25% for pelvic osteosarcoma and 1.7% for limb osteosarcoma. The most common imaging features associated with histopathologically proven VTT were enhancement with contrast (n = 12; 100%), venous enlargement (n = 10; 83%), vessel encasement (n = 8; 66%), and visible intraluminal osteoid matrix (n = 6; 50%). Disease-specific survival (DSS) for patients with VTT was 95% at 12 months (95% CI 0.87 to 1.00), 50% at three years (95% CI 0.31 to 0.80), and 31% at five years (95% CI 0.14 to 0.71). VTT was associated with worse DSS (hazard ratio 2.3 (95% CI 1.11 to 4.84). Conclusion. VTT is rare with osteosarcoma and occurs more commonly in the pelvis than the limbs. Imaging features suggestive of VTT include enhancement with contrast, venous dilation, and vessel encasement. VTT portends a worse prognosis for patients with osteosarcoma, with a similar survivability to metastatic disease. Cite this article: Bone Joint J 2024;106-B(8):865–870

Aims. The aim of this study was to determine the risk of local recurrence and survival in patients with osteosarcoma based on the proximity of the tumour to the major vessels. Patients and Methods. A total of 226 patients with high-grade non-metastatic osteosarcoma in the limbs were investigated. Median age at diagnosis was 15 years (4 to 67) with the ratio of male to female patients being 1.5:1. The most common site of the tumour was the femur (n = 103) followed by tibia (n = 66). The vascular proximity was categorized based on the preoperative MRI after neoadjuvant chemotherapy into four types: type 1 > 5 mm; type 2 ≤ 5 mm, > 0 mm; type 3 attached; type 4 surrounded. Results. Limb salvage rate based on the proximity type was 92%, 88%, 51%, and 0% for types 1 to 4, respectively, and the overall survival at five years was 82%, 77%, 57%, and 67%, respectively (p < 0.001). Local recurrence rate in patients with limb-salvage surgery was 7%, 8%, and 22% for the types 1 to 3, respectively (p = 0.041), and local recurrence at the perivascular area was observed in 1% and 4% for type 2 and 3, respectively. The mean microscopic margin to the major vessels was 6.9 mm, 3.0 mm, and 1.4 mm for types 1 to 3, respectively. In type 3, local recurrence-free survival with limb salvage was significantly poorer compared with amputation (p = 0.025), while the latter offered no overall survival benefit. In this group of patients, factors such as good response to chemotherapy or limited vascular attachment to less than half circumference or longitudinal 10 mm reduced the risk of local recurrence. Conclusion. The proximity of osteosarcoma to major blood vessels is a poor prognostic factor for local control and survival. Amputation offers better local control for tumours attached to the blood vessels but does not improve survival. Limb salvage surgery offers similar local control if the tumour attachment to blood vessels is limited. Cite this article: Bone Joint J 2019;101-B:1024–1031

Dupuytren’s disease is a chronic inflammatory process which produces contractures of the fingers. The nodules present in Dupuytren’s tissue contain inflammatory cells, mainly lymphocytes and macrophages. These express a common integrin known as VLA4. The corresponding binding ligands to VLA4 are vascular cell adhesion molecule-1 (VCAM-1) present on the endothelial cells and the CS1 sequence of the fibronectin present in the extracellular matrix. Transforming growth factor-beta (TGF-ß) is a peptide hormone which has a crucial role in the process of fibrosis. We studied tissue from 20 patients with Dupuytren’s disease, four samples of normal palmar fascia from patients undergoing carpal tunnel decompression and tissue from ten patients who had received perinodular injections of depomedrone into the palm five days before operation. The distribution of VLA4, VCAM-1, CS1 fibronectin and TGF-ß was shown by immunohistochemistry using an alkaline phosphorylase method for light microscopy. In untreated Dupuytren’s tissue CS1 fibronectin stained positively around the endothelial cells of blood vessels and also around the surrounding myofibroblasts, principally at the periphery of many of the active areas of the Dupuytren’s nodule. VCAM-1 stained very positively for the endothelial cells of blood vessels surrounding and penetrating the areas of high nodular activity. VCAM-1 was more rarely expressed outside the blood vessels. VLA4 was expressed by inflammatory cells principally in and around the blood vessels expressing VCAM-1 and CS1 but also on some cells spreading into the nodule. TGF-ß stained positively around the inflammatory cells principally at the perivascular periphery of nodules. These cells often showed VLA4 expression and co-localised with areas of strong production of CS1 fibronectin. Normal palmar fascia contained only scanty amounts of CS1 fibronectin, almost no VCAM-1 and only an occasional cell staining positively for VLA4 or TGF-ß. In the steroid-treated group, VCAM-1 expression was downregulated in the endothelium of perinodular blood vessels and only occasional inflammatory cell expression remained. Expression of CS1 fibronectin was also much reduced but still occurred in the blood vessels and around the myofibroblast stroma. VLA4-expressing cells were also reduced in numbers. A similar but reduced distribution of production of TGF-ß was also noted. Our findings show that adherence of inflammatory cells to the endothelial wall and the extravasation into the periphery of the nodule may be affected by steroids, which reduce expression of VCAM-1 in vivo. This indicates that therapeutic intervention to prevent the recommencement of the chronic inflammatory process and subsequent fibrosis necessitating further surgery may be possible

We have studied cellular and vascular changes in different stages of full thickness tears of the rotator cuff. We examined biopsies from the supraspinatus tendon in 40 patients with chronic rotator cuff tears who were undergoing surgery and compared them with biopsies from four uninjured subscapularis tendons. Morphological and immunocytochemical methods using monoclonal antibodies directed against leucocytes, macrophages, mast cells, proliferative and vascular markers were used. Histological changes indicative of repair and inflammation were most evident in small sized rotator cuff tears with increased fibroblast cellularity and intimal hyperplasia, together with increased expression of leucocyte and vascular markers. These reparative and inflammatory changes diminished as the size of the rotator cuff tear increased. Marked oedema and degeneration was seen in large and massive tears, which more often showed chondroid metaplasia and amyloid deposition. There was no association between the age of the patient and the duration of symptoms. In contrast, large and massive tears showed no increase in the number of inflammatory cells and blood vessels. Small sized rotator cuff tears retained the greatest potential to heal, showing increased fibroblast cellularity, blood vessel proliferation and the presence of a significant inflammatory component. Tissue from large and massive tears is of such a degenerative nature that it may be a significant cause of re-rupture after surgical repair and could make healing improbable in this group

We obtained intervertebral discs with cartilage endplates and underlying cancellous bone at operation from patients with degenerative disc disease and then used immunohistochemical techniques to localise the nerves and nerve endings in the specimens. We used antibodies for the ubiquitous neuronal protein gene product 9.5 (PGP 9.5). Immunoreactivity to neuropeptide Y was used to identify autonomic nerves and calcitonin gene-related peptide (CGRP) and substance P to identify sensory nerves. Blood vessels were identified by immunoreactivity with platelet-endothelial cell-adhesion molecule (CD31; PECAM). In a control group with no known history of chronic back pain, nerve fibres immunoreactive to PGP 9.5 and neuropeptide Y were most closely related to blood vessels, with occasional substance P and CGRP immunoreactivity. In patients with severe back pain and markedly reduced disc height, proliferation of blood vessels and accompanying nerve fibres was observed in the endplate region and underlying vertebral bodies. Many of these nerves were immunoreactive to substance P or CGRP, and in addition, substance P- and CGRP-immunoreactive nociceptors were seen unrelated to blood vessels. Quantification by image analysis showed a marked increase in CGRP-containing sensory nerve fibres compared with normal control subjects. We speculate that a chemotactic response to products of disc breakdown is responsible for the proliferation of vascularity and CGRP-containing sensory nerves found in the endplate region and vertebral body adjacent to degenerate discs. The neuropeptides substance P and CGRP have potent vasodilatory as well as pain-transmitting effects. The increase in sensory nerve endings suggests increase in blood flow, perhaps as an attempt to augment the nutrition of the degenerate disc. The increase in the density of sensory nerves, and the presence of endplate cartilage defects, strongly suggest that the endplates and vertebral bodies are sources of pain; this may explain the severe pain on movement experienced by some patients with degenerative disc disease

Our aim was to develop a clinically relevant model of atrophic nonunion in the rat to test the hypothesis that the vessel density of atrophic nonunion reaches that of normal healing bone, but at a later time-point. Atrophic nonunion is usually attributed to impaired blood supply and is poorly understood. We determined the number of blood vessels at the site of an osteotomy using immunolocalisation techniques in both normally healing bones and in atrophic nonunion. At one week after operation there were significantly fewer blood vessels in the nonunion group than in the healing group. By eight weeks, the number in the atrophic nonunion group had reached the same level as that in the healing group. Our findings suggest that the number of blood vessels in atrophic nonunion reaches the same level as that in healing bone, but at a later time-point. Diminished vascularity within the first three weeks, but not at a later time-point, may prevent fractures from uniting

We studied the vascular pattern of human posterior tibial tendons by injection techniques and immunohistochemically using antibodies against laminin. The intravascular volume of the posterior tibial tendon was determined using a new method of injection of a solution of . 99m. Tc and gelatin ink into the lower legs of cadavers. Three segments of 1 cm length from different regions of the human posterior tibial tendon were measured using a gamma well counter. The main blood supply arises from the posterior tibial artery. Blood vessels enter the paratenon of the posterior tibial tendon via a mesotenon from the posterior aspect. From the paratenon, the blood vessels penetrate the posterior tibial tendon and anastomose with a longitudinally orientated intratendinous network. The number of vessels in the substance of the tendon is consistently less than that in the surrounding paratenon. The distribution of blood vessels within the posterior tibial tendon is not homogeneous. In the retromalleolar region the intravascular volume was significantly reduced with a mean value of 15 μl/g of tendon tissue. There was no significant difference between the mean intravascular volumes of the proximal and distal areas (distal, 27.7 μl/g tendon tissue; proximal, 30 μl/g tendon tissue). The immunohistochemical investigation showed that there was no immunostaining for laminin in the anterior part of the tendon in the region where it passes behind the medial malleolus. This region is avascular. The most frequent site of rupture of the posterior tibial tendon is in the region behind the medial malleolus. A potential endogenous risk factor may be the limited healing potential of avascular tissue

Neuropathic changes in the foot are common with a prevalence of approximately 1%. The diagnosis of neuropathic arthropathy is often delayed in diabetic patients with harmful consequences including amputation. The appropriate diagnosis and treatment can avoid an extensive programme of treatment with significant morbidity for the patient, high costs and delayed surgery. The pathogenesis of a Charcot foot involves repetitive micro-trauma in a foot with impaired sensation and neurovascular changes caused by pathological innervation of the blood vessels. In most cases, changes are due to a combination of both pathophysiological factors. The Charcot foot is triggered by a combination of mechanical, vascular and biological factors which can lead to late diagnosis and incorrect treatment and eventually to destruction of the foot. This review aims to raise awareness of the diagnosis of the Charcot foot (diabetic neuropathic osteoarthropathy and the differential diagnosis, erysipelas, peripheral arterial occlusive disease) and describe the ways in which the diagnosis may be made. The clinical diagnostic pathways based on different classifications are presented. Cite this article: Bone Joint J 2016;98-B:1155–9

The belief that an intervertebral disc must degenerate before it can herniate has clinical and medicolegal significance, but lacks scientific validity. We hypothesised that tissue changes in herniated discs differ from those in discs that degenerate without herniation. Tissues were obtained at surgery from 21 herniated discs and 11 non-herniated discs of similar degeneration as assessed by the Pfirrmann grade. Thin sections were graded histologically, and certain features were quantified using immunofluorescence combined with confocal microscopy and image analysis. Herniated and degenerated tissues were compared separately for each tissue type: nucleus, inner annulus and outer annulus. Herniated tissues showed significantly greater proteoglycan loss (outer annulus), neovascularisation (annulus), innervation (annulus), cellularity/inflammation (annulus) and expression of matrix-degrading enzymes (inner annulus) than degenerated discs. No significant differences were seen in the nucleus tissue from herniated and degenerated discs. Degenerative changes start in the nucleus, so it seems unlikely that advanced degeneration caused herniation in 21 of these 32 discs. On the contrary, specific changes in the annulus can be interpreted as the consequences of herniation, when disruption allows local swelling, proteoglycan loss, and the ingrowth of blood vessels, nerves and inflammatory cells. In conclusion, it should not be assumed that degenerative changes always precede disc herniation. Cite this article: Bone Joint J 2013;95-B:1127–33

The main findings in this experimental work on rats fed on lathyrus odoratus (sweet-pea) meal are as follows:. 1. Growth is retarded. 2. The growth plate is disorganised and normal ossification at the metaphysis is interfered with. 3. The small blood vessels are seriously affected and probably contribute quite largely to the disorganisation and lack of calcification. 4. Alkaline phosphatase activity is increased. 5. Raising of the periosteum and laying down of new bone result in exostoses. The possible underlying etiology and the role of cement substance, endocrine factors and the blood vessels are discussed

1. Periosteal bone is supplied by periosteal vessels and endochondral bone by the nutrient artery. 2. In the earliest stages of development the metaphysis is supplied by vessels derived only from the nutrient artery. Later, metaphysial arteries derived from the periosteum take over the supply of its peripheral part, the extent of their area of supply progressively increasing. 3. In injected specimens the blood vessels approaching the epiphysial cartilaginous plate end in saccular dilations. Histological sections show these dilations to be blood-filled cartilage lacunae, with no endothelial lining and into which open the blood vessels approaching the epiphysial plate

1. In five out of eleven cases of osteoclastoma it was found that osteoclasts were present inside clearly defined blood vessels either within the tumours or in the tissues immediately surrounding the tumours. In two further cases it was found that osteoclasts protruded into the vessels although they were not lying free within the vessels. 2. The possible modes of entry of these cells into the blood stream are discussed. Although accidental dissemination of osteoclasts into damaged blood vessels could not be excluded, it was felt that the process was equally likely to be related to some inherent property of the osteoclasts. From further observations it is suggested that osteoclasts are capable of local destruction of the connective tissues of the vessel walls, probably by enzyme action. Such an action might be analogous to the processes by which, in the opinion of many, osteoclasts bring about the resorption of bone. 3. There did not seem to be any relationship between the finding of intravascular osteoclasts and the malignancy of the tumour, assessing the latter either on histological or clinical grounds. The finding of intravascular osteoclasts does not therefore appear to be of any prognostic significance

Our aim was to investigate whether nitric oxide synthase (NOS) isoforms, responsible for the generation of NO, are expressed during the healing of fractures. To localise the sites of expression compared with those in normal bone we made standardised, stabilised, unilateral tibial fractures in male Wistar rats. Immunostaining was used to determine the precise tissue localisation of the different NOS isoforms. Western blotting was used to assess expression of NOS isoform protein and L-citrulline assays for studies on NOS activity. Control tissue was obtained from both the contralateral uninjured limb and limbs of normal rats. Immunohistochemistry showed increased expression of endothelial NOS (eNOS) to be strongest in the cortical blood vessels and in osteocytes in the early phase of fracture repair. Western blot and image analysis confirmed this initial increase. Significantly elevated calcium-dependent NOS activity was observed at day 1 after fracture. Inducible NOS (iNOS) was localised principally in endosteal osteoblasts and was also seen in chondroblasts especially in the second week of fracture healing. Western blotting showed a reduction in iNOS during the early healing period. Significantly reduced calcium-independent NOS activity was also seen. No neuronal NOS was seen in either fracture or normal tissue. Increased eNOS in bone blood vessels is likely to mediate the increased blood flow recognised during fracture healing. eNOS expression in osteocytes may occur in response to changes in either mechanical or local fluid shear stress. The finding that eNOS is increased and iNOS reduced in early healing of fractures may be important in their successful repair

1. Idiopathic necrosis of the femoral head is generally considered to be a rare disease but it appears to be rather frequent in France in view of the fact that 139 cases were recorded in the orthopaedic clinic of Hôpital Cochin between 1959 and 1963. Ninety cases treated by operation have been analysed in this paper. Men are nearly exclusively affected between the ages of eighteen and seventy, with the highest incidence between thirty and fifty years of age. Both hips are affected in 52 per cent of cases. 2. The etiology is unknown, but steroid therapy was noted in 36 per cent of the cases and some history of slight injury in 30 per cent. The sudden onset of pain in half the cases suggests the obliteration of one of the blood vessels supplying the femoral head. 3. Radiographs are often normal at the time of onset of the symptoms but later they show increased density of the head localised to the antero-superior aspect, and later still collapse of this weight-bearing region. The extent of the lesion appears to be determined from the very beginning rather than to be progressive. The superior joint space is never reduced and may in fact be widened. 4. Pathological examination of the head and neck confirms necrosis of the cancellous bone and the integrity of the overlying cartilage, but shows deep to the necrotic region a highly reactive zone characterised by hypervascularity and raised metabolism. These features have been demonstrated by injection of the blood vessels and also by the uptake of phosphorus 32 and by the succino-deshydrogenase test. 5. In six cases microscopic vascular lesions were found in the antero-lateral pedicle of the femoral head. 6. The high degree of activity of the tissue deep to the necrotic zone gives some hope for revascularisation of the necrotic segment. For this reason protection from pressure may be the way to prevent dramatic collapse of the head. Rest, medical treatment and freedom from weight bearing, however, do not achieve adequate protection. Varus or rotation osteotomy of the femoral neck not only gives relief from pain but appears to prevent collapse of the femoral head. 7. When destruction of the head has already taken place good results may be expected from the insertion of a metallic prosthesis, provided the acetabulum is sound. The results are less favourable when the acetabulum has been altered by secondary arthritic change, and arthrodesis may have to be considered if the disease is unilateral or when a prosthesis has been successfully inserted on the other side

1. Autografts, isografts and homografts of fibrocartilaginous callus were observed in the anterior chamber of the eye in rats. Proliferation of cartilage ceased, endochondral ossification followed, and the end-product was a new and complete ossicle with a cortex and a marrow cavity. The size and shape of the ossicle was determined by the size and shape of the sample of callus. Thus the callus in the eye performed the function of a cartilage model like that of the developing epiphysis or a healing fracture of a long bone. 2. Fibrocartilaginous callus, heavily labelled with . 3. H-thymidine, was transplanted to the eye twenty-four hours after the last injection, when there was little if any radioactive thymidine circulating in the blood. A few small chondrocytes with labelled nuclei persisted in the cores of new bone trabeculae, but the largest part of the labelled callus was resorbed and replaced by unlabelled new bone. 3. Homografts of labelled callus produced the same results as autografts at twenty-five days, but between twenty-five and forty-five days the donor cells were destroyed by the immune response of the host. 4. Isogenous transplants in host rats treated with . 3. H-thymidine between nine and thirteen days, when the callus was invaded by new blood vessels, produced many osteogenetic cells with labelled nuclei and made it possible to trace the origin of the new bone. The label appeared in the progenitor cells within twenty-four hours. While remaining thereafter in progenitor cells, it appeared also in osteoclasts (or chondroclasts) and osteoblasts in forty-eight to seventy-two hours, and in osteocytes in ninety-six to 120 hours. Chondrocytes did not proliferate and were not labelled in the eye. 5. Homogenous transplants in host rats treated with . 3. H-thymidine between five and one days before the operation also produced new bone, but contained no labelled osteoprogenitor or bone cells after twenty-five days in the eye. At forty-five days the donor tissue had been destroyed by the immune response of the host. 6. Devitalised callus was encapsulated in inflammatory connective tissue and scar. When the dead callus was absorbed by the capillaries of the host new bone formation by induction produced a scanty deposit as a delayed event in a few instances. 7. Irrespective of whether it originated in the donor or the host, a connective-tissue cell type that proliferated rapidly and became labelled with . 3. H-thymidine was identified as a progenitor cell. Differentiation and specialisation as osteoprogenitor cells occurred after the growth of blood vessels into the interior of the callus, and developed inside of excavation chambers in cartilage. Except that the interaction of the donor tissue and host cells leading to new bone formation by induction takes place in the interior of the excavation chamber, the biophysico-chemical mechanism is unknown

The ability of mesenchymal stem cells (MSCs) to differentiate in vitro into chondrocytes, osteocytes and myocytes holds great promise for tissue engineering. Skeletal defects are emerging as key targets for treatment using MSCs due to the high responsiveness of bone to interventions in animal models. Interest in MSCs has further expanded in recognition of their ability to release growth factors and to adjust immune responses. Despite their increasing application in clinical trials, the origin and role of MSCs in the development, repair and regeneration of organs have remained unclear. Until recently, MSCs could only be isolated in a process that requires culture in a laboratory; these cells were being used for tissue engineering without understanding their native location and function. MSCs isolated in this indirect way have been used in clinical trials and remain the reference standard cellular substrate for musculoskeletal engineering. The therapeutic use of autologous MSCs is currently limited by the need for ex vivo expansion and by heterogeneity within MSC preparations. The recent discovery that the walls of blood vessels harbour native precursors of MSCs has led to their prospective identification and isolation. MSCs may therefore now be purified from dispensable tissues such as lipo-aspirate and returned for clinical use in sufficient quantity, negating the requirement for ex vivo expansion and a second surgical procedure. In this annotation we provide an update on the recent developments in the understanding of the identity of MSCs within tissues and outline how this may affect their use in orthopaedic surgery in the future. Cite this article: Bone Joint J 2014;96-B:291–8

Aims

Given the possible radiation damage and inaccuracy of radiological investigations, particularly in children, ultrasound and superb microvascular imaging (SMI) may offer alternative methods of evaluating new bone formation when limb lengthening is undertaken in paediatric patients. The aim of this study was to assess the use of ultrasound combined with SMI in monitoring new bone formation during limb lengthening in children.

The blood supply of the vertebral column of the rabbit has been studied. A description of the embryological development of the blood supply is followed by a description of the blood vessels supplying the adult vertebra

Aims

The aim of this study was to evaluate the optimal deep tissue specimen sample number for histopathological analysis in the diagnosis of periprosthetic joint infection (PJI).

A 59-year-old woman with calcific tendinitis in her right shoulder underwent extracorporeal shock-wave lithotripsy. Three years and four months later she presented with osteonecrosis of the head of the right humerus. It is known that shock waves in patients with urological disorders can damage blood vessels. A possible reason for the development of osteonecrosis in this patient may have been damage to the blood supply of the head of the humerus

Angiogenin, a potent blood vessel inducing protein, was implanted into experimentally injured menisci of 75 New Zealand white rabbits. Localised neovascularisation occurred in 52% of the angiogenin-treated animals, and in 9% of the controls. Neovascularisation induced by angiogenin may enhance healing of injuries within the poorly vascularised meniscal fibrocartilage, and improve the results of meniscal repair

1. The behaviour of various types of cortical bone graft has been studied in rabbits by histological and injection techniques. 2. The results suggest that penetration of the graft by blood vessels plays an important part in the incorporation of autogenous and homogenous grafts. 3. Autogenous and homogenous grafts are both incorporated–the latter more slowly than the former–but heterogenous grafts are rejected. The reasons for this rejection are discussed

In an eight-year period we treated 51 cases of vascular injury associated with fractures and/or dislocations or soft-tissue injuries of the limbs. We relied on a clinical diagnosis and immediate exploration of blood vessels rather than the time-consuming procedure of arteriography. All patients were operated on by the orthopaedic residents on duty and not by vascular surgeons. Only 17 (33%) were repaired within six hours of injury. Limb viability with good function was obtained in 38. Complications included six deaths, four amputations, two renal failures and delayed occlusion in one case

Revascularisation of syngeneic and allogeneic intramuscular bone grafts have been studied using radioactive microspheres to measure the ingrowth of blood vessels. New bone formation and resorption were measured by 85strontium uptake and by graft weight reduction. Revascularisation, and mineralisation rate were significantly higher in syngeneic grafts than in allogeneic grafts at two, three and six weeks after implantation. The syngeneic grafts lost weight faster indicating that the allogeneic grafts resorbed more slowly. The ingrowth of new vessels is impaired in allogeneic bone, and this probably inhibits the rate of bone formation and resorption of the grafts

An experimental method is described which permits observations on the early stages of repair after acute displacement of the upper femoral epiphysis. Because the epiphysis is intra-articular, displacement brings about avascular necrosis which is slowly repaired by ingrowth of callus and blood vessels from the stump of the neck. As the bulk of the epiphysial plate remainsattached to the epiphysis, it acts as a barrier to successful revascularisation. Deliberate removal of the epiphysial cartilage allows earlier revascularisation. It is suggested that in clinical cases reduction be done through the epiphysial plate rather than through the neck, and that it be accompanied by curettage of the remaining part of the epiphysial plate from the under surface of the head

We studied the morphology of the haversian canals in the osteopenic cortical bone of the medial femoral neck from patients with rheumatoid arthritis and compared the findings with those in patients with osteoarthritis and with uncomplicated coxa valga. In the rheumatoid bone, the diameters of the canals were larger and many more contained osteoclasts. Fewer haversian canals showed only lining cells than in the osteoarthritic or coxa valga patients. In bone from rheumatoid patients, especially in canals with osteoclasts, small blood vessels were frequently lined by tall endothelial cells with an infiltration of mononuclear cells. These morphological differences are discussed with reference to the possible mechanisms of loss of cortical bone in rheumatoid arthritis and other conditions

1. This case is presented to illustrate two etiological factors in tendon rupture occurring in one patient. 2. The rupture of the long head of the biceps brachii muscle appears to have been of acute traumatic origin. 3. Bilateral simultaneous rupture of the calcaneal tendons is rare, but it seems probable that the cortico-steroid therapy was the etiological factor in this case. 4. It has been suggested that degeneration in the tendon is caused by ischaemia, secondary to hypertrophy of the tunica media and narrowing of the medium calibre blood vessels. Betamethazone could possibly have aggravated, or may even have caused these changes, and the periarteriolar changes found in the biopsy specimen would tend to support this theory

In this work the role of the blood vessels surrounding the epiphysial growth plate has been studied. The nutritional dependence of the proliferative cells on the epiphysial vessels has been established whereas the metaphysial vessels were seen to take part in calcification and ossification at the metaphysis. As it does not seem likely that the blood circulating in the two systems of vessels had a different constitution, particularly in hormones and vitamins, it seems permissible to assume that it is the characteristics, particularly in shape and number, of such vessels that make growth the orderly process it is, with the repeated birth of a cell at the top of a column and burial at the bottom end. But, despite this undeniable role of the vessels, growth depends on the ability of the cartilage cell to form a matrix which, in due course, will be avid for apatite crystals

1. The form and distribution of the blood vessels within the adult human femoral head are described. 2. It has been found possible to delimit the proximal femoral epiphysis in mature years by reference to arterial form alone. 3. Two morphologically different sets of vessels are described interposed between the arterioles and venules of the bone marrow. One, a true capillary bed, lies mainly within the fat marrow; the other, constituted by sinusoids, lies within the red marrow. The departure of these findings from current views is noted. 4. A capillary system is described in relationship to the calcified zone of the articular cartilage. 5. No evidence has been found in support of the common belief that the circulation within the femoral head decreases quantitatively with advancing age

1. Twenty-five lower limbs, amputated above the knee for senile atherosclerosis with peripheral gangrene, have been investigated radiologically and histologically to determine the vascular patterns in ischaemic bone with particular reference to the tibia. These have been contrasted with the patterns found in non-atherosclerotic tubular bone. 2. The principal changes are the development of a diffuse vascularisation of compact and spongy bone; a widening of Haversian spaces which come to contain a variable number of sinusoidal blood vessels; and an increasing periosteal participation in cortical nutrition which is related to the severity and chronicity of the ischaemic process. 3. Views on the normal blood supply of long bones are discussed, and evidence is presented for regarding this as discrete and end-arterial in nature; in particular it is suggested that the normal cortex has a wholly medullary, centrifugal, arterial supply

We studied the presence of sensory nerves by immunohistochemistry in the interface membranes of hip prostheses after aseptic loosening. Substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) were analysed as was protein gene product (PGP) 9.5, a general marker for nerve fibres. We identified nerve fibres in all samples but differences in their density were found. SP- and NKA-positive fibres were predominantly non-vascular, forming varicose nerve terminals. CGRP-immunoreactive nerve fibres with varicose terminals were seen mostly close to blood vessels, but also as free nerve endings. Sensory neuropeptides participate not only in nociception but also stimulate immune cells to release cytokines. The presence of sensory nerves in the interface membrane may reflect a pathophysiological response contributing to the aseptic loosening of hip prostheses

Aims

The aim of this study was to determine the rate of indocyanine green (ICG) staining of bone and soft-tissue tumours, as well as the stability and accuracy of ICG fluorescence imaging in detecting tumour residuals during surgery for bone and soft-tissue tumours.

1. Serial arteriograms show not only the anatomical distribution of blood vessels but also the functional state and activity of the peripheral circulation. The technique is of value in the diagnosis of tumours of soft tissues and bone, and particularly in the differential diagnosis of bone tumours from chronic osteomyelitis. It may be used to assess the response of malignant bone tumours to treatment by irradiation. 2. In malignant bone tumours, serial arteriograms show irregular formation of new vessels of uniform diameter, "blood pools," and increased rapidity of flow from the arterial to the venous systems. 3. In osteoclastomas there is new vessel formation and an appearance of "blood pools," but less rapid filling of the veins. In simple tumours there is no new formation of vessels. The tumour itself is often relatively avascular. 4. In osteomyelitis there is no new formation of vessels but only dilatation of existing vessels. The vessels retain their orderly and regular arrangement of successive branches of gradually decreasing diameter

Aims

Surgical site infection (SSI) after soft-tissue sarcoma (STS) resection is a serious complication. The purpose of this retrospective study was to investigate the risk factors for SSI after STS resection, and to develop a nomogram that allows patient-specific risk assessment.

Pathological fractures due to metastasis with destruction of the acetabulum and central dislocation of the hip present a difficult surgical challenge. We describe a series using a single technique in which a stable and long-lasting reconstruction was obtained using standard primary hip replacement implants augmented by strong, fully-threaded steel rods with cement and steel mesh, where required. Between 1997 and 2006, 19 patients with a mean age of 66 years (48 to 83) were treated using a modified Harrington technique. Acetabular destruction was graded as Harrington class II in six cases and class III in 13. Reconstruction was achieved using three 6.5 mm rods inserted through a separate incision in the iliac crest followed by augmentation with cement and a conventional cemented Charnley or Exeter primary hip replacement. There were no peri-operative deaths. At the final follow-up (mean 25 months (5 to 110)) one rod had fractured and one construct required revision. Of the 18 patients who did not require revision, 13 had died. The mean time to death was 16 months (5 to 55). The mean follow-up of the five survivors was 31 months (18 to 47). There were no cases of dislocation, deep infection or injury to a nerve, the blood vessels or the bladder

1. A study has been made of the blood supply of the human patella. There are two main systems, one penetrating the middle third of the anterior surface and the other entering the lower pole of the bone behind the patellar ligament. 2. The relationship between these findings and the complication of avascular necrosis of the upper fragment of the patella after fracture is discussed. Forty-one cases of necrosis after operation have been studied and notes made on the pathological, clinical and radiological evolution of the condition. Whatever the severity of the ischaemic necrosis the prognosis was not substantially affected and good function was observed in all knees six months after injury. 3. The surgical implications of the vascular anatomy are discussed. It is pointed out that surgical intervention may damage the blood vessels entering the anterior surface of the bone and that circumferential repair of patellar fractures may strangle the vessels in their peripatellar course. 4. If removal of one-half of the patella after a transverse fracture is indicated, vascular studies indicate that the upper fragment should be removed

1. Volkmann’s ischaemia is a real and threatening complication of fracture of the femur, and it is more common than reports in the literature would suggest. 2. The early signs and symptoms in the calf are ominous whereas the early vascular signs of a good tibial pulse, colour and temperature are often misleading. 3. Muscle decompression with or without arterial exploration has proved to be of no value. 4. Early recognition and radical treatment are imperative. Temporary paralysis of the lumbar sympathetic outflow has been shown to be an effective measure. 5. Transfixion of the calcaneum with a Kirschner wire for traction has the advantage of eliminating all bandages, suspending the tender calf and preventing an equinovarus deformity. 6. The only essential difference between the histological appearance of muscle which recovers and that which does not appears to be degeneration of muscle nuclei. The significance of engorged blood vessels remains in doubt. 7. Histological studies suggest that despite the typical gross appearance of an infarct some regeneration of muscle may occur

1. A study of late segmental collapse in twelve femoral heads shows that it may not develop until two and a half years after the fracture. 2. Until the articular surfaces had collapsed the patients usually had no symptoms. The fractures were united and there was no obvious radiographic evidence of ischaemic necrosis. 3. There was histological evidence that the whole of the femoral heads had been necrotic at one time. The term late segmental collapse is more appropriate than late segmental necrosis. 4. The blood vessels of the ligamentum teres played little or no part in revascularisation which, when it occurred, was almost entirely across the fracture line. 5. In only one femoral head was revascularisation approaching completion and apparently continuing. In the other eleven much of the head remained necrotic and the process appeared to have halted. 6. An increase in radiological density was caused by new bone laid down on unresorbed necrotic trabeculae and was most prominent behind the line of revascularisation when the process had halted. 7. Trabecular collapse was evident within dead bone. In ten of the femoral heads it occurred in the subchondral region and in four just beyond the junction of reossified and dead bone. 8. Osteoarthritic changes occurred in the cartilage covering revascularised bone at the periphery of the head, especially when collapse was severe

Osteoarthritis, as seen in the hip, is a disease which eventually embraces all the tissues of the joint but begins as a reaction of the juxta-chondral blood vessels to a degeneration of the articular cartilage; this reaction results in a hyperaemia of the bone. To our surprise we found that daily use preserves rather than "wears out" articular cartilage; indeed inadequate use is the commonest cause of cartilage degeneration and ensuing vascular invasion. To this factor are added the effects of excessive pressure in the many patients who require surgical treatment for advanced osteoarthritis of a hip the seat of some anatomical incongruity. This etiology based on cartilage suffering does not exclude, but indeed explains, the osteoarthritis implanted on joints of a normal shape which have been previously affected by acute or chronic inflammation or by hormonal dysfunction, such as acromegalic osteoarthritis. The stimulus to vessel growth and invasion is the same in all these cases—namely cartilage damage. Once the vessels have entered the cartilage the bone and marrow of the osteophyte are inevitably laid down. What is so damaging in osteoarthritis seems to be not the degeneration of the cartilage but the vigorous and persistent attempt at repair, an attempt which aggravates the already disordered function of the joint not only by osteophyte formation but by the hypervascularity which weakens the structure of the bone beyond the point where it can carry its increased load. The collapse that follows provokes further reparative efforts with the same deplorable results. The osteoarthritic process thus appears to be an attempt to transform a decaying joint into a youthful one and for this, as in the miraculous rejuvenation depicted in Goethe's Faust, a high price must ultimately be paid

Aims

The aim of this study is to develop a core set of outcome domains that should be considered and reported in all future trials of childhood limb fractures.

1. Loss of osteocytes in the bone trabeculae of the femoral heads of "normal" elderly patients was patchy and distinguishable from that resulting from avascular necrosis after fracture. 2. Changes in the haemopoietic marrow were the earliest and most sensitive indicators of ischaemia, loss of osteocytes rarely being complete until three or four weeks after fracture. 3. In 109 femoral heads removed more than sixteen days after fracture the viability could be determined by histological means. All of these had suffered some damage to the vascular supply but in a number the head remained alive apart from the region of the fracture line. These heads were nourished by the blood vessels of the ligamentum teres and sometimes by retinacular arteries, usually of the inferior group. 4. Some femoral heads became completely necrotic following fracture, others were only partly affected. A variable amount of the subfoveal region commonly remained alive and it was from this site that revascularisation spread into the head. The upper segment of the femoral head least often remained alive and its subchondral region was usually the last to revascularise. 5. In a group of unselected femoral heads a third remained alive following fracture and two-thirds were partly or completely necrotic. 6. Femoral heads which were partly necrotic appeared capable of uniting and completely revascularising, there being invasion of the necrotic bone by vessels from across the fracture line and from the ligamentum teres. This contrasted with the completely necrotic femoral heads described elsewhere in this issue which united but in the absence of proliferation of ligamenturn teres vessels failed to revascularise completely and developed late segmental collapse. 7. Avascular necrosis did not appear to be the sole cause of non-union. 8. Necrotic bone showed no alteration in radiological density. Reossifying bone in areas of revascularisation sometimes caused an absolute increase of radiodensity especially when associated with halted revascularisation. This increase of radiological opacity was the result of deposition of new on dead bone with broadening of the trabeculae. Marrow calcification was minimal. 9. Obliterative sclerosis of venules in the ligamentum teres was found in "normal" patients even in infancy. No thrombosis was seen in the ligaments following fracture but where the femoral heads were completely necrotic and not revascularised the ligaments were often also necrotic. 10. There appeared to be no increase in degenerative changes in the articular cartilage of the femoral heads following fracture compared with fifty elderly controls. Some loss of chondrocytes in the deep zone of the weight-bearing area was found in about a quarter of the femoral heads. In only one head was the cartilage almost completely acellular. An almost normal depth and a smooth contour of the articular cartilage were retained

Aims

We have previously reported cryoablation-assisted joint-sparing surgery for osteosarcoma with epiphyseal involvement. However, it is not clear whether this is a comparable alternative to conventional joint arthroplasty in terms of oncological and functional outcomes.

Aims

The aim of this study was to analyze the complications and outcomes of treatment in a series of previously untreated patients with a primary aneurysmal bone cyst (ABC) who had been treated by percutaneous sclerosant therapy using polidocanol.

Aims

Although internal hemipelvectomy is associated with a high incidence of morbidity, especially wound complications, few studies have examined rates of wound complications in these patients or have identified factors associated with the consequences. The present study aimed to: 1) determine the rate of wound and other complications requiring surgery after internal hemipelvectomy; and 2) identify factors that affect the rate of wound complications and can be used to stratify patients by risk of wound complications.

Aims

It is increasingly appreciated that coordinated regulation of angiogenesis and osteogenesis is needed for bone formation. How this regulation is achieved during peri-implant bone healing, such as osseointegration, is largely unclear. This study examined the relationship between angiogenesis and osteogenesis in a unique model of osseointegration of a mouse tibial implant by pharmacologically blocking the vascular endothelial growth factor (VEGF) pathway.

Stem cells are defined by their potential for self-renewal and the ability to differentiate into numerous cell types, including cartilage and bone cells. Although basic laboratory studies demonstrate that cell therapies have strong potential for improvement in tissue healing and regeneration, there is little evidence in the scientific literature for many of the available cell formulations that are currently offered to patients. Numerous commercial entities and ‘regenerative medicine centres’ have aggressively marketed unproven cell therapies for a wide range of medical conditions, leading to sometimes indiscriminate use of these treatments, which has added to the confusion and unpredictable outcomes. The significant variability and heterogeneity in cell formulations between different individuals makes it difficult to draw conclusions about efficacy. The ‘minimally manipulated’ preparations derived from bone marrow and adipose tissue that are currently used differ substantially from cells that are processed and prepared under defined laboratory protocols. The term ‘stem cells’ should be reserved for laboratory-purified, culture-expanded cells. The number of cells in uncultured preparations that meet these defined criteria is estimated to be approximately one in 10 000 to 20 000 (0.005% to 0.01%) in native bone marrow and 1 in 2000 in adipose tissue. It is clear that more refined definitions of stem cells are required, as the lumping together of widely diverse progenitor cell types under the umbrella term ‘mesenchymal stem cells’ has created confusion among scientists, clinicians, regulators, and our patients. Validated methods need to be developed to measure and characterize the ‘critical quality attributes’ and biological activity of a specific cell formulation. It is certain that ‘one size does not fit all’ – different cell formulations, dosing schedules, and culturing parameters will likely be required based on the tissue being treated and the desired biological target. As an alternative to the use of exogenous cells, in the future we may be able to stimulate the intrinsic vascular stem cell niche that is known to exist in many tissues. The tremendous potential of cell therapy will only be realized with further basic, translational, and clinical research.

Cite this article: Bone Joint J 2019;101-B:361–364.

Aims

The Intraosseous Transcutaneous Amputation Prosthesis (ITAP) may improve quality of life for amputees by avoiding soft-tissue complications associated with socket prostheses and by improving sensory feedback and function. It relies on the formation of a seal between the soft tissues and the implant and currently has a flange with drilled holes to promote dermal attachment. Despite this, infection remains a significant risk. This study explored alternative strategies to enhance soft-tissue integration.

Vascular injuries during total hip arthroplasty (THA) are rare but when they occur, have serious consequences. These have traditionally been managed with open exploration and repair, but more recently there has been a trend towards percutaneous endovascular management.

We performed a systematic review of the literature to assess if this change in trend has led to an improvement in the overall reported rates of morbidity and mortality during the last 22 years in comparison with the reviews of the literature published previously.

We found a total of 61 articles describing 138 vascular injuries in 124 patients. Injuries because of a laceration were the most prevalent (n = 51, 44%) and the most common presenting feature, when recorded, was bleeding (n = 41, 53.3%). Delay in diagnosis was associated with the type of vascular lesion (p < 0.001) and the clinical presentation (p = 0.002).

Open exploration and repair was the most common form of management, however percutaneous endovascular intervention was used in one third of the injuries and more constantly during the last 13 years.

The main overall reported complications included death (n = 9, 7.3%), amputation (n = 2, 1.6%), and persistent ischaemia (n = 9, 7.3%). When compared with previous reviews there was a similar rate of mortality but lower rates of amputation and permanent disability, especially in patients managed by endovascular strategies.

Cite this article: Bone Joint J 2015;97-B:1447–55.

The number of arthroplasties being performed increases each year. Patients undergoing an arthroplasty are at risk of venous thromboembolism (VTE) and appropriate prophylaxis has been recommended. However, the optimal protocol and the best agent to minimise VTE under these circumstances are not known. Although many agents may be used, there is a difference in their efficacy and the risk of bleeding. Thus, the selection of a particular agent relies on the balance between the desire to minimise VTE and the attempt to reduce the risk of bleeding, with its undesirable, and occasionally fatal, consequences.

Acetylsalicylic acid (aspirin) is an agent for VTE prophylaxis following arthroplasty. Many studies have shown its efficacy in minimising VTE under these circumstances. It is inexpensive and well-tolerated, and its use does not require routine blood tests. It is also a ‘milder’ agent and unlikely to result in haematoma formation, which may increase both the risk of infection and the need for further surgery. Aspirin is also unlikely to result in persistent wound drainage, which has been shown to be associated with the use of agents such as low-molecular-weight heparin (LMWH) and other more aggressive agents.

The main objective of this review was to summarise the current evidence relating to the efficacy of aspirin as a VTE prophylaxis following arthroplasty, and to address some of the common questions about its use.

There is convincing evidence that, taking all factors into account, aspirin is an effective, inexpensive, and safe form of VTE following arthroplasty in patients without a major risk factor for VTE, such as previous VTE.

Cite this article: Bone Joint J 2017;99-B:1420–30.