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Trauma & Orthopaedics Revision
BASIC SCIENCES - Go to Main Contents
Normal bone is lamellar bone, which can be cortical or cancellous. Immature or pathologic bone is Woven bone. Cortical bone makes up 80% of the skeleton and is composed of tightly packed osteons or haversian systems. It has relatively high Young's modulus. Cancellous bone is spongy or trabecular, less dense but undergoes more remodelling. Bone cells are osteoblasts, osteocytes, bone lining cells, osteoclasts and osteoprogenitor cells.
Osteoblasts originate from mesenchymal progenitor cells Osteocytes originate from osteoblasts. Macrophages and osteoclasts share a common origin.
Osteoblasts produce type I collagen.
Composition of bone matrix: Bone tissue wet weight is 70% mineralised matrix, 25% organic matrix and cells and 5% water. 40% of the dry weight of the bone is organic component. 90% of organic matrix is collagen and rest of the organic matrix is made up of proteoglycans, non-collageneous matrix protein (glycoproteins, phospholipids, phosphoproteins), growth factors and cytokines. Collagen is a triple helix of tropocollagen. Hole zones and pores exist within the collagen fibrils for mineral deposition.
Matrix proteins are osteonectin, osteocalcin, osteopontin and others. They promote mineralisation and bone formation. Growth factors and cytokines include transforming growth factor beta, insulin like growth factor, interleukins and bone morphogenic proteins BMP 1 to 6. These play a role in bone cell differentiation, activation, growth and turn over of the bone.
Non-collageneous proteins in bone matrix are dermaton sulphate, heparan sulphate, keratan sulphate and chondroitan sulphate. Chondroitan sulphate is the most abundant. Function of proteoglycan is not well established. 60% of the dry weight of the bone is made up of inorganic mineral component. This consists mainly of calcium hydroxyapatite Formula - CA10PO4 (6OH2). This is responsible for the compressive strength of the bone whereas collagen is responsible for the tensile strength of the bone. Osteocalcium phosphate is also part of the inorganic matrix.
Bone remodelling - Wolff's law - Bones remodels according to the stress applied to it. More the stress, more the bone formation. Piezo electric charges also affect the bone remodelling. Compression side is Electro negative; tension side is Electro positive. Cortical bone remodels by osteoclastic tunnelling (cutting cone). Cancelleous bone remodels by osteoclastic re-absorption, followed by osteoblasts, which lay down new bone.
Major influence on bone metabolism:
(1) Parathyroid hormone
(2) Vitamin D and its metabolism
(3) Calcitonin
The factors, which have beneficial effect on bone formation, are
(1) Sex hormone
(2) Transforming growth factor beta,
(3) Insulin like growth factor
(4) Colony stimulating factor
(5) Interleukin 1, interleukin 6
(6) Bone morphogenetic protein. More than 7 are recognised. BMP's belong to TGF beta super family.
Factors having inhibitory effect on bone formation are -
(1) Thyroid hormones
(2) Glucocorticoid hormones
(3) Tumour necrosis factor alpha
(4) Prostaglandin F2 and E2
(5) Leukotreines
Bone circulation 3 main systems
(1) Nutrient artery or high pressure system
(2) Metaphyseal epiphyseal system and
(3) Periosteal system which is low pressure system
Mechanical properties of the bone: Bone- strength is derived from Composite nature of the material i.e. tensile property of the collagen and compressile behaviour of the mineral and secondly the nature of the bone structure consisting of Haversian, circumferential and interstitial lamellae working synergistically to avoid yield or ultimate strain. Yield strain of the bone is approximately 7000 micro strain. Ultimate strain in bone is approximately 15000 micro strains in normal bone.
There are 2 types of physis
(1) Horizontal growth plate
(2) Spherical growth plate that allows growth of the epiphyses.
Zones of Horizontal growth plate:
(1) Reserve zone
(2) Proliferative zone
(3) Hypertrophic zone which is subclassified into:
Zone of maturation,
Zone of degeneration and
Zone of provisional calcification.
Proliferative zone is kinetically active zone of the growth plate. In the lower hypertropic zone calcium is packed in vesicles and deposited into the surrounding matrix. Most of growth plate synthesises type II collagen, only lower hypertrophic zone synthesises type X collagen. Type I collagen appears in the metaphyses.
Heuter Volkmann' s law of growth plate states that increased pressure causes decreased growth and decreased pressure causes increased growth. This is opposite to Wolff's law.
Rickets and osteomalacia tends to have abnormal provisional calcification zone i.e. the last zone of the growth plate is abnormal because of inappropriate calcification. Mucopolysaccharidosis affects the maturation and degenerative part of the hypertrophic zone. Achondroplasia affects proliferative zone and pseudoachondroplasia affects reserve zone. Osteopetrosis, osteogenesis imperfecta, scurvy and metaphyseal dysplasias affect the secondary spongiosa zone of the metaphyses.
Joint development is divided into three phases:
Phase 1 is blastimal condensation of skeletal elements,
Phase 2 is joint cavitation, the
Phase 3 is synovium and intra articular structural development.
ARTICULAR CARTILAGE & ARTHRITIS
PH of articular cartilage is 7.4. 65 to 80% of wet weight is water. Collagen forms 10 to 20% of the wet weight or more than 50% of dry weight. 90 to 95% Collagen in the articular cartilage is type II collagen. Collagen gives tensile strength to the cartilage. Type X collagen is associated with calcification of cartilage. Proteoglycan forms 10 to 15% of the wet weight of articular cartilage (collagen forms 10 to 20 % of it). This gives compressive strength to the cartilage. Proteoglycans play an important role of inhibiting calcification. Chondrocytes form 5% of the wet weight.
Layers of articular cartilage are
(1) Superficial layer forms 10 to 20%
(2) Middle layer forms 40 to 60% and
(3) Deep layer forms 30% and the
(4) Tide mark
(5) Last layer close to the ossific nucleus is Calcified cartilage.
Layers of cartilage are also grouped as follows:
(1) Gliding zone
(2) Transitional zone
(3) Radial zone
(4) Tide mark and
(5) Calcified zone
Cartilage is a shock absorbing structure. Nutrients and metabolic mediators are provided via the synovial fluid and help to maintain the metabolic state of the cartilage.
Early events in osteoarthritis are characterised by a possibly reversible loss of proteoglycans and an activation of repair mechanism in the chondrocytes. Chondroitin/Keratan sulphate ratio is reversed in OA. Late event includes the modulation of extra cellular matrix into a variant with inferior biomechanical properties. Damaged cartilage fails to repair to its normal zonal organisation and the collagen regenerated is usually unsuitable for repetitive load bearing.
Synovial fluid is produced by the Type B fibroblast like cells of the synovium. Synovial fluid is made up of proteinase, collagenase, hyaluronic acid and prostaglandins.
Main functions
(1) Nourishment of the cartilage
(2) Lubrication
Main mechanism of lubrication in the joint is hydrodynamic and boundary.
Other types of lubrication are weeping & boosted lubrication. Hydrodynamic lubrication is where fluid separates the surfaces under load and boundary lubrication takes place on the slippery surfaces.
Failed attempts of chondrocytes to repair damaged cartilage, characterised by increased water content, alterations in the proteoglycans, collagen abnormalities, binding of proteoglycans to hyaluronic acid is osteoarthritis. Two types are primary and secondary OA.
X-ray features are osteophytes, subchondral cysts and joint space narrowing. Knee is the most commonly affected joint.
Common causes are:
(1) Diabetes
(2) Tabes dorsalis
(3) Syringomyelia
(4) Syphilis
(5) Meningocoele
(6) Congenital insensitivity to pain
(7) Other neurologic problems
Acute rheumatic fever
5 major and 5 minor Jones criteria. Two major criteria or one major and two minor criteria are required to diagnose rheumatic fever.
5 Major criteria are:
(1) Carditis
(2) Polyarthritis
(3) Chorea
(4) Erythema marginatum
(5) Subcutaneous nodules.
Minor criteria are:
(1) Fever
(2) Arthralgia
(3) Previous rheumatic fever
(4) Elevated ESR
(5) Prolonged PR interval on ECG
Most commonly affects hands. Aetiology is unclear, may be cell mediated immune response. HLA focus, HLA-DR4 and DW4. Subcutaneous nodules are seen in 20% of rheumatoid arthritis. Synovium and soft tissues are affected first. Elevated ESR, C reactive Protein and positive rheumatoid factor is present in 80% of cases.
Felty's syndrome is rheumatoid arthritis with splenomegaly and leukopenia. Still's disease is acute onset rheumatoid arthritis with fever, rash and splenomegaly.
In RA Treatment is directed to:
(1) Symptoms & Synovitis
(2) Joint destruction and
(3) Deformities
(4) Cervical spine evaluation
Radiological features in RA: periarticular erosion and osteopenia. Protrusio acetabuli
Systemic lupus erythematosus, fever, butterfly malar rash, pan cytopenia, pericarditis, nephritis and polyarthritis. Joint destruction is not as destructive as rheumatoid arthritis.
JUVENILE RHEUMATOID ARTHRITIS (JRA)
(1) Systemic - 20%
(2) polyarticular - 50% and
(3) pauciarticular - 30%
5 or more joints are involved in polyarticular and 4 or less joint are involved in pauciarticular JRA
Polyarticular JRA can be
(1) Sero-negative
(2) Sero- positive depending on positive rheumatoid factor.
Pauciarticular JRA can be
(1) Early onset usually associated with iridocyclitis
(2) Late onset is the only type of Rheumatoid more common in boys
Characterised by positive HLA-B27 and negative rheumatoid factor.
(1) Ankylosing spondylosis
(2) Reiter's syndrome
(3) Psoriatic arthropathy
(4) Enteropathic arthritis
(1) Gout
(2) Chondrocalcinosis
(3) Calcium hydroxyapatite crystal deposition disease
In pyogenic infectious arthritis joint fluid will have more than 80,000WBC's with more than 75% polymorpho nucleocytes, positive gram stain, low glucose and turbid fluid.
13 types have been described.
Type I - Bone, tendon, meniscus, intervertebral disc annulus and skin
Type II - Articular cartilage and nucleus pulposus of the disc
Type III - Skin, blood vessels
Type IV - Basement membrane
Type V & VI - Small amounts in the articular cartilage
Type VII & VIII - Basement membrane
Type IX - Small amounts in the cartilage
Type X - Abnormal cartilage with calcification
Type XI - Small amounts in articular cartilage
Type XII - Tendon
Type XIII - Endothelial cells
Sarcomere consists of thick and thin filaments in an intricate arrangement that allows fibres to slide on each other. Thick filament is myosin and thin filaments have troponin and tropomycin. H zone thick filaments. I band solely thin actin filament.
Types of muscle contraction are
(1) Isotonic which is constant tension in the muscle, which can be concentric or eccentric. Concentric is when muscle is shortening and eccentric is when muscle is lengthening.
(2) Isometric where length of the muscle remains same
Types of muscle fibres:
(1) Slow twitch or Type I fibres. Slow red ox specialise in endurance activities or otherwise called aerobic activities
(2) Fast twitch or Type II fibres are anaerobic activities in sprinters
Seddon's Classification: Neuropraxia, axonotmesis and neurotmesis.
Sunderland has classified the same injury into 5 groups:
(1) Neuropraxia
(2) Axon injury with intact endoneurium
(3) Axon injury with intact perineurium
(4) Axon injury with intact epineurium
(5) Complete nerve disruption or neurotmesis.
Recovery of nerve injury has got 3 basic mechanism:
(1) Re-myelination through areas of focal neuropraxia
(2) Collateral sprouting from surviving axon motor terminals to denervated muscle
(3) Nerve regeneration from the site of injury
Main Diagnostic Electro-physiologic procedures are:
(1) Nerve conduction studies and
(2) Needle Electro myography.
Nerve conduction study:
Motor nerve conduction and
Sensory nerve conduction studies
Motor nerve conduction studies -
(1) Conduction velocity
(2) Distal motor latency and
(3) Amplitudes are the parameters to be measured
Sensory nerve conduction studies:
(1) Sensory nerve action potential,
(2) Amplitude and conduction velocity
Needle Electro myography has got 2 main aspects -
(1) Muscle at rest and
(2) During the voluntary muscle action.
Normal muscle at rest is electrically silent.
METABOLIC AND ENDOCRINE SYNDROMES affecting bone
PRIMARY HYPER PARATHYROIDISM
1 in 1000 subjects, calcium and parathormone both are elevated with hypercalcaemia. Most common cause is adenoma - 80%. Increases calcium resorption from the bone, increases calcium absorption from the intestine and increases calcium excretion from the renal system.
X-ray findings - Osteitis fibrosa cystica, osteopenia, localised boned resorption at the terminal phalanges or distal clavicle and changes in skull films. Subcortical bone resorption in the jaw produces Brown tumours.
It is an absolute or relative deficiency or inadequacy of parathyroid function. If it is associated with parathyroid hormone resistance it is pseudohypo-parathyroidism otherwise called Albright's hereditary osteo dystrophy. Shortening of the metacarpals and metatarsals particularly the fourth metacarpal, brachydactyly and exostoses.
It is a complex bone disorder in patients with chronic renal failure, which leads to inability to excrete phosphate with compensatory reduction in serum calcium.
(1) Vitamin D deficiency rickets
(2) Hereditary vitamin D dependant rickets
(3) Familial hypophosphataemic rickets (vitamin D resistance rickets)
All groups of rickets alkaline phosphatase is increased.
Vitamin D deficiency rickets:
Harrison's groove of the sternum, rachitic rosary is enlargement of costochondral junction.
X-ray findings - Physes appears enlarged and cupped metaphyses.
Treatment is 5000 units of Vit. D.
Vitamin D dependant rickets:
It is the defect in renal 1 alpha hydroxylation of 25-dihydroxy vitamin D3. Treatment here is very high doses of vitamin D upto 20,000 to 100,000 units of vitamin D daily.
Vitamin D resistance rickets is X linked recessive otherwise called hypo phosphatemic rickets. Decreased phosphate level in the blood and increased alkaline phosphatase. Treatment: Combination of phosphate with vitamin D is the treatment.
It is an autosomal recessive condition where there is low alkaline phosphatase in the blood gives typical features of rickets but alkaline phosphatase is low. There is no satisfactory treatment for this condition.
(Adult counterpart of rickets)
Aetiology can be dietary, renal tubular acidosis or tumour induced osteomalacia. Serum calcium may be low, alkaline phosphatase is high. Bone biopsy: - increased width of unmineralised bone.
X-ray shows looser's zone or pseudo fractures on the concave surface of long bones as well as on flat bones. It lacks calcium, so compression side is weaker than the tensile side - so pseudofractures are on the concave side. In osteogenesis imperfecta the tensile side is weak because of abnormal collagen so looser's zone is usually on the convex side.
SCURVY or vitamin C deficiency
Leads to abnormal collagen in the bone resulting in bone pains and deformities. Metaphyseal clefts are characteristics of scurvy.
Is diminution of bone mass.
Mainly 2 types -
Primary osteoporosis
Secondary osteoporosis
Primary osteoporosis:
Type I or Type II
Type I has excessive loss of cancellous bone, at the time of menopause
Type II has excessive loss of cancellous as well as cortical bone. 15 to 20 years after menopause and elderly men - this is because of senile bone mass diminution or senile osteoporosis. Type II osteoporosis is also called Low Turnover osteoporosis.
Type I has got more predilection for cancellous bone fractures, like wrist fractures whereas type II tends to have cortical as well as cancellous bone loss resulting in inter-trochantric and femur fracture.
Secondary osteoporosis is due to underlying bone conditions like hyper parathyroidism, hyper thyroidism etc., which increase the rate of the bone remodelling as well as the rate of bone loss. This is also called High turnover osteoporosis.
Evaluation of vertebral fractures in the osteoporotic patient:
Mnemonic TOMEO:
T - Tumour screening
O - Osteopenia screening
M - Marrow screening
E - Endocrine screening
O - For osteomalacia screening
(1) Tumour screening is x-ray, bone scan, MRI and CT;
(2) Osteopenia screening is DEXA scan
(3) Marrow screening is full blood count, serum electrophoresis for myeloma
(4) Endocrine screening for parathyroid cortisol, thyroid function, diabetes
(5) Osteomalacia screening for rickets before making a diagnosis for osteoporosis. So TOMEO for osteoporosis after vertebral fractures
Measurement of bone scan mainly DEXA scan, dual energy x-ray absorptiometry or quantitative CT.
Treatment
(1) Decrease the bone loss by phosphate or diphosphanate
(2) Halt the bone loss by calcium, vitamin D, calcitonin, oestrogen, mild exercises
(3) Increase the bone mass by fluoride with calcium, fluoride with vitamin D, fluoride with oestrogen, fluoride with calcitonin, exercises or combinations of above.
Preventive therapy: Women at risk - recommend increased physical activity. Oestrogen is used to halt the bone loss in early postmenopausal years and is currently highly recommended in those who do not have the risk of this treatment. Progestin probably diminishes the risk of endometrial cancer.
3 to 4% of the population over the age of 50 years suffer from Paget's disease. Pathologically classified as lytic and sclerotic phases, eventually end up as a mixed phase. Paramyxo virus antibodies have been identified in the Paget's disease suggestive of chronic viral infection.
Clinical manifestation and complications of Paget's disease -
Mnemonic - ABCD (PM)2:
A - Arthritis
B - Blood flow
C - Cranial nerves
D - Deformity
P - Pain
P - Pseudoarthrosis
M - Metabolic complications and
M - Malignant transformation
Arthritis can be due to
(1) Articular bone deformation
(2) Abnormal joint bio-mechanic
(3) Sub capital support loss or
(4) Gout
Blood flow complications are due to hyper dynamic circulation.
Cranial nerve palsy's are common with Paget's disease. Hearing is most commonly impaired.
Deformities are due to the abnormal bone structure.
Pain is associated with active disease.
Pseudoarthrosis may result in a fracture with delayed or non-union.
Metabolic complications are hyper calciurea and hyper calcaemia mainly after immobilisation.
Malignant bone tumour is very rare about 1% incidence.
X-ray picture: of Paget's disease will show mixed picture of osteolysis and osteosclerosis. Enlargement of the vertebral body is a hallmark of Paget's disease of the spine.
Treatment is again addressed to these ABCD (PM)2. Treatment for arthritis, treatment for increased blood flow (hyperdynamic circulation) during operations, treatment for cranial nerve palsy, treatment for deformities, treatment for pain, treatment for pseudoarthrosis and non-unions, treatments for metabolic disorders like hyper calcemia during the operation and after the operation and treatment for malignant transformation of the bone.
Medical management: Calcitonin therapy and biphosphonates. Biphosphonates are first generation, second generation and new generation. First generation is etidronate; second generation is pamidronate and third is alendronate.
Total hip arthroplasties in Paget's disease poses special problems.
(1) Technical difficulties
(2) Medical management to avoid hyper-calcemia, acidosis and bleeding. Though not proven, Calcitonins and biphosphonates are commonly used.
(3) Heterotopic ossification - it is as high as 5%
(4) Early prosthetic loosening is not been statistically proved.
Most common lysozomal storage disease resulting from an inborn error of glycosphingo lipid metabolism. Autosomal recessive.
Haematological problems Anaemia, thrombocytopenia and hepato-splenomegaly.
Pathogenesis is incompletely understood. Progressive marrow infiltration leading to loss of trabecular bone and lytic lesions so called bone crisis. Gaucher cells are not directly involved in bone resorption but they cause intra-medullary expansion and intra-osseous increased pressure resulting in extra vascular compression and ischaemia.
Orthopaedic problems in Gaucher's disease:
(1) Osteonecrosis AVN of femur or humeral head and
(2) Vertebral compression fractures
Radiological changes have been staged into:
Stage 1 - Osteopenia
Stage 2- Medullary expansion
Stage 3 - Localised destruction or osteolysis giving ground glass appearance
Stage 4 - Osteonecrosis and
Stage 5 - Diffuse destruction, epiphyseal collapse and osteoarthritis
Two complications of Gaucher's-
AVN and Bone crisis
Treatment - enzyme replacement therapy particularly when treatment is initiated early in the disease
Treatment of complications:
(1) Bone crisis supportive management
(2) Osteonecrosis core decompression during the early acute phase.
(3) Degenerative joint disease -may need joint replacement
(4) Pathologic fractures - may need internal fixation
(5) Neurologic compression syndrome - may need spinal decompression
Kinematics is the study of motion in terms of displacement, velocity and acceleration without reference to the cause of the motion.
Kinetics relates the action of forces and Kinesiology is the study of human movement and motion.
Newton's Laws
First law is Law of Inertia - If a zero net external force acts on a body, the body will remain at rest or move uniformly
Second Law - Law of Acceleration - The acceleration A of an object of mass M is directly proportional to the force applied to the object. F = M x A
Third Law is Law of Reaction - For every action there is equal and opposite reaction.
Vector has 4 characteristics -
(1) Magnitude, (2) Direction, (3) Point of application and (4) Line of action.
Rotational effect of a force on a body about a fulcrum is movement.
Work is Force multiplied by distance
Energy is the ability to perform work, which can be either potential energy (stored energy) or kinetic energy (energy due to motion).
Force acting on a body is load.
Deformation can be
(1) Elastic deformity or otherwise called temporary deformity
(2) Plastic deformity or otherwise called permanent deformity. P for P. Plastic for Permanent
Stress = Force / Area. Stress is the intensity of internal force, which can be compressive or tensile.
Strain = Relative measure of a deformation.
Stress is proportional to strain up to a limit or otherwise called proportional limit. This is Hooke's law.
Young's modulus is a measure of the stiffness of a material or its ability to resist deformation. It is represented as E.
E = Stress divided by Strain.
Stress strain curve:
(1) Yield point is the point where the material from its elastic region goes on to plastic region i.e. permanent deformity is plastic deformity
(2) Ultimate strength is the maximum strength obtained by the material
(3) Breaking point is when material breaks
Plastic deformation is change in length after removing the load
Material can be
(1) Brittle material has minimal or no plastic deformation before it breaks. e.g. is poly methyl methacrylate cement
(2) Ductile material which has large amount of plastic deformation e.g. metal
(3) Viscoelastic material exhibits stress strain behaviour that is time, rate dependent. e.g. bone.
Important points to remember about the metal is
Fatigue point - fatigue failure occurs with repetitive loading cycles at stress below the ultimate tensile strength. If a stress is less than a predetermined amount of stress, called the endurance limit, material may be loaded cyclically, infinite number of times without breaking.
Creep: is progressive deformation of metal over an extended period.
Corrosion is dissolving of metal. Corrosion can be
(1) Galvanic corrosion which is due to dissimilar metal
(2) Crevice corrosion due to low oxygen tension
(3) Stress corrosion due to high stress gradients
(4) Fretting corrosion which is from small movements abrading the outside layers and
(5) Miscellaneous corrosion due to intra granular inclusions
The following is the order of materials with decreasing level of Young's modules:
(1) Ceramic
(2) Cobalt chrome
(3) Stainless steel
(4) Titanium
(5) Cortical bone
(6) Matrix polymers
(7) PMMA
(8) Cancellous bone
(9) Polyethylene
(10) Tendon or ligament
(11) Cartilage
Force is a vector quantity with magnitude and direction, which will accelerate the body in the direction of application.
Types of forces in joint biomechanics:
(1) External force which is ground reaction force, gravitational force and applied force through contact
(2) Internal force which is muscle contracting force. Joint contact and sheer forces as well as capsulo ligamentous contractions.
Joint movements are:
Gliding motion
Spinning motion and
Rocking motion
Ceramics are non-metallic materials that can be either bioactive or inorganic.
Bioactive ceramics are glasses such as silicon dioxide and calcium phosphate ceramics. Calcium phosphate ceramics are hydroxyapatite, tricalcium phosphate and fluorapatite.
Inorganic oxide ceramics are alumina and zirconia.
Types of wear in the arthroplasties:
(1) Abrasive wear
(2) Adhesive wear and
(3) Third body wear
IMAGING OF THE MUSCULO-SKELETAL SYSTEM
First radiograph ever made was of a hand of the wife of Wilhelm Conrad Roentgen in 1895.
Nuclear medicine: SPECT full form is - Single Photon Emission Computed Tomography.
Bone scan, intravenously administered technetium 99m methylene diphosphanate (MDP) is incorporated into bone by adsorption on to hydroxyapatite.
Tracer uptake is reflection of osteoblastic activity. Has 3 phases.
(1) First Phase - radio nuclide angiogram every 2 to 5 seconds for 30 to 60 seconds
(2) Static blood pool which is second phase - reflects soft tissue distribution and
(3) Skeletal phase which is delayed phase when the radioactive material is taken up by the osteoblasts
Major areas of application: infection, trauma, AVN, neoplasia.
Acute osteomyelitis has got sensitivity and specificity reported to be more than 90%. Specificity drops to 33% when underlying bone pathology is present. Most authors believe the leukocyte imaging is superior to gallium imaging for cases of complicated osteomyelitis. Leukocyte imaging is not related to bone turnover of the tracer and is more specific for infection where, neutrophils are in abundance.
Weakness of leukocyte scans are
(1) Non-bacteria infections where neutrophils are not the major responders
(2) Leukocyte imaging of the vertebral osteomyelitis has less accuracy specially the cold spots
(3) Technically more difficult
(4) Neutropenic patients may not be well labelled
Ultrasound is based on the transmission of sound waves through tissue and the time it takes for the waves to be reflected back to the transducing probe.
Computed tomography uses a tightly collimated, fan like beam of x-rays to produce tomographic images.
Magnetic resonance imaging: nuclear spin is the underlying principle of MRI. Only those nuclei with an odd number of proton or neutrons possess nuclear spin. Hydrogen nucleus is utilised in medical MRI because of its natural abundance in the human body.
Magnetic field is created around the body to be imaged and the radio frequency pulse is used to deflect the orientation of the protons. Two aspects to consider are:
(1) Time required for 63% of the signal to disappear irreversibly is called the T2 relaxation time and
(2) Time required restoring 63% of the equilibrium population of the magnetic movement to be aligned with the external magnetic field after being deflected by a 900 pulse is T1 relaxation time
In simple words all the hydrogen ions are directed to one external magnetic field that is the first step.
Second step is - the deflection of these ions by radio frequency waves.
Third step - calculating the time required for 63% of the signal to return to the externally aligned magnetic field is T1 relaxation
Fourth step - Time required for 63% of the signal to disappear completely when the external magnetic field is taken away is T2 relaxation time.
Water in inflamed tissues is bright on T2 images of the MR scan. Annulus pulposus, infection and inflammation of the soft tissue as well as bone infection are bright on T2 images. Fat is bright on T1 images. (H2O for T2. 2 for 2 is easy to remember)
MRI scan is a better imaging modality for the structures with more water content. Bone does not have a lot of water content so CT scan is a better imaging modality compared to MRI scan for bones.
Statistical Hypothesis:
(1) Null (H0): No difference between the groups. ( No association between the disease & risk factor)
(2) Alternative(H1): There is difference between the groups.(Some association between the disease and the risk factor)
Type I error: Rejecting the null hypothesis by mistake. Alpha is the probability of making this error. ({Alpha 0.05 means 5% chance of making an error}{convicting an innocent person})
Type II error: Fail to reject the null hypothesis when in fact null hypothesis is false. Beta is the probability of making this error. (Setting a guilt person free). 1 - beta is the power of the study. More the number higher the power. (Number is power)
Incidence: New cases in a population at a given time
Prevalence: Total number of cases at a given time
Sensitivity: Number of true positive cases detected (True positives / all with the disease)
Specificity: Number of true negative cases not detected. (True negatives / all without disease)
Positive Predictive value: Number of true positives / number who have tested positive
Negative Predictive value: Number of true negatives / number who have tested negative. (Predictive values are for evaluating the tests)
P-value: Probability of the difference between the groups has occurred by chance. (P = 0.05, means 5% probability of the difference is a chance occurrence.)
T-test: Calculates the difference between the two means (Blood pressure readings of two groups mean values, parametric data)
Paired T-test: Two values of the same population compared with the two values of another population. (2 blood pressure readings of each person in group A compared with two blood pressure readings of each person in group B)
ANOVA test: Comparing three or more than three variables (groups).
Chi-square test: Compares two or more percentages or proportions of categorical outcomes (Not mean values)
Mann-Whitney U-test, Rank tests: Comparing two non-parametric data (e.g.: pain and other subjective data)
Meta-analysis: Pooling data from several studies (may be literature) to achieve greater statistical power.
Case control studies: Observational study. Often retrospective. Sample chosen based on presence (cases) and absence (control) of the disease.
Cohort Study: Observational study. Sample chosen based on presence or absence of risk factors. Subjects followed over a period of time for development of the disease.
Clinical trials: Experimental study. Difficult to conduct. Compares therapeutic benefits of
