Aims. The glenohumeral joint is the most frequently dislocated articulation, but possibly due to the lower prevalence of posterior shoulder dislocations, approximately 50% to 79% of posterior glenohumeral dislocations are missed at initial presentation. The aim of this study was to systematically evaluate the most recent evidence involving the aetiology of posterior glenohumeral dislocations, as well as the diagnosis and treatment. Materials and Methods. A systematic search was conducted using PubMed (MEDLINE), Web of Science, Embase, and Cochrane (January 1997 to September 2017), with references from articles also evaluated. Studies reporting patients who experienced an acute posterior glenohumeral joint subluxation and/or dislocation, as well as the aetiology of posterior glenohumeral dislocations, were included. Results. A total of 54 studies met the inclusion criteria. In total, 182 patients were included in this analysis; study sizes ranged from one to 66 patients, with a mean age of 44.2 years (. sd. 13.7). There was a higher proportion of male patients. In all, 216 shoulders were included with 148 unilateral injuries and 34 bilateral. Seizures were implicated in 38% of patients (n = 69), with falls, road traffic accidents, electric shock, and iatrogenic reasons also described. Time to diagnosis varied across studies from immediate up to a delay of 25 years. Multiple associated injuries are described. Conclusion. This review provides an up-to-date insight into the aetiology of posterior shoulder dislocations. Our results showed that seizures were most commonly implicated. Overall, reduction was achieved via open means in the majority of shoulders. We also found that delayed diagnosis is common

Femoroacetabular impingement causes pain in the hip in young adults and may predispose to the development of osteoarthritis. Genetic factors are important in the aetiology of osteoarthritis of the hip and may have a role in that of femoroacetabular impingement. We compared 96 siblings of 64 patients treated for primary impingement with a spouse control group of 77 individuals. All the subjects were screened clinically and radiologically using a standardised protocol for the presence of cam and pincer deformities and osteoarthritis. The siblings of those patients with a cam deformity had a relative risk of 2.8 of having the same deformity (66 of 160 siblings hips versus 23 of 154 control hips, p < 0.00001). The siblings of those patients with a pincer deformity had a relative risk of 2.0 of having the same deformity (43 of 116 sibling hips versus 29 of 154 control hips, p = 0.001). Bilateral deformity occurred more often in the siblings (42 of 96 siblings versus 13 of 77 control subjects, relative risk 2.6, p = 0.0002). The prevalence of clinical features in those hips with abnormal morphology was also greater in the sibling group compared with the control group (41 of 109 sibling hips versus 7 of 46 control hips, relative risk 2.5, p = 0.007). In 11 sibling hips there was grade-2 osteoarthritis according to Kellgren and Lawrence versus none in the control group (p = 0.002). Genetic influences are important in the aetiology of primary femoroacetabular impingement. This risk appears to be manifested through not only abnormal joint morphology, but also through other factors which may modulate progression of the disease

1. During a fifteen-year period a clinical, radiological and in some cases a surgical study has been made of 319 patients suffering from spondylolisthesis–that is, forward slipping of one lumbar vertebra on another or forward sagging of the whole lumbar spine in relation to the sacrum. 2. The five etiological factors are described, and the cases are assigned to five groups according to the factor responsible for the slip. In every case slipping is permitted by a lesion of the apparatus which normally resists the forward thrust of the lower lumbar spine–that is, the hook of the neural arch composed of the pedicle, the pars interarticularis and the inferior articular facet engaging caudally over the superior articular facet of the vertebra below. 3. In Group I (congenital spondylolisthesis–sixty-six cases) the lesion is a congenital defect of the facets. In Group II (spondylolytic spondylolisthesis–164 cases) the lesion occurs in the region of the pars interarticularis and is either an elongation of the bone or a break in continuity. There are reasons for thinking that the lesion is caused by stress over a long period rather than by acute injury or by a congenital anomaly of ossification. In Group IV (degenerative spondylolisthesis–eighty cases) the lesion of the facets is degenerative. There are no good grounds for thinking that an abnormality of the angle between the facets and the pedicles is the primary lesion behind the degenerative change. 4. Group III and V comprise few cases. In the former (traumatic spondylolisthesis–three cases) the lesion–a fracture of the neural arch–is caused by a single severe injury. In Group V (pathological spondylolisthesis–six cases) the slipping is caused by weakness of bone from various causes. 5. A full description is given of the etiological and biomechanical features of each group. A special investigation has been made into the etiological factors in degenerative spondylolisthesis. 6. The incidence of involvement of nerve tissues is highest in degenerative spondylolisthesis; the most severe degrees of slip are found in congenital spondylolisthesis

1 . Current theories of the etiology of chondromalacia patellae do not explain satisfactorily either its great frequency or its common site of origin on the medial patellar facet. 2. The etiology can be more logically explained by the presence of a ridge on the upper anterior border of the cartilage of the medial femoral condyle, in most knees. This ridge, consisting of cartilage, or cartilage and bone, varies considerably in height and, in normal knee joint movement, causes considerable friction on the medial patellar facet. 3. The degenerative changes were found to be greater in the presence of the larger ridges, and–because of longer wear and tear–in the older patients. 4. This study indicates that chondromalacia was more severe in women than in men, and in patients overweight. Although the activity of the individual and the power of the quadriceps mechanism must play an extremely important part in this condition, it was not possible to assess this. 5. Two factors previously considered to be important in the etiology of this condition, namely, the length of the patellar tendon and Wiberg's Type III patellar shape, have not been confirmed in this study. 6. Resulting from the present investigation certain precautions are suggested in rehabilitation after operations on the knee, and a surgical method for discouraging the progress of this common, and sometimes disabling, condition has been devised

A nationwide study of Perthes’ disease in Norway was undertaken over a five-year period from January 1996. There were 425 patients registered, which represents a mean annual incidence of 9.2 per 100 000 in subjects under 15 years of age, and an occurrence rate of 1:714 for the country as a whole. There were marked regional variations. The lowest incidence was found in the northern region (5.4 per 100 000 per year) and the highest in the central and western regions (10.8 and 11.3 per 100 000 per year, respectively). There was a trend towards a higher incidence in urban (9.5 per 100 000 per year) compared with rural areas (8.9 per 100 000 per year). The mean age at onset was 5.8 years (1.3 to 15.2) and the male:female ratio was 3.3:1. We compared 402 patients with a matched control group of non-affected children (n = 1 025 952) from the Norwegian Medical Birth Registry and analysed maternal data (age at delivery, parity, duration of pregnancy), birth length and weight, birth presentation, head circumference, ponderal index and the presence of congenital anomalies. Children with Perthes’ disease were significantly shorter at birth and had an increased frequency of congenital anomalies. Applying Sartwell’s log-normal model of incubation periods to the distribution of age at onset of Perthes’ disease showed a good fit to the log-normal curve. Our findings point toward a single cause, either genetic or environmental, acting prenatally in the aetiology of Perthes’ disease

1. Chondromalacia of the patella starts most frequently on the medial facet. 2. The anatomy of the medial femoral condyle is described, including the rim at its superior border, and the different arrangement at the upper border of the lateral femoral condyle. 3. Rubbing of the medial patellar facet on the rim at the upper border of the medial femoral condyle can explain in part the etiology of chondromalacia

A five-year prospective trial involving 120 patients was undertaken to investigate the aetiology and treatment of coccydynia. The cause lies in some localised musculoskeletal abnormality in the coccygeal region. Lumbosacral disc prolapse is not a significant factor. The condition is genuine and distressing and we found no evidence of neurosis in our patients. Physiotherapy was of little help in treatment but 60% of patients responded to local injections of corticosteroid and local anaesthesia. Manipulation and injection was even more successful and cured about 85%. Coccygectomy was required in almost 20% and had a success rate of over 90%

At the apex of an idiopathic scoliotic curve there is a greater proportion of "slow twitch" muscle fibres in multifidus on the convex as compared to the concave side. To determine whether this represents a primary muscular imbalance relevant to the aetiology of idiopathic scoliosis or merely a secondary change, the lengths of multifidus on opposite sides of the curve were measured. Multifidus is shorter on the convex side. This is consistent with the theory of primary muscular imbalance, in which the more tonically acting muscle with its higher proportion of "slow twitch" fibres contracts and shortens as the deformity is produced. The paradox of multifidus being shorter on the convex rather than on the concave side is explained by consideration of its action

A study of the natural history and aetiology of deep vein thrombosis in 499 patients after total hip replacement is presented. Deep vein thrombosis was diagnosed by scanning the leg for 125Iodine-labelled fibrinogen for a period of 14 to 18 days and by ascending phlebography. It has been shown that deep vein thrombosis occurs ater than in patients who have undergone abdominal operations, and the risk period is longer. The peak of onset of thrombosis is on the fourth day after the hip replacement. Attempts at prophylaxis using subcutaneous heparin or intermittent pneumatic compression of the calves delay the appearance of thrombosis. Analysis of possible aetiology factors shows that the age of the patient, the degenerative disease of the hip, the surgical approach, and under-transfusion of blood, all have a significant effect on the incidence of thrombosis

1. Breech malposition and hormonal joint laxity produce atraumatic posterior dislocations in the hip joints of young rabbits. 2. Experimental studies were shown to cause the development of a limbus and other softtissue changes similar to those found in human congenital dislocations. 3. The development of femoral retroversion and anteversion in the presence of joint laxity is described. 4. The co-existence of breech malposition and hormonal joint laxity in utero, and their importance as prime factors in the etiology of congenital dislocation of the hip, are discussed

1. Peroneal spastic flat foot is a term loosely and often inaccurately used to describe rigid valgus feet developing from widely different causes. 2. The most common causes are two anomalies of the bones of the tarsus—the calcaneonavicular bar, and the talocalcaneal bridge. The first was described in 1921 by Sloman and in 1927 by Badgley; the other is described for the first time in this paper as an etiological factor in rigid flat foot though it has been recognised by anatomists for fifty years as a skeletal variation. The term peroneal spastic flat foot, as applied to these cases, is inaccurate since there is no spasm of the peroneal muscles. The deformity is a fixed structural deformity due to anomalous bone structure, and the apparent spasm of peroneal muscles is in reality an adaptive shortening. A better term would be rigid flat foot due to talocalcaneal bridge or calcaneonavicular bar. 3. The smaller group of patients who suffer from inflammatory lesions of the tarsal joints, chiefly due to rheumatoid arthritis, do in fact develop valgus deformity from peroneal spasm. The resemblance between the two groups is superficial and it is limited to the apparent similarity of the deformity. Though it might be justifiable to designate this type as peroneal spastic flat foot, it would be better to use the more accurate title—arthritic flat foot with peroneal spasm. 4. Lipping of the upper margin of the talonavicular joint strongly suggests the existence of one or other of the congenital anomalies. Both anomalies are visualised only by special radiological projections

A prospective study was made of 119 children with transient synovitis or any other cause for synovial effusion and elevated intra-articular pressure. During a follow-up of one year not one case of Perthes' disease was diagnosed and the late clinical and radiographic changes were minimal with moderate overgrowth of the femoral head in 33% and widening of the joint space in 14.2%. Our results do not support the widely accepted concept that Perthes' disease develops as a result of the period of elevated intra-articular pressure found in transient synovitis. Further research into this and Perthes' disease should follow the premise that they are two different diseases without any aetiological connection

1. The clinical features of hyperostosis cranii are briefly reviewed. In large series of cases the syndrome has been found to occur almost entirely in females. 2. In recent studies of dystrophia myotonica, it is apparent that hyperostosis cranii is one of the variable features of the disorder. This disease occurs equally among males and females and the hyperostosis cranii also is distributed equally among males and females. 3. Hyperostosis cranii also occurs in patients with Morgagni's syndrome, with acromegaly, and as "senile hyperostosis.". 4. The etiology of hyperostosis is still a matter for speculation. More recent studies have focused attention on the endocrine system, and it seems probable, in view of the sex distribution in dystrophia myotonica, that the key to the problem may be found in this disorder. 5. In dystrophia myotonica the characteristic skull changes are hyperostosis cranii, a small pituitary fossa, excessive sinus formation and prognathism. These are acromegaloid changes. Gonadal atrophy is a common feature and endocrine study suggests that the endocrine defect is primarily a failure of the androgenic function of the adrenals and the testes. 6. In rodents and in humans ablation of the gonads leads to overactivity of gonadotrophic cells and, at times, of somatotrophic cells. Sometimes pituitary tumours develop. 7. Acromegaloid features may occur in eunuchs, and it is likely that the acromegaloid changes in dystrophia myotonica are of the same order from overactivity of growth hormone. 8. In animals excess of growth hormone produces thickening of the skull. 9. In dystrophia myotonica, acromegaly, and Morgagni's syndrome, it is suggested that hyperostosis cranii is an expression of unrestrained activity of growth hormone

We report four patients who showed hundreds of brilliant white loose bodies at arthroscopy of the knee after a short history of pain and crepitus. Histological, historical and clinical evidence is presented which indicates that the aetiology of this condition is the culture of chondrocytes in synovial fluid. It is suggested that reversal of the usually accepted order of events in synovial osteochondromatosis could provide a better and unified explanation for both that condition and multiple loose bodies. The term 'snow storm knee' is proposed to describe the dramatic picture seen at arthroscopy

We have shown that stress fractures can be induced in the tibial diaphysis of an animal model by the repeated application of non-traumatic impulsive loads. The right hind limbs of 31 rabbits were loaded for three to nine weeks and changes in the bone were monitored by radiography and bone scintigraphy. The presence of stress fractures was confirmed histologically in some cases. Most animals sustained a stress fracture within six weeks and there was a positive correspondence between scintigraphic change and radiological evidence. Microscopic damage was evident at the sites of positive bone scans. The progression, location, and time of onset of stress fractures in this animal model were similar to those in clinical reports, making the model a useful one for the study of the aetiology of stress fractures

Heritable thrombophilic disorders have been proposed as one of the causes for Legg-Calvé-Perthes disease. A total of 62 patients diagnosed with this disease between 1988 and 1997 and 50 controls were screened for thrombophilia. The incidence and relationship of thrombophilia to the severity of the disease were evaluated. One patient and none of the controls had protein S deficiency. One of the control group and one of the patients had protein C deficiency with the latter child also having a combined deficiency with a mutant factor V gene. The number of children with a mutant factor V gene, protein C deficiency, who were homozygous for the C 677T polymorphism of methylenetetra-hydrofolate reductase or were heterozygous for mutant G20210A prothrombin did not differ statistically in the study and the control groups. No patient had antithrombin deficiency or positive lupus anticoagulant. We found no correlation between thrombophilia and the extent of the disease. The most common risk factors for arteriovenous thromboembolism showed no statistical significance in our patients compared with the control group or with the general population. These data do not confirm an aetiological role for thrombophilia in Perthes’ disease

We performed electrophysiological studies on both legs of 52 children, aged from 3 months to 15 years, with idiopathic club foot. In only nine (17%) was no abnormality found. Isolated peroneal nerve damage was seen in 14 (27%). Abnormality of both peroneal and posterior tibial nerves was found in five (10%). Four patients (8%) had evidence of isolated spinal-cord dysfunction, whereas combined spinal-cord and peripheral-nerve lesions were seen in 14 (27%). Six patients (11%) had variable neurogenic electrophysiological patterns. In 13 patients in whom the studies were repeated neither progression nor improvement of the electrophysiological parameters was observed. Pathological electrophysiological findings were found in 66% of conservatively-treated patients. In the 43 patients treated surgically, all 16 with fair and poor results had pathological electrophysiological findings and 12 required further operations. Multiplicity of the pathological findings was related to the severity of the deformity of the foot; normal studies represent a good prognostic sign. Electrophysiological studies are useful in idiopathic club foot with residual deformities after conservative or operative treatment. Our findings support the theory that muscle imbalance is an aetiological factor in idiopathic club foot

1. An anatomical study of the bony structure of the pars interarticularis of the fourth and fifth lumbar vertebrae has been made in specimens from seven cadavers aged seventeen to sixty-seven. 2. Layers of cortical bone have been described antero-laterally and postero-medially which are thickest in the narrowest region of the pars. 3. In one specimen from a seventeen-year-old male, a healing fracture was found in the antero-lateral layer of cortical bone in the right neural arch of the fourth lumbar vertebra. 4. The stresses to which the pars is subject consist primarily of shear forces applied to the articular processes. The significance of these stresses to the etiology of spondylolysis is discussed

Aims

The number of revision total knee arthroplasties (TKA) that are performed is expected to increase. However, previous reports of the causes of failure after TKA are limited in that they report the causes at specific institutions, which are often dependent on referral patterns. Our aim was to report the most common indications for re-operations and revisions in a large series of posterior-stabilised TKAs undertaken at a single institution, excluding referrals from elsewhere, which may bias the causes of failure.

We report a study of 112 patients with primary anteromedial osteoarthritis of the knee and their families. Sibling risk was determined using randomly selected single siblings. Spouses were used as controls. The presence of symptomatic osteoarthritis was determined using an Oxford knee score of ≥ 29 supported by a Kellgren and Lawrence radiological score of II or greater.

Using Fisher’s exact test we found that there was a significant increased risk of anteromedial osteoarthritis (OA) relative to the control group (p = 0.031). The recurrence risk of anteromedial OA to siblings was 3.21 (95% confidence interval 1.12 to 9.27).

These findings imply that genetic factors may play a major role in the development of anteromedial OA of the knee.