Lower limb muscle power is thought to influence outcome following
total knee replacement (TKR). Post-operative deficits in muscle
strength are commonly reported, although not explained. We hypothesised
that post-operative recovery of lower limb muscle power would be
influenced by the number of satellite cells in the quadriceps muscle at
time of surgery. Biopsies were obtained from 29 patients undergoing TKR. Power
output was assessed pre-operatively and at six and 26 weeks post-operatively
with a Leg Extensor Power Rig and data were scaled for body weight.
Satellite cell content was assessed in two separate analyses, the
first cohort (n = 18) using immunohistochemistry and the second
(n = 11) by a new quantitative polymerase chain reaction (q-PCR)
protocol for Pax-7 (generic satellite cell marker) and Neural Cell
Adhesion Molecule (NCAM; marker of activated cells).Objectives
Methods
The aim of this study was to determine the association
between the Oxford knee score (OKS) and direct assessment of outcome,
and to examine how this relationship varied at different time-points
following total knee replacement (TKR). Prospective data consisting
of the OKS, numerical rating scales for ‘worst pain’ and ‘perceived
mean daily pain’, timed functional assessments (chair rising, stairs
and walking ability), goniometry and lower limb power were recorded
for 183 patients pre-operatively and at six, 26 and 52 weeks post-operatively.
The OKS was influenced primarily by the patient’s level of pain
rather than objective functional assessments. The relationship between report
of outcome and direct assessment changed over time: R2 =
35% pre-operatively, 44% at six weeks, 57% at 26 weeks and 62% at
52 weeks. The relationship between assessment of performance and report
of performance improved as the patient’s report of pain diminished,
suggesting that patients’ reporting of functional outcome after
TKR is influenced more by their pain level than their ability to
accomplish tasks.
Small animal models of fracture repair primarily investigate
indirect fracture healing via external callus formation. We present
the first described rat model of direct fracture healing. A rat tibial osteotomy was created and fixed with compression
plating similar to that used in patients. The procedure was evaluated
in 15 cadaver rats and then Objectives
Methods
We describe three cases of infantile tibia vara
resulting from an atraumatic slip of the proximal tibial epiphysis
upon the metaphysis. There appears to be an association between
this condition and severe obesity. Radiologically, the condition
is characterised by a dome-shaped metaphysis, an open growth plate
and disruption of the continuity between the lateral borders of
the epiphysis and metaphysis, with inferomedial translation of the
proximal tibial epiphysis. All patients were treated by realignment
of the proximal tibia by distraction osteogenesis with an external
circulator fixator, and it is suggested that this is the optimal
method for correction of this complex deformity. There are differences
in the radiological features and management between conventional
infantile Blount’s disease and this ‘slipped upper tibial epiphysis’
variant.
To evaluate the neck strength of school-aged rugby players, and
to define the relationship with proxy physical measures with a view
to predicting neck strength. Cross-sectional cohort study involving 382 rugby playing schoolchildren
at three Scottish schools (all male, aged between 12 and 18 years).
Outcome measures included maximal isometric neck extension, weight,
height, grip strength, cervical range of movement and neck circumference.Objectives
Methods
This review is aimed at clinicians appraising
preclinical trauma studies and researchers investigating compromised bone
healing or novel treatments for fractures. It categorises the clinical
scenarios of poor healing of fractures and attempts to match them
with the appropriate animal models in the literature. We performed an extensive literature search of animal models
of long bone fracture repair/nonunion and grouped the resulting
studies according to the clinical scenario they were attempting
to reflect; we then scrutinised them for their reliability and accuracy
in reproducing that clinical scenario. Models for normal fracture repair (primary and secondary), delayed
union, nonunion (atrophic and hypertrophic), segmental defects and
fractures at risk of impaired healing were identified. Their accuracy
in reflecting the clinical scenario ranged greatly and the reliability
of reproducing the scenario ranged from 100% to 40%. It is vital to know the limitations and success of each model
when considering its application.
The aim of this study was to determine whether exposure of human articular cartilage to hyperosmotic saline (0.9%, 600 mOsm) reduces Using confocal laser scanning microscopy, we identified a sixfold (p = 0.04) decrease in chondrocyte death following mechanical injury in the superficial zone of human articular cartilage exposed to hyperosmotic saline compared with normal saline. These data suggest that increasing the osmolarity of joint irrigation solutions used during open and arthroscopic articular surgery may reduce chondrocyte death from surgical injury and could promote integrative cartilage repair.
The aim of this study was to determine whether subchondral bone influences in situ chondrocyte survival. Bovine explants were cultured in serum-free media over seven days with subchondral bone excised from articular cartilage (group A), subchondral bone left attached to articular cartilage (group B), and subchondral bone excised but co-cultured with articular cartilage (group C). Using confocal laser scanning microscopy, fluorescent probes and biochemical assays, in situ chondrocyte viability and relevant biophysical parameters (cartilage thickness, cell density, culture medium composition) were quantified over time (2.5 hours vs seven days). There was a significant increase in chondrocyte death over seven days, primarily within the superficial zone, for group A, but not for groups B or C (p <
0.05). There was no significant difference in cartilage thickness or cell density between groups A, B and C (p >
0.05). Increases in the protein content of the culture media for groups B and C, but not for group A, suggested that the release of soluble factors from subchondral bone may have influenced chondrocyte survival. In conclusion, subchondral bone significantly influenced chondrocyte survival in articular cartilage during explant culture. The extrapolation of bone-cartilage interactions in vitro to the clinical situation must be made with caution, but the findings from these experiments suggest that future investigation into in vivo mechanisms of articular cartilage survival and degradation must consider the interactions of cartilage with subchondral bone.
This paper reviews the current literature concerning the main clinical factors which can impair the healing of fractures and makes recommendations on avoiding or minimising these in order to optimise the outcome for patients. The clinical implications are described.
The risk of venous thromboembolism in patients following arthroplasty may be reduced by continuing chemical thromboprophylaxis for up to 35 days post-operatively. This prospective cohort study investigated the compliance of 40 consecutive consenting patients undergoing lower limb arthroplasty with self-administration of a recommended subcutaneous chemotherapeutic agent for six weeks after surgery. Compliance was assessed by examination of the patient for signs of injection, number of syringes used, and a self-report diary at the end of the six-week period. A total of 40 patients, 15 men and 25 women, were recruited. One woman was excluded because immediate post-operative complications prevented her participation. Self-administration was considered feasible in 87% of patients (95% confidence interval (CI) 76 to 98) at the time of discharge. Among this group of 34 patients, 29 (85%) were compliant (95% CI 73 to 97). Patients can learn to self-administer subcutaneous injections of thromboprophylaxis, and compliance with extended prophylaxis to six weeks is good.
Little is known about the increase in length of tendons in postnatal life or of their response to limb lengthening procedures. A study was carried out in ten young and nine adult rabbits in which the tibia was lengthened by 20% at two rates 0.8 mm/day and 1.6 mm/day. The tendon of the flexor digitorum longus (FDL) muscle showed a significant increase in length in response to lengthening of the tibia. The young rabbits exhibited a significantly higher increase in length in the FDL tendon compared with the adults. There was no difference in the amount of lengthening of the FDL tendon at the different rates. Of the increase in length which occurred, 77% was in the proximal half of the tendon. This investigation demonstrated that tendons have the ability to lengthen during limb distraction. This occurred to a greater extent in the young who showed a higher proliferative response, suggesting that there may be less need for formal tendon lengthening in young children.
This prospective, longitudinal study documents the muscle strength and baseline function of 18 patients undergoing closed femoral shortening for discrepancy in limb length. Patients were studied for two years following surgery. Function was measured by a self-reported questionnaire, timed tests of performance and measurements of muscle strength and power. After two years, the self-reported function and ability to complete timed functional tests had returned to or improved on the pre-operative values. Muscle strength remained slightly below the pre-operative value and was more marked in the quadriceps than the hamstrings. This study suggests that small decreases in muscle strength and power following closed femoral shortening do not adversely affect the patients’ ability to perform everyday activities.
We performed a prospective genotype-phenotype study using molecular screening and clinical assessment to compare the severity of disease and the risk of sarcoma in 172 individuals (78 families) with hereditary multiple exostoses. We calculated the severity of disease including stature, number of exostoses, number of surgical procedures that were necessary, deformity and functional parameters and used molecular techniques to identify the genetic mutations in affected individuals. Each arm of the genotype-phenotype study was blind to the outcome of the other. Mutations There was a wide variation in the severity of disease. Children under ten years of age had fewer exostoses, consistent with the known age-related penetrance of this condition. The severity of the disease did not differ significantly with gender and was very variable within any given family. The sites of mutation affected the severity of disease with patients with The sarcoma risk in
There are few reports on function after limb salvage surgery using the Ilizarov technique, and none that document the pattern of recovery or predict when maximum function returns. This prospective, longitudinal study documents the baseline functional abilities of 40 consecutive patients with nonunion of a fracture in the lower limb. Patients were studied for at least two and a half years following the completion of surgery. Function was measured by timed tests of functional performance and by the Toronto Extremity Salvage Score self-reported patient questionnaire. Recovery was slowest in the early stages after removal of the frame and greatest between six months and one year. Statistically significant improvement continued up to, but not beyond two years. This observation has important implications for the length of follow-up incorporated into the rehabilitation programmes for patients, predictions of patient status in regard to compensation and for the design of future studies to evaluate functional outcome.
Our aim was to develop a clinically relevant model of atrophic nonunion in the rat to test the hypothesis that the vessel density of atrophic nonunion reaches that of normal healing bone, but at a later time-point. Atrophic nonunion is usually attributed to impaired blood supply and is poorly understood. We determined the number of blood vessels at the site of an osteotomy using immunolocalisation techniques in both normally healing bones and in atrophic nonunion. At one week after operation there were significantly fewer blood vessels in the nonunion group than in the healing group. By eight weeks, the number in the atrophic nonunion group had reached the same level as that in the healing group. Our findings suggest that the number of blood vessels in atrophic nonunion reaches the same level as that in healing bone, but at a later time-point. Diminished vascularity within the first three weeks, but not at a later time-point, may prevent fractures from uniting.
A knowledge of bacteriological profiles in previously treated cases is helpful as a guide to management of infected joint replacements, especially in those cases where bacteriology results are not available. The object of this study was to assess the changing trends of the bacteriology of infected total knee replacements (TKR) over 2 decades. The records of 79 patients undergoing revision for infected TKR between 1979 and 1999 were reviewed. There were 30 males and 49 females, average age 63 years, range 36 – 82 years. The types and sensitivities of bacteria identified, and the use of prophylactic systematic and cement antibiotics, was recorded. The Chi-squared test was used to test statistical significance. 70 organisms were identified in 62 patients: 29 Staphylococcus aureus; 27 Coagulase Negative Staphylococci (CNS); 8 Streptococci; 6 Coliforms. In the 1980s S. aureus accounted for 55% of infections, CNS 25%. In the 1990s S. aureus 38%, CNS 41%. Following the use of systematic antibiotics (3 x cefuroxime) or antibiotic cement (bacitracin/erythromycin/colistin – BEC) at primary TKR, fewer CNS infections were seen (p<
0. 05). There was only 1 case of methicillin resistant S. aureus. Coagulase negative staphylococci had a 36% resistance to flucloxacillin. With BEC cement there was a tendency to increased erythromycin resistance in CNS, but this did not achieve statistical significance. At revision for infected TKR, different bacterial profiles were observed depending on prophylactic antibiotic usage. As CNS now causes >
40% of infections, patients undergoing revision TKR should have antibiotics effective against CNS until definitive results are available.
To determine whether the spectrum of genetic mutation in Hereditary Multiple Exostoses supports a neoplastic aetiology for this condition. Historically, experts have been cautious in attributing neoplastic qualities to the osteochondroma. Solomon states ‘[osteochondromas] are not neoplastic in the ordinary sense of the word’; Morton that it ‘is not a tumour but a growth-aberration; Peterson that the ‘osteochondroma is not a true neoplasm’; and Schmale that ‘exostoses are the result of dysplasia of the lateral apect of the growth-plate’. There are, however, several features of osteochondroma behaviour common to other neoplasms which suggest a neoplastic aetiology:
the existence of an autosomal dominant inherited multiple form, in which lesions are histologically identical to the solitary form. lesions which are distributed randomly and perhaps asymmetrically at ‘high-risk’ anatomical sites (usually adjacent to those physes with greatest growth potential). evidence of behavioural or cellular disorder. a potential for malignant transformation. Recent genetic data has supported a fresh look at the neoplastic nature of osteochondromas. EXT1 and EXT2 genes are responsible for Hereditary Multiple Exostoses (HME). EXT1 codes for a protein which alters the synthesis and display of cell-surface heparan sulphate glycosaminoglycans; molecules which affect cellular growth, differentiation, motility and adhesion. Loss-of-function of such a gene may initiate a neoplastic pathogenesis in osteochondromas. From 1996–1999, 51 families with HME were screened for EXT mutation, with mutations identified in 41 families. EXT mutation was assessed by means of fluorescent single-strand conformational polymorphism (f-SSCP) screening, followed by sequencing analysis.
All frame-shift, splice-site and nonsense mutations are loss-of-function. Missense mutations may result in partial or complete dysfunction if a crucial folding or binding site is involved. Since no missense mutations were new, this suggested their mutation sites are important, and may effectively result in loss-of-function. These data strongly support a tumour suppressor gene function for EXT genes, and a neoplastic pathogenesis for HME.