This study aimed to analyze the correlation between transverse
process (TP) fractures of the fourth (L4) and fifth (L5) lumbar
vertebrae and biomechanical and haemodynamic stability in patients
with a pelvic ring injury, since previous data are inconsistent. The study is a retrospective matched-pair analysis of patients
with a pelvic fracture according to the modified Tile AO Müller
and the Young and Burgess classification who presented to a level
1 trauma centre between January 2005 and December 2014.Aims
Patients and Methods
The diagnosis of periprosthetic joint infection (PJI) remains
demanding due to limitations of all the available diagnostic tests.
The synovial fluid marker, α-defensin, is a promising adjunct for
the assessment of potential PJI. The purpose of this study was to
investigate the qualitative assessment of α-defensin, using Synovasure
to detect or exclude periprosthetic infection in total joint arthroplasty. We studied 50 patients (28 women, 22 men, mean age 65 years;
20 to 89) with a clinical indication for revision arthroplasty who
met the inclusion criteria of this prospective diagnostic study.
The presence of α-defensin was determined using the qualitative
Synovasure test and compared with standard diagnostic methods for
PJI. Based on modified Musculoskeletal Infection Society (MSIS)
criteria, 13 cases were categorised as septic and 36 as aseptic revisions.
One test was inconclusive.Aims
Patients and Methods
The objectives of this study were: 1) to examine osteophyte formation, subchondral bone advance, and bone marrow lesions (BMLs) in osteoarthritis (OA)-prone Hartley guinea pigs; and 2) to assess the disease-modifying activity of an orally administered phosphocitrate ‘analogue’, Carolinas Molecule-01 (CM-01). Young Hartley guinea pigs were divided into two groups. The first group (n = 12) had drinking water and the second group (n = 9) had drinking water containing CM-01. Three guinea pigs in each group were euthanized at age six, 12, and 18 months, respectively. Three guinea pigs in the first group were euthanized aged three months as baseline control. Radiological, histological, and immunochemical examinations were performed to assess cartilage degeneration, osteophyte formation, subchondral bone advance, BMLs, and the levels of matrix metalloproteinse-13 (MMP13) protein expression in the knee joints of hind limbs.Objectives
Methods
The exact aetiology and pathogenesis of microdamage-induced long bone fractures remain unknown. These fractures are likely to be the result of inadequate bone remodelling in response to damage. This study aims to identify an association of osteocyte apoptosis, the presence of osteocytic osteolysis, and any alterations in sclerostin expression with a fracture of the third metacarpal (Mc-III) bone of Thoroughbred racehorses. A total of 30 Mc-III bones were obtained; ten bones were fractured during racing, ten were from the contralateral limb, and ten were from control horses. Each Mc-III bone was divided into a fracture site, condyle, condylar groove, and sagittal ridge. Microcracks and diffuse microdamage were quantified. Apoptotic osteocytes were measured using TUNEL staining. Cathepsin K, matrix metalloproteinase-13 (MMP-13), HtrA1, and sclerostin expression were analyzed.Objectives
Methods
The aim of this study was to identify the most effective regimen
of multiple doses of oral tranexamic acid (TXA) in achieving maximum
reduction of blood loss in total knee arthroplasty (TKA). In this randomized controlled trial, 200 patients were randomized
to receive a single dose of 2.0 g of TXA orally two hours preoperatively
(group A), a single dose of TXA followed by 1.0 g orally three hours
postoperatively (group B), a single dose of TXA followed by 1.0 g
three and nine hours postoperatively (group C), or a single dose
of TXA followed by 1.0 g orally three, nine, and 15 hours postoperatively
(group D). All patients followed a routine enhanced-recovery protocol.
The primary outcome measure was the total blood loss. Secondary
outcome measures were hidden blood loss (HBL), reduction in the
level of haemoglobin, the rate of transfusion and adverse events.Aims
Patients and Methods
Intermittently administered parathyroid hormone (PTH 1-34) has been shown to promote bone formation in both human and animal studies. The hormone and its analogues stimulate both bone formation and resorption, and as such at low doses are now in clinical use for the treatment of severe osteoporosis. By varying the duration of exposure, parathyroid hormone can modulate genes leading to increased bone formation within a so-called ‘anabolic window’. The osteogenic mechanisms involved are multiple, affecting the stimulation of osteoprogenitor cells, osteoblasts, osteocytes and the stem cell niche, and ultimately leading to increased osteoblast activation, reduced osteoblast apoptosis, upregulation of Wnt/β-catenin signalling, increased stem cell mobilisation, and mediation of the RANKL/OPG pathway. Ongoing investigation into their effect on bone formation through ‘coupled’ and ‘uncoupled’ mechanisms further underlines the impact of intermittent PTH on both cortical and cancellous bone. Given the principally catabolic actions of continuous PTH, this article reviews the skeletal actions of intermittent PTH 1-34 and the mechanisms underlying its effect.
This study aimed to investigate the role of quantitative histological
analysis in the diagnosis of fracture-related infection (FRI). The clinical features, microbiology culture results, and histological
analysis in 156 surgically treated nonunions were used to stratify
the likelihood of associated infection. There were 64 confirmed
infected nonunions (one or more confirmatory criteria: pus, sinus,
and bacterial growth in two or more samples), 66 aseptic nonunions
(no confirmatory criteria), and 26 possibly infected nonunions (pathogen
identified from a single specimen and no confirmatory criteria).
The histological inflammatory response was assessed by average neutrophil
polymorph (NPs) counts per high-power field (HPF) and compared with
the established diagnosis.Aims
Patients and Methods
The aim of this study was to investigate the role of miR-126 in the development of osteoarthritis, as well as the potential molecular mechanisms involved, in order to provide a theoretical basis for osteoarthritis treatment and a novel perspective for clinical therapy. Human chondrocyte cell line CHON-001 was administrated by different doses of interleukin (IL)-1β to simulate inflammation. Cell viability, migration, apoptosis, IL-6, IL-8, and tumour necrosis factor (TNF)-α expression, as well as expression of apoptosis-related factors, were measured to assess inflammation. miR-126 expression was measured by quantitative polymerase chain reaction (qPCR). Cells were then transfected with miR-126 inhibitor to assess the effect of miR-126 on IL-1β-injured CHON-001 cells. Expression of B-cell lymphoma 2 (Bcl-2) and the activity of mitogen-activated protein kinase (MAPK) / Jun N-terminal kinase (JNK) signaling pathway were measured by Western blot to explore the underlying mechanism through which miR-126 affects IL-1β-induced inflammation.Objectives
Methods
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
Deep bone and joint infections (DBJI) are directly intertwined with health, demographic change towards an elderly population, and wellbeing. The elderly human population is more prone to acquire infections, and the consequences such as pain, reduced quality of life, morbidity, absence from work and premature retirement due to disability place significant burdens on already strained healthcare systems and societal budgets. DBJIs are less responsive to systemic antibiotics because of poor vascular perfusion in necrotic bone, large bone defects and persistent biofilm-based infection. Emerging bacterial resistance poses a major threat and new innovative treatment modalities are urgently needed to curb its current trajectory. We present a new biphasic ceramic bone substitute consisting of hydroxyapatite and calcium sulphate for local antibiotic delivery in combination with bone regeneration. Gentamicin release was measured in four setups: 1) Objectives
Materials and Methods
To compare the effect of femoral bone tunnel configuration on tendon-bone healing in an anterior cruciate ligament (ACL) reconstruction animal model. Anterior cruciate ligament reconstruction using the plantaris tendon as graft material was performed on both knees of 24 rabbits (48 knees) to mimic ACL reconstruction by two different suspensory fixation devices for graft fixation. For the adjustable fixation device model (Socket group; group S), a 5 mm deep socket was created in the lateral femoral condyle (LFC) of the right knee. For the fixed-loop model (Tunnel group; group T), a femoral tunnel penetrating the LFC was created in the left knee. Animals were sacrificed at four and eight weeks after surgery for histological evaluation and biomechanical testing.Objectives
Methods
The aims of this study were to increase the diagnostic accuracy
of the analysis of synovial fluid in the differentiation of prosthetic
joint infection (PJI) by the addition of inexpensive biomarkers
such as the levels of C-reactive protein (CRP), adenosine deaminase
(ADA), alpha-2-macrogloblulin (α2M) and procalcitonin. Between January 2013 and December 2015, synovial fluid and removed
implants were requested from 143 revision total joint arthroplasties.
A total of 55 patients met inclusion criteria of the receipt of
sufficient synovial fluid, tissue samples and removed implants for
analysis. The diagnosis of PJI followed the definition from a recent International
Consensus Meeting to create two groups of patients; septic and aseptic.
Using receiver operating characteristic curves we determined the
cutoff values and diagnostic accuracy for each marker.Aims
Patients and Methods
To determine whether there is any association between glomerular
filtration rate (GFR) and blood cobalt (Co) and chromium (Cr) levels
in patients with metal-on-metal (MoM) hip arthroplasty. We identified 179 patients with a unilateral 36 mm diameter head
as part of a stemmed Summit-Pinnacle MoM hip arthroplasty. GFR was
calculated using the Modification of Diet in Renal Disease formula.Aims
Patients and Methods
The aim of this study was to investigate the effect of hyperglycaemia on oxidative stress markers and inflammatory and matrix gene expression within tendons of normal and diabetic rats and to give insights into the processes involved in tendinopathy. Using tenocytes from normal Sprague-Dawley rats, cultured both in control and high glucose conditions, reactive oxygen species (ROS) production, cell proliferation, messenger RNA (mRNA) expression of NADPH oxidase (NOX) 1 and 4, interleukin-6 (IL-6), matrix metalloproteinase (MMP)-2, tissue inhibitors of matrix metalloproteinase (TIMP)-1 and -2 and type I and III collagens were determined after 48 and 72 hours Objectives
Methods
Cite this article: A. A. Abubakar, M. M. Noordin, T. I. Azmi, U. Kaka, M. Y. Loqman. The use of rats and mice as animal models in
The use of large-diameter metal-on-metal (MoM)
components in total hip arthroplasty (THA) is associated with an increased
risk of early failure due to adverse local tissue reaction to metal
debris (ARMD) in response to the release of metal ions from the
bearing couple and/or head-neck taper corrosion. The aim of this
paper was to present a review of the incidence and natural history
of ARMD and the forms of treatment, with a focus on the need for
and extent of resection or debulking of the pseudotumour. An illustrative
case report is presented of a patient with an intra-pelvic pseudotumour
associated with a large diameter MoM THA, which was treated successfully
with revision of the bearing surface to a dual mobility couple and
retention of the well-fixed acetabular and femoral components. The
pseudotumour was left Cite this article:
