ABSTRACT There has recently been discussion regarding the term “clinical anatomy”: how can it be defined, and what makes an anatomist “clinical”? Is there any difference between “anatomy” and “clinical anatomy”? What makes an anatomist “clinical” as opposed to being simply “an anatomist”? With the wide range of educator backgrounds now teaching anatomy in higher education institutions, it is highly relevant to ask this question. In this Viewpoint article, members of Council of The British Association of Clinical Anatomists (BACA) discuss these issues in relation to anatomical education in the UK. We acknowledge that anatomy education in the UK has undergone significant changes, which reflect broader changes in medical education. BACA's approach of including members regardless of whether or not they hold clinical qualifications, while maintaining rigorous healthcare‐related standards, aligns with the perspective that the clinical anatomist is defined not by credentials alone, but by a commitment to collaborate with other healthcare disciplines, integrating anatomical knowledge with clinical relevance.

ObjectiveThe relationship between the index (2D) to ring finger (4D) is one of the most commonly studied anthropometric measures, which is believed to offer insight into early growth and the foetal...

BACKGROUND AND OBJECTIVES:Perthes disease is a childhood precipitant to osteoarthritis of the hip, for which the etiology and mechanism are unknown. There is mounting evidence to suggest a vascular insult is responsible for disease, and it is suggested that this may have long-term implications for the vascular health of affected individuals. This study sought to use ultrasound measures to investigate vascular structure and function in children affected by Perthes disease.METHODS:This case control study encompassed 149 cases and 146 controls, frequency matched for age and gender. Endothelial function was measured by using the technique of flow-mediated dilation of the brachial artery, and alterations in arterial flow were recorded in response to an ischemic stimulus.RESULTS:There was a significant structural alteration in the vasculature among individuals with Perthes disease (resting brachial artery diameter (cases 2.97 mm versus controls 3.11 mm; P = .01), which remained even after adjusting for height. In addition, there was a notable reduction in blood velocity (cases 33.84 cm/s versus controls 37.83 cm/s; P = .01) and blood flow (cases 149.82 mL/min versus controls 184.67 mL/min; P = .001), which was independent of baseline arterial size. There was no evidence to suggest that flow-mediated dilation of the brachial artery was impaired among affected individuals (P = .71).CONCLUSIONS:Children with Perthes disease exhibit small artery caliber and reduced function, which is independent of body composition. These data imply that that Perthes disease may reflect a wider vascular phenomenon that could have long-term implications for the vascular health of affected individuals.

Aim:Right-Handed Girls With Rt-Ais Measured Using Holtain Equipment Have Upper Arm Length Asymmetry (Right-Minus-Left) Which Is: 1) Relatively Longer On Scoliosis Curve Convexity; 2) Significantly ...

This paper formulates a novel multifactorial Cascade Concept for the pathogenesis of adolescent idiopathic scoliosis (AIS). This Concept stems from the longitudinal findings of Clark et al. (J Bone Miner Res 29(8):1729-36, 2014) who identified leptin body composition factors at 10 years of age associated with a scoliosis deformity found at 15 years. We interpret these findings in the light of some concepts for AIS pathogenesis. In particular, we speculate that the leptin body composition effect is linked to central nervous system development and the initiation of the asynchronous neuro-osseous growth mechanism that involves the creation of a neuraxis tether of relative anterior vertebral overgrowth. The latter mechanism in combination with age and gender-related anatomical variants of vertebral backward tilt (dorsal shear concept), human upright posture, adolescent growth factors, Hueter-Volkmann effect in vertebrae and vertebral bone mass abnormalities, lead to AIS, possibly both initiation and progression of scoliosis curvatures. Being multifactorial, while the Cascade Concept cannot be tested for all its components, some components should be testable by the method of numerical simulation. Clark et al. (J Bone Miner Res 29(8):1729-36, 2014) also suggested the origin of scoliosis was in the embryonic stages of life from cell types, including adipocytes and osteoblasts, derived from the same progenitor cells, and myoblasts from mesodermal somites. The involvement of cell types from different developmental origins suggests a process acting in embryonic life at a similar time, probably environmental, as previously proposed from anthropometric studies. As a Complex disease, AIS will involve genetic, environmental and life style factors operating in development and growth; this possibility needs evaluating in epidemiological studies.

BACKGROUND CONTEXT: Adolescent idiopathic scoliosis (AIS) affects humans and not non-human primates. This difference is generally attributed to factors associated with human bipedalism and spinopelvic balance. In AIS, there is increasing evidence of underlying subclinical neurological disorders and cerebral asymmetries which may contribute with skeletal growth and other factors to pathogenesis. The evidence suggests that in some subjects with AIS, any cerebral dysfunction with asymmetry that may initiate the scoliosis could have its root in the complex organisation of the cortical network of the human brain acquired by hominins in evolution.

This Editorial initiates a Thematic Series on the aetiology, pathogenesis and pathomechanisms (scoliogeny) of adolescent idiopathic scoliosis (AIS). It introduces the Series and invites contributions from researchers in the field and from interested parties. The aim is to develop a wideranging online discussion based on evidence and theoretical interpretations, In doing this, it will extend the role of the electronic focus group of the International Federated Body on Scoliosis Etiology (IBSE) which discussed nine selected topics from 2003 to 2013 [1,2]. While the relationship between scoliosis and growth was recognized forty years ago [3], progress in understanding the causation of AIS was fettered by a relative paucity of basic biological and biomechanical scientific data. Since then and subsequent to emphasis in pathogenesis on sagittal spinal plane [4] and relative anterior spinal overgrowth [5], advances in biological knowledge have enabled scoliogenic understanding to progress particularly after the year 2000 [6-8]. Knowledge limtation still restricts scoliogenic understanding for example in relation to the biochemistry and endocrinology of AIS [9] and the abnormal extra-spinal skeletal length asymmetries of AIS girls which are of unknown pathogenetic significance [2,10,11]. Research on the genetic variant hypothesis of disease for AIS has led to significant achievements [12]. Within the research forum of the British Scoliosis Research Foundation [13] there is a separate, private forum for the International Scoliosis Genetics Interest Group (ISGIG), a specialist group formed at the 2011 International Phillip Zorab Symposium. A possible role for environmental and epigenetic factors in AIS scoliogeny is

Adolescent idiopathic scoliosis frequently develops around puberty and involves both translational and angular asymmetry of the rib cage and back surface vertebrae. This article examines various invasive methods used to measure the spine and back and reviews research on non-invasive measurement systems. This should allow clinicians and therapists with an interest in the spine and back to be informed of the different approaches undertaken for clinical evaluation and research in this field. Optoelectronic gait analysis systems have been used to measure dynamic back movements, but there remains need to optimize marker placement procedures. The importance of trunk movement in human gait has been established in many studies, although quantifying spinal deformities and the range of spine and trunk movement has concentrated on the static position of the body. Additionally, there is paucity of data detailing the actual relative motion between the back and lower limb during gait. This article highlights the need for quantitative information examining the relationship between load and the spinal curve.

BACKGROUND:Legg-Calve-Perthes Disease (LCPD) is a childhood precursor to hip osteoarthritis, for which the etiology is unknown. There is a widespread belief that affected individuals are "hyperactive," propagating a theory that such children may have sustained an epiphyseal injury that precipitated the onset of LCPD. This study seeks to quantify the association with hyperactivity, and the wider psychological burden of the disease. METHODS:A case-control study was conducted among 146 cases of LCPD and 142 hospital controls, frequency matched by age and sex. Psychological domains were measured using the Strength and Difficulties Questionnaire. Adjustment was made for age, sex, and socioeconomic deprivation. Results were stratified by the time elapsed since LCPD was diagnosed. RESULTS:Significant associations (P<0.05) existed with the majority of the psychological domains captured by the Strength and Difficulties Questionnaire [odds ratio (OR) for "high" level of difficulties-Emotion OR 3.2, Conduct OR 2.1, Inattention-Hyperactivity OR 2.7, Prosocial Behavior OR 1.9]. Hyperactivity was especially marked among individuals within 2 years of diagnosis (OR 8.6; P<0.001), but not so among individuals over 4 years from diagnosis. Emotional symptoms persisted long after resolution of the active phase of disease. CONCLUSIONS:There was a marked psychological burden among individuals with LCPD, which was most marked amongst individuals with a recent diagnosis. The breadth and inferred temporality of these disturbances may be a function of the disease process, through restriction of activities and disability, or may be a fundamental disease characteristic related directly to disease or to its etiological determinant.

There is no generally accepted scientific theory for the cause of adolescent idiopathic scoliosis (AIS). As part of its mission to widen understanding of scoliosis etiology, the International Federated Body on Scoliosis Etiology (IBSE).introduced the electronic focus group (EFG) as a means of increasing debate on knowledge of important topics. This has been designated as an on-line Delphi discussion. The text for this debate was written by Dr TB Grivas. It is based on published research from Athens, Greece evaluating schoolchildren age 11-17 years for the relation of body mass index (BMI) to each of truncal asymmetry (TA) and menarcheal status. Girls with relatively lower BMI were found to have a significant excess of severe TAs and significantly later menarche confirming the well-known relation of BMI to menarche. Together with other evidence linking nutritional status to skeletal growth, the observations suggest energy balance via the hypothalamus is related to trunk asymmetry. As with a recent speculative hypothesis for the pathogenesis of AIS in girls, Grivas et al. suggest that the severe TAs involve a genetically-determined selectively increased sensitivity (up-regulation) of the hypothalamus to circulating leptin with asymmetry as an adverse response to stress (hormesis). The TA is expressed bilaterally via the sympathetic nervous system to produce left-right asymmetry in ribs and/or vertebrae leading to severe TAs when beyond the capacity of postural mechanisms of the somatic nervous system to control the shape distortion in the trunk. This EFG discusses the findings and interpretations of the paper by Grivas and colleagues as research at the borderland between the genesis of TA (physiogenesis) and AIS (pathogenesis). It is suggested that TAs, here regarded in common with AIS, result from the combination of secondary sexual development affecting body composition, adolescent skeletal growth velocity, and an asymmetry process. The possible involvement of epigenetic factors is not considered.

This paper aims to integrate into current understanding of AIS causation, etiopathogenetic information presented at two Meetings during 2012 namely, the International Research Society of Spinal Deformities (IRSSD) and the Scoliosis Research Society (SRS). The ultimate hope is to prevent the occurrence or progression of the spinal deformity of AIS with non-invasive treatment, possibly medical. This might be attained by personalised polymechanistic preventive therapy targeting the appropriate etiology and/or etiopathogenetic pathways, to avoid fusion and maintain spinal mobility. Although considerable progress had been made in the past two decades in understanding the etiopathogenesis of adolescent idiopathic scoliosis (AIS), it still lacks an agreed theory of etiopathogenesis. One problem may be that AIS results not from one cause, but several that interact with various genetic predisposing factors. There is a view there are two other pathogenic processes for idiopathic scoliosis namely, initiating (or inducing), and those that cause curve progression. Twin studies and observations of family aggregation have revealed significant genetic contributions to idiopathic scoliosis, that place AIS among other common disease or complex traits with a high heritability interpreted by the genetic variant hypothesis of disease. We summarize etiopathogenetic knowledge of AIS as theories of pathogenesis including recent multiple concepts, and blood tests for AIS based on predictive biomarkers and genetic variants that signify disease risk. There is increasing evidence for the possibility of an underlying neurological disorder for AIS, research which holds promise. Like brain research, most AIS workers focus on their own corner and there is a need for greater integration of research effort. Epigenetics, a relatively recent field, evaluates factors concerned with gene expression in relation to environment, disease, normal development and aging, with a complex regulation across the genome during the first decade of life. Research on the role of environmental factors, epigenetics and chronic non-communicable diseases (NCDs) including adiposity, after a slow start, has exploded in the last decade. Not so for AIS research and the environment where, except for monozygotic twin studies, there are only sporadic reports to suggest that environmental factors are at work in etiology. Here, we examine epigenetic concepts as they may relate to human development, normal life history phases and AIS pathogenesis. Although AIS is not regarded as an NCD, like them, it is associated with whole organism metabolic phenomena, including lower body mass index, lower circulating leptin levels and other systemic disorders. Some epigenetic research applied to Silver-Russell syndrome and adiposity is examined, from which suggestions are made for consideration of AIS epigenetic research, cross-sectional and longitudinal. The word scoliogeny is suggested to include etiology, pathogenesis and pathomechanism.

Perthes' disease is an osteonecrosis of the juvenile hip, the aetiology of which is unknown. A number of comorbid associations have been suggested that may offer insights into aetiology, yet the strength and validity of these are unclear. This study explored such associations through a case control study using the United Kingdom General Practice Research database. Associations investigated were those previously suggested within the literature. A total of 619 cases of Perthes' disease were included, as were 2544 controls. The risk of Perthes' disease was significantly increased with the presence of congenital anomalies of the genitourinary and inguinal region, such as hypospadias (odds ratio (OR) 4.04 (95% confidence interval (CI) 1.41 to 11.58)), undescended testis (OR 1.83 (95% CI 1.12 to 3.00)) and inguinal herniae (OR 1.79 (95% CI 1.02 to 3.16)). Attention deficit hyperactivity disorder was not associated with Perthes' disease (OR 1.01 (95% CI 0.48 to 2.12)), although a generalised behavioural disorder was (OR 1.55 (95% CI 1.10 to 2.17)). Asthma significantly increased the risk of Perthes' disease (OR 1.44 (95% CI 1.17 to 1.76)), which remained after adjusting for oral/parenteral steroid use. Perthes' disease has a significant association with congenital genitourinary and inguinal anomalies, suggesting that intra-uterine factors may be critical to causation. Other comorbid associations may offer insight to support or refute theories of pathogenesis.

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This entry summarizes research about cyber behavior with wikis. Wikis are collaborative websites allowing the easy creation of interlinked webpages using text editors. The first wiki tool was created by Ward Cunningham, and the first online wiki-based encyclopedia, Wikipedia, appeared in 2001. Currently, three types of wikis exist: public, organizational, and private/educational wikis. This article identifies six areas of wiki research and its leading researchers. These areas are: (1) the wiki way (wikis as part of the suite of Web2.0 tools), and Wikipedia; (2) wiki growth and contributor roles; (3) what motivates people to contribute to wikis; (4) how the authenticity of wiki articles is ensured; (5) the use of wikis in education; and finally (6) how researchers consider the way wikis have impacted on various aspects of human life. The entry closes with suggestions about possible future research directions on online behavior with wikis.

OBJECTIVE Little is known about Legg-Calvé-Perthes disease, a common childhood precursor to osteoarthritis of the hip. This study was undertaken to analyze the incidence of Legg-Calvé-Perthes disease in the UK, with respect to geographic and temporal trends over a 19-year period. METHODS The General Practice Research database was analyzed to identify incident cases between 1990 and 2008 in children ages 0-14 years. Incidence rates were calculated by year and by region (National Health Service Strategic Health Authority regions in England, and Scotland, Wales, and Northern Ireland), and the association with regional markers of deprivation examined. RESULTS Over the 19-year period there was a dramatic decline in Legg-Calvé-Perthes disease incidence, with annual rates among children 0-14 years old declining from 12.2 per 100,000 to 5.7 per 100,000 (P < 0.001). There was also marked geographic variation, with incidence rates in Scotland more than twice those in London (10.39 [95% confidence interval 8.05-13.2] versus 4.6 [95% confidence interval 3.4-6.1] per 100,000 0-14-year-olds). A more rapid decline in incidence was apparent in the Northern regions compared to Southern regions. The quintile with the highest degree of deprivation had the highest disease incidence (rate ratio 1.49 [95% confidence interval 1.10-2.04]) and, with the exception of London, regional incidence showed a strong linear relationship with regional deprivation score (P < 0.01). CONCLUSION The incidence of Legg-Calvé-Perthes disease in the UK has a strong North-South divide, with a greater disease incidence within the Northern regions of the UK. There was a marked decline in incidence over the study period, which was more marked in Northern areas. The declining incidence, along with the geographic variation, suggests that a major etiologic determinant in Legg-Calvé-Perthes disease is environmental and closely linked to childhood deprivation.

Legg-Calvé-Perthes' disease (Perthes' disease) is a childhood osteonecrosis of the hip for which the disease determinants are poorly understood. In this review, the authors identify studies of Perthes' disease incidence published up to December 2010 and make denominator populations comparable in order to allow meaningful between-study evaluation. Incidence rates and confidence intervals were determined, and, where appropriate, denominator populations were obtained from national statistical offices. Poisson regression was used to determine the influence of race and geography. The review included 21 studies that described 27 populations in 16 countries, with 124 million person-years of observation. The annual incidence among children under age 15 years ranged from 0.2 per 100,000 to 19.1 per 100,000. Race was a key determinant, with East Asians being least affected and whites most affected, though data were insufficient to consider incidence among blacks (for South Asians vs. East Asians, incidence rate ratio = 2.9, 95% confidence interval (CI): 2.4, 3.5; for whites vs. East Asians, incidence rate ratio = 8.8, 95% CI: 8.2, 9.6). Latitude was a strong predictor of disease, even after adjustment for race. Each 10° increase in latitude was associated with an incidence increase of 1.44 (95% CI: 1.30, 1.58) times. While much of the international variation appears to be a function of race, latitude demonstrates a strong association. This observation may offer new epidemiologic insights into the determinants of Perthes' disease.

Although considerable progress had been made in the past two decades in understanding the etiopathogenesis of adolescent idiopathic scoliosis (AIS), it still lacks an agreed theory of etiopathogenesis. One problem may be that AIS results not from one cause, but several that interact with various genetic predisposing factors. There is a view there are two other pathogenic processes for idiopathic scoliosis namely, initiating (or inducing), and those that cause curve progression. Twin studies and observations of family aggregation have revealed significant genetic contributions to idiopathic scoliosis, that place AIS among other common disease or complex traits with a high heritability interpreted by the genetic variant hypothesis of disease. We summarize etiopathogenetic knowledge of AIS as theories of pathogenesis including recent multiple concepts, and blood tests for AIS based on predictive biomarkers and genetic variants that signify disease risk. There is increasing evidence for the possibility of an underlying neurological disorder for AIS, research which holds promise. Like brain research, most AIS workers focus on their own corner and there is a need for greater integration of research effort. Epigenetics, a relatively recent field, evaluates factors concerned with gene expression in relation to environment, disease, normal development and aging, with a complex regulation across the genome during the first decade of life. Research on the role of environmental factors, epigenetics and chronic non-communicable diseases (NCDs) including adiposity, after a slow start, has exploded in the last decade. Not so for AIS research and the environment where, except for monozygotic twin studies, there are only sporadic reports to suggest that environmental factors are at work in etiology. Here, we examine epigenetic concepts as they may relate to human development, normal life history phases and AIS pathogenesis. Although AIS is not regarded as an NCD, like them, it is associated with whole organism metabolic phenomena, including lower body mass index, lower circulating leptin levels and other systemic disorders. Some epigenetic research applied to Silver-Russell syndrome and adiposity is examined, from which suggestions are made for consideration of AIS epigenetic research, cross-sectional and longitudinal. The word scoliogeny is suggested to include etiology, pathogenesis and pathomechanism.