1 . The magnitude of the problem of congenital anomalies becomes evident when one takes into consideration the fact that they cause the death of approximately one quarter of the human race either before or shortly after birth, and handicap an appreciable proportion of the survivors throughout their lives. Further, a significant percentage of infants judged to be normal at birth are found in later life to suffer from "disguised" anomalies of the skeleton and soft tissues. Though the study of genetic factors leading to congenital defects has attracted a great deal of attention during the last few decades, the importance of environmental causes of human malformations has received relatively less emphasis. The association of congenital anomalies such as cataract and cardiac septal defects with maternal intercurrent infection of rubella during the early months of pregnancy demonstrates clearly that changes in the germplasm cannot always be invoked as the cause of developmental abnormalities. Congenital malformations that are sometimes genetically determined, such as microphthalmos, cleft palate, and certain skeletal abnormalities, can be caused in the offspring not only by maternal nutritional deficiencies and x-radiation but also, at least in some animals, such as chickens, rats and rabbits, by the introduction of certain substances like insulin into the environment of the embryo during its development. 2. Since very little is known of the detailed histology of the early human embryo, the histological examination of cases of perverted growth is mainly limited to aborted foetuses which, unfortunately, tend to present varying degrees of post-mortem degeneration before accurate histological methods can be applied. It is exactly in this field that animal experiments can offer valuable help. According to Mall and other embryologists the pathological changes that take place in human foetuses and those obtained experimentally in animals are not merely "analogous or similar but identical.". 3. An attempt has been made to review, in some detail, the more important work which has been carried out on experimental teratogenesis, on the epidemiological implications of developmental arrests in humans, and on foetal abnormalities associated with maternal metabolic and hormonal disorders during pregnancy. 4. The technique employed for injection of insulin into the egg yolk has been described. Methods used for the estimation of blood sugar in chick embryos at various stages after injection of insulin and special histochemical techniques for localising polysaccharides in cartilage have been outlined. 5. A few salient experimental results have been tabulated, and some of the insulin-induced abnormalities have been illustrated. 6. The possible mechanism of action of insulin in the causation of the various developmental anomalies has been discussed. Broadly speaking, insulin seems to affect primarily the part or tissue which is in the most active stage of growth or differentiation at the time of the injection. Within the range of 0·05 to 6 units of insulin employed, the incidence, severity and distribution of the deformities appear to increase with the dose of the hormone. It has been observed that the hypoglycaemia caused by insulin injection is not counteracted till about the twelfth day of incubation, presumably because of excessive accumulation of glycogen in the yolk-sac membrane immediately after the injection, and because of lack of glycogen storage in the embryonic liver and the absence of active secretion in the endocrine glands concerned with the carbohydrate metabolism of the embryo. It has been suggested that this unchecked hypoglycaemia may deprive the mesenchyme, pre-cartilage and cartilage of glycogen and mucopolysaccharides (chondroiten-sulphuric acid complexes), depending on the time of injection and the dose of insulin, and thus not only give rise to a variety of single and multiple deformities in the cartilaginous skeleton but also interfere with the normal endochondral ossification, resulting in a generalised developmental disturbance of bone resembling osteogenesis imperfecta in the human. 7. Insulin-induced abnormalities can be prevented to a remarkable extent by injecting nicotinamide and riboflavin into eggs along with insulin. 8. The question of the practical application of the knowledge gained from experimental observations on insulin-induced developmental abnormalities in explaining the possible causation of congenital anomalies in humans by genetic and environmental teratogenic factors, has been discussed. It is suggested that the orderly progression from the mesenchymatous condensation to cartilage, and then through calcified cartilage to bone, may be disturbed by these teratogenic factors at critical phases during the development of the embryo, and a variety of single and multiple skeletal deformities may thus be induced. 9. A plea is made for routine pathological and radiological examination of aborted foetuses and stillborn infants more or less on the lines followed for experimentally induced deformities with a view to applying the knowledge gained from animal experiments to a better understanding of the etiology and pathology of human congenital anomalies. 10. As regards the possible prevention of these deformities, it is not always easy to offer sound eugenic advice in the cases of congenital malformations determined partly or completely by genetic factors, for two important reasons. First, it is often difficult to distinguish between genetically determined congenital anomalies and their phenocopies. Secondly, genetically determined developmental defects sometimes show surprisingly variable expressivity and penetrance. For the conditions in which both genetic and environmental factors are involved, the most profitable immediate line of attack would be on the environmental factors. A relatively simpler problem is presented by the malformations which are, for all practical purposes, entirely caused by environmental factors. Measures to prevent congenital anomalies caused by prenatal rubella, such as exposure of girls to the disease during childhood and protection of pregnant women during the early stages of pregnancy by immune serum, are under active consideration. 11 . Further energetic investigation of the causes of permaturity, stillbirths, monstrosities and congenital malformations is urgently needed, before embarking on a successful programme for prevention. "The day of successful prophylaxis is not yet, but it is much nearer than seemed possible a few years ago."

Persistent post-surgical pain remains a problem after knee replacement with some studies reporting up to 20% incidence. Pain is usually felt by those who do not operate to be a monolithic entity. All orthopaedic surgeons know that this is not the case. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is fortunately becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain. Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions. The name neuropathic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed especially by the author of this abstract. The optimum treatment I have found is lumbar sympathetic blocks. Perceived pain is the largest group. It does not matter what you tell the patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Some of this pain is actually mechanical, especially in those with no benefits such as hairstylists. Perceived pain is widespread. The classic treatise on this is Dr. Ian McNabb's book “Backache”. It should be studied by all orthopaedic surgeons, who wish to understand pain complaints.

Any experienced knee surgeon will have his list of red flags or caveats. These are often politically incorrect and this information is transferred to young surgeons, usually in dim bars late at night. I will list only a few. If the patient comes in with a form asking for a disability pension on the first visit. If the patient's mother answers the questions. If the patient comes in taking massive doses of opiates. If the patient is referred to you by a surgeon, who does more knee replacements than you do. There is also the recently described Fern Silverman's syndrome.

Persistent post-surgical pain (PPSP) remains a problem after knee replacement with some studies reporting up to 20% incidence. Pain is usually felt by those who do not operate to be a monolithic entity. All orthopaedic surgeons know that this is not the case. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain. Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions. The name neuropathic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS-type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed. The optimum treatment I have found is lumbar sympathetic blocks. Lyrica, Gabapentin and Cymbalta may also help. Perceived pain is the largest group. It does not matter what you tell the patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Perceived pain is widespread. The classic treatise, Dr. Ian McNabb's book “Backache”, should be studied by all who wish to understand pain complaints.

Any experienced knee surgeon will have his list of red flags or caveats. I will list only a few. If the patient comes in with a form asking for a disability pension on the first visit. If the patient's mother answers the questions. If the patient comes in taking massive doses of opiates. If the patient is referred to you by a surgeon who does more knee replacements than you do.

There are other issues such as good old fibromyalgia, which appears to have gone the way of the dodo. It has been replaced by something equally silly called central sensitization. The theory of central sensitization is that if one has pain somewhere or other for three months or six months or whatever, there are going to be changes in the brain and spinal cord. It then does not matter what happens to the original pain, i.e. whether or not it goes away, the pain will persist because of the changes in the brain, hence, the title of the pain in the brain syndrome. If this theory was correct, we might as well all go home because we have all been wasting our time for the last 30 years because none of our patients would get any better. After all, all of our patients have had pain for a lot longer than three months, many of them have been involved in trauma and sometimes, compensation is at issue. The pain in the brain theory, therefore, sounds about as realistic as the flat earth society or the treatment of Galileo.

Persistent post-surgical pain (PPSP) remains a problem after knee replacement with some studies reporting up to 20% incidence. At its most basic level, pain can be divided into two categories, mechanical and non-mechanical.

Mechanical pain is like the pain of a fresh fracture. If the patient does not move, the pain is less. This type of pain is relieved by opiates. Mechanical pain is seen following knee replacement, but is fortunately becoming less frequent. It is caused by a combination of malrotations and maltranslations, often minor, which on their own would not produce problems. The combination of them, however, may produce a knee in which there is overload of the extensor mechanism or of the medial stabilizing structures. If these minor mechanical problems can be identified, then corrective surgery will help.

Non-mechanical pain is present on a constant basis. It is not significantly worsened by activities. Opiates may make the patient feel better, but they do not change the essential nature of the pain. Non-mechanical pain falls into three broad groups, infection, neuropathic and perceived pain.

Infection pain is usually relieved by opiates. Since some of this pain is probably due to pressure, its inclusion in the non-mechanical pain group is questionable, but it is better left there so that the surgeon always considers it. Low grade chronic infection can be extremely difficult to diagnose. Loosening of noncemented knee components is so rare that when it is noted radiologically, infection should be very high on the list of suspicions.

The name neurogenic pain suggests that we know much more about it than we do in reality. Causalgia or CRPS-type two is rare following knee replacement. CRPS type one or reflex sympathetic dystrophy probably does exist, but it is probably over-diagnosed especially by the author of this abstract. The optimum treatment I have found is lumbar sympathetic blocks. Lyrica, Gabapentin and Cymbalta may also help.

Perceived pain is the largest group. It does not matter what you tell patient, some believe a new knee should be like a new car, i.e. you step into it and drive away. The fact that they have to work to make it work is horrifying. Some of this pain is actually mechanical, especially in those with no benefits such as hairstylists. Perceived pain is widespread. The classic treatment on this is Dr. Ian McNabb's book “Backache”. It should be studied by all orthopaedic surgeons, who wish to understand pain complaints.

There are other issues such as good old fibromyalgia, which appears to have gone the way of the dodo. It has been replaced by something equally silly called central sensitization. The theory of central sensitization is that if one has pain somewhere or other for three months or six months or whatever, there are going to be changes in the brain and spinal cord. It then does not matter what happens to the original pain, i.e. whether or not it goes away, the pain will persist because of the changes in the brain, hence, the title of the pain in the brain syndrome.

If this theory was correct, we might as well all go home because we have all been wasting our time for the last 30 years because none of our patients would get any better. After all, all of our patients have had pain for a lot longer than three months, many of them have been involved in trauma and sometimes, compensation is at issue. The pain in the brain theory, therefore, sounds about as realistic as the flat earth society or the treatment of Galileo.

There are two types of pain, mechanical and non-mechanical. Mechanical pain hurts with movement/use, is not constant and is helped by morphine-type products. Non-mechanical pain is different. It is present 24 hours a day, often worse at night, and except for the pain of infection, is not relieved by morphine-type products.

If the cause of mechanical pain can be determined, it can be corrected by an operation. The usual cause of postoperative mechanical knee pain nowadays is multifactorial, i.e. a combination of minor errors, none of which on their own would require revision.

Non-mechanical pain, other than infection, is much more difficult to handle. The commonest cause is not really a pain complaint, it is disappointment due to a failure of expectation. It does not matter how often you tell patients, some patients still think they should step in a drive away. A lot of these failures of expectations become much more realistic by the end of year one.

There are several other categories. Incipient osteoarthritis or sensitive people (The Princess and the Pea). If the pain complaints were severe with minimal arthritis, an operation is not likely to help.

The patient on disability for no clear reason is unlikely to get a good result and Workmen's Compensation Board and motor vehicle accident patients are also a very bad prognostic sign and will often produce the postoperative painful knee. Preoperative use of large doses of morphine is also a very bad sign. It is not clear if it is the morphine, which influences the patient or the patient, who influences the morphine.

There are several pain syndromes, some of which are purely psychiatric such as Conversion Disorders and Somatoform Pain Disorders. Treatment of purely psychiatric conditions should be a referral to a psychiatrist is in order.

Complex regional pain syndrome is an organic pain disorder. Type 2 is causalgia or an actual nerve injury. This is unusual following knee replacement other than the odd drop foot, which even after recovery, leaves an area of dysaethesia on the dorsum of the foot. Type 1 used to be called reflex sympathetic dystrophy. This is not uncommon after total knee replacement. I managed to collect more than 40 cases. One problem is that the diagnosis to some extent is a diagnosis of exclusion. If the diagnosis can be made, then treatment is available including Cymbalta, Lyrica or Gabapentin. I have found most success with lumbar sympathetic blocks, but it is difficult to find someone, who can do these. Some patients have been treated with implantable electrical spinal stimulators with variable results.

The current flavour of the month pain syndrome is called central sensitization. The theory is that if someone has pain for more than six months, then there will be changes in the brain, which will remain after the original pain goes away, hence, the title the pain in the brain syndrome. If this theory were correct, then we as arthroplasty surgeons have been collectively wasting our time for the last 40 years as no patient would have recovered. The likelihood, therefore, of this theory having any basis in reality is pretty remote.

Fortunately, by the end of year one, the vast majority of our knee replacement patients are reasonably content with the procedure.

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.

Introduction and Objective. Malunion after trauma can lead to coronal plane malalignment in the lower limb. The mechanical hypothesis suggests that this alters the load distribution in the knee joint and that that this increased load may predispose to compartmental arthritis. This is generally accepted in the orthopaedic community and serves as the basis guiding deformity correction after malunion as well as congenital or insidious onset malalignment. Much of the literature surrounding the contribution of lower limb alignment to arthritis comes from cohort studies of incident osteoarthritis. There has been a causation dilemma perpetuated in a number of studies - suggesting malalignment does not contribute to, but is instead a consequence of, compartmental arthritis. In this investigation the relationship between compartmental (medial or lateral) arthritis and coronal plane malalignment (varus or valgus) in patients with post traumatic unilateral limb deformity was examined. This represents a specific niche cohort of patients in which worsened compartmental knee arthritis after extra-articular injury must rationally be attributed to malalignment. Materials and Methods. The picture archiving system was searched to identify all 1160 long leg x ray films available at a major metropolitan trauma center over a 12-year period. Images were screened for inclusion and exclusion criteria, namely patients >10 years after traumatic long bone fracture without contralateral injury or arthroplasty to give 39 cases. Alignment was measured according to established surgical standards on long leg films by 3 independent reviewers, and arthritis scores Osteoarthritis Research Society International (OARSI) and Kellegren-Lawrence (KL) were recorded independently for each compartment of both knees. Malalignment was defined conservatively as mechanical axis deviation outside of 0–20 mm medial from centre of the knee, to give 27 patients. Comparison of mean compartmental arthritis score was performed for patients with varus and valgus malalignment, using Analysis of Variance and linear regression. Results. In knees with varus malalignment there was a greater mean arthritis score in the medial compartment compared to the contralateral knee, with OARSI scores 5.69 vs 3.86 (0.32, 3.35 95% CI; p<0.05) and KL 2.92 vs 1.92 (0.38, 1.62; p<0.005). There was a similar trend in valgus knees for the lateral compartment OARSI 2.98 vs 1.84 (CI −0.16, 2.42; p=0.1) and KL 1.76 vs 1.31 (CI −0.12, 1.01; p=0.17), but the evidence was not conclusive. OARSI arthritis score was significantly associated with absolute MAD (0.7/10mm MAD, p<0.0005) and Time (0.6/decade, p=0.01) in a linear regression model. Conclusions. Malalignment in the coronal plane is correlated with worsened arthritis scores in the medial compartment for varus deformity and may similarly result in worsened lateral compartment arthritis in valgus knees. These findings support the mechanical hypothesis that arthritis may be related to altered stress distribution at the knee, larger studies may provide further conclusive evidence

Aims. Idiopathic scoliosis is the most common spinal deformity in adolescents and children. The aetiology of the disease remains unknown. Previous studies have shown a lower bone mineral density in individuals with idiopathic scoliosis, which may contribute to the causation. The aim of the present study was to compare bone health in adolescents with idiopathic scoliosis with controls. Methods. We included 78 adolescents with idiopathic scoliosis (57 female patients) at a mean age of 13.7 years (8.5 to 19.6) and 52 age- and sex-matched healthy controls (39 female patients) at a mean age of 13.8 years (9.1 to 17.6). Mean skeletal age, estimated according to the Tanner-Whitehouse 3 system (TW3), was 13.4 years (7.4 to 17.8) for those with idiopathic scoliosis, and 13.1 years (7.4 to 16.5) for the controls. Mean Cobb angle for those with idiopathic scoliosis was 29° (SD 11°). All individuals were scanned with dual energy x-ray absorptiometry (DXA) and peripheral quantitative CT (pQCT) of the left radius and tibia to assess bone density. Statistical analyses were performed with independent-samples t-test, the Mann-Whitney U test, and the chi-squared test. Results. Compared with controls, adolescents with idiopathic scoliosis had mean lower DXA values in the left femoral neck (0.94 g/cm. 2. (SD 0.14) vs 1.00 g/cm. 2. (SD 0.15)), left total hip (0.94 g/cm. 2. (SD 0.14) vs 1.01 g/cm. 2. (SD 0.17)), L1 to L4 (0.99 g/cm. 2. (SD 0.15) vs 1.06 g/cm. 2. (SD 0.17)) and distal radius (0.35 g/cm. 2. (SD 0.07) vs 0.39 g/cm. 2. (SD 0.08; all p ≤ 0.024), but not in the mid-radius (0.72 g/cm. 2. vs 0.74 g/cm. 2. ; p = 0.198, independent t-test) and total body less head (1,559 g (SD 380) vs 1,649 g (SD 492; p = 0.0.247, independent t-test). Compared with controls, adolescents with idiopathic scoliosis had lower trabecular volume bone mineral density (BMD) on pQCT in the distal radius (184.7 mg/cm. 3. (SD 40.0) vs 201.7 mg/cm. 3. (SD 46.8); p = 0.029), but not in other parts of the radius or the tibia (p ≥ 0.062, Mann-Whitney U test). Conclusion. In the present study, idiopathic scoliosis patients seemed to have lower BMD at central skeletal sites and less evident differences at peripheral skeletal sites when compared with controls. Cite this article: Bone Joint J 2020;102-B(2):268–272

The evolution of orthopedic implants has witnessed a great evolution and allowed insights into the various metals and alloys compatible with the human body. However, some recent reports have raised concerns regarding hypersensitivity to several metals used in orthopedic implants. These cases are mostly documented in the field of arthroplasty. Metal ion release following hip or knee arthroplasty is a known phenomenon and associated immune reactions to these metal ions have been implicated in the causation of these hypersensitivity reactions. These reactions frequently lead to poor outcome following these implant surgeries. We here present two rare cases of metal induced hypersensitivity reactions following orthopedic surgeries. We have also reviewed the literature in this context to look into the various causes of metal reactions, types of implant involved in hypersensitivity, methods of testing and management options in these cases

Introduction: Recent cadaveric studies have identified neovascularisation and neoneuralisation as probable mechanisms in the causation of discogenic pain. Calcium pyrophosphate deposits have been observed in discs in several studies. Their significance in the causation of discogenic pain is unclear. Direct correlation between the pain site and histological features can be verified by aware state endoscopic visualisation. Aim and Objectives: The study aims to examine and correlate the presence of neovascularisation, crystalline pyrophosphate deposits in the disc, and discogenic pain by spinal probing and discography under endoscopic visualisation. Material and Methods: Tissue removed from intervertebral discs of 224 patients during surgery was examined directly, and polarised microscopy was used to identify the presence of calcium pyrophosphate and neovascularisation. Their presence was correlated to diagnostic provocative findings of spinal probing and discography and intradiscal distortion during aware state endoscopy. Results: Calcium Pyrophosphate: Twenty out of 224 patients (9%) demonstrated calcium pyrophosphate in the discs. Fourteen had pain reproduced on probing or discography. Thirteen out of 20 patients (65%) had either an annular collection or leak at the index level. 6 had an extradiscal cause of pain. One hundred percent of the patients with annular collections or leaks had pain on spinal probing or discography. Sixteen patients with pyrophosphate deposits did not have neovascularisation. Neovascularisation: Thirty seven out of 224 patients (16.5%) showed neovascularisation in the disc. Four discs had crystalline pyrophosphate deposits. Thirty three out of 37 (90%) had pain on probing and/or discography. Out of four patients who had no pain on probing or discography, two had demonstrated tears during previous discographic procedures which were treated with laser annealing. These patients had disc bulges and compressive radiculopathy. Conclusion: The presence of pyrophosphate in the disc without a tear or leak does not directly render them tender to provocation. The presence of pyrophosphate is not correlated to neovascularisation. Annular tears or leaks are not directly correlated to the presence of pyrophosphates. There is a high correlation between pain provocation and neovascularisation

The medical model of history, examination and investigation forms the bedrock of diagnosis and management of all patients. The essence is the recognition of patterns of symptoms and signs. In the modern era there are an increasing number of non-medical resources ranging from web-based information, computer diagnostic aids and non-specialist healthcare professionals to provide a diagnosis and commence management of a wide range of conditions, including knee problems. We analysed the quality and patterns of clinical presentation in order to answer the question how closely clinical symptoms and examination findings correlate to diagnosis based on MRI scan and/or arthroscopic findings. The analysis was a dataset of a consecutive series of patients, aged 18 to 45, with no past history of knee problems or end stage arthritis, presenting to a single specialist triage physiotherapist, working within an integrated knee service, who fully completed a standardised knee assessment proforma of presenting symptoms and signs at a large district general hospital. The study comprises 86 patients and 98 knees. We analysed this data based on diagnostic findings of MRI scan or arthroscopy to provide definitive intra-articular diagnosis. Based on standard textbook descriptions of common presentations, we went on to define the patients' presentation history and examination as typical or atypical, with typical meaning the symptoms and signs correlated with the diagnosis. The null hypothesis is that patients have a high chance of typical presentations for common knee conditions. In the 75% of patients with a significant intra-articular pathology we found the majority had chondral rather than meniscal tears 1.7 to 1. Forty four percent of patients had atypical symptoms and 71% had atypical clinical signs, 30% and only 26% of the cohort had both typical symptoms and signs together, reflecting a surprisingly low positive predictive probability of symptoms and signs in this group of patients, particularly those with chondral lesions which was 44%. In this cohort, 57% of the cohort has 3 or more multiple diagnoses. In the diagnostically normal group, 43% had symptoms and signs typical for a meniscal tear. We conclude that clinical symptoms and signs surprisingly inaccurate in guiding intra-articular pathology within the knee, even in a sub-set considered the easy and accurate to assess. The number of multiple diagnoses and the incidence of false positive results also means that simplistic interpretations of non-definitive diagnoses and linear causation of pain pathways should be treated cautiously

Shoulder injury related to vaccine administration (SIRVA) is a prolonged episode of shoulder dysfunction that commences within 24 to 48 hours of a vaccination. Symptoms include a combination of shoulder pain, stiffness, and weakness. There has been a recent rapid increase in reported cases of SIRVA within the literature, particularly in adults, and is likely related to the mass vaccination programmes associated with COVID-19 and influenza. The pathophysiology is not certain, but placement of the vaccination in the subdeltoid bursa or other pericapsular tissue has been suggested to result in an inflammatory capsular process. It has been hypothesized that this is associated with a vaccine injection site that is “too high” and predisposes to the development of SIRVA. Nerve conduction studies are routinely normal, but further imaging can reveal deep-deltoid collections, rotator cuff tendinopathy and tears, or subacromial subdeltoid bursitis. However, all of these are common findings within a general asymptomatic population. Medicolegal claims in the UK, based on an incorrect injection site, are unlikely to meet the legal threshold to determine liability.

Cite this article: Bone Joint J 2023;105-B(8):839–842.

Aims

The Chopart joint complex is a joint between the midfoot and hindfoot. The static and dynamic support system of the joint is critical for maintaining the medial longitudinal arch of the foot. Any dysfunction leads to progressive collapsing flatfoot deformity (PCFD). Often, the tibialis posterior is the primary cause; however, contrary views have also been expressed. The present investigation intends to explore the comprehensive anatomy of the support system of the Chopart joint complex to gain insight into the cause of PCFD.

The importance of registries has been brought into focus by recent UK national reports focusing on implant (Cumberlege) and surgeon (Paterson) performance. National arthroplasty registries provide real-time, real-world information about implant, hospital, and surgeon performance and allow case identification in the event of product recall or adverse surgical outcomes. They are a valuable resource for research and service improvement given the volume of data recorded and the longitunidal nature of data collection. This review discusses the current value of registry data as it relates to both clinical practice and research.

Cite this article: Bone Joint J 2023;105-B(4):356–360.

The aim of this study was to investigate the relationship between the geometry of the proximal femur and the incidence of intra-operative fracture during uncemented total hip arthroplasty (THA). We studied the pre-operative CT scans of 100 patients undergoing THA with an uncemented femoral component. We measured the anteroposterior and mediolateral dimensions at the level of division of the femoral neck to calculate the aspect ratio of the femur. Wide variations in the shape of the femur were observed, from round, to very narrow elliptic. The femurs of women were narrower than those of men (p < 0.0001) and small femurs were also narrower than large ones. Patients with an intra-operative fracture of the calcar had smaller and narrower femurs than those without a fracture (p < 0.05) and the implanted Corail stems were smaller in those with a fracture (mean size 9 vs 12, p < 0.0001). The variability of the shape of the femoral neck at the level of division contributes to the understanding of the causation of intra-operative fractures in uncemented THA. Cite this article: Bone Joint J 2015;97-B:741–8

Objectives. A successful outcome following treatment of nonunion requires the correct identification of all of the underlying cause(s) and addressing them appropriately. The aim of this study was to assess the distribution and frequency of causative factors in a consecutive cohort of nonunion patients in order to optimise the management strategy for individual patients presenting with nonunion. Methods. Causes of the nonunion were divided into four categories: mechanical; infection; dead bone with a gap; and host. Prospective and retrospective data of 100 consecutive patients who had undergone surgery for long bone fracture nonunion were analysed. Results. A total of 31% of patients had a single attributable cause, 55% had two causes, 14% had three causes and 1% had all four. Of those (31%) with only a single attributable cause, half were due to a mechanical factor and a quarter had dead bone with a gap. Mechanical causation was found in 59% of all patients, dead bone and a gap was present in 47%, host factors in 43% and infection was a causative factor in 38% of patients. In all, three of 58 patients (5%) thought to be aseptic and two of nine (22%) suspected of possible infection were found to be infected. A total of 100% of previously treated patients no longer considered to have ongoing infection, had multiple positive microbiology results. Conclusion. Two thirds of patients had multiple contributing factors for their nonunion and 5% had entirely unexpected infection. This study highlights the importance of identifying all of the aetiological factors and routinely testing tissue for infection in treating nonunion. It raises key points regarding the inadequacy of a purely radiographic nonunion classification system and the variety of different definitions for atrophic nonunion in the current mainstream classifications used for nonunion. Cite this article: L. Mills, J. Tsang, G. Hopper, G. Keenan, A. H. R. W. Simpson. The multifactorial aetiology of fracture nonunion and the importance of searching for latent infection. Bone Joint Res 2016;5:512–519. DOI: 10.1302/2046-3758.510.BJR-2016-0138