Locomotion 1 Flashcards
How do radio-graphic projections work in terms of terminology
- Refers to the path taken by the X-ray beam through the structure where the primary beam enters the tissue and the second part where the beam exits
where does beam go with ventrodorsal projection
beam enters the abdomen ventrally and exits dorsally
Left lateral recumbency where does beam go
right side up, left side down -> gives left lateral projection
○ Names after the side through which the beam exits the body
What are the 3 main types of joints
1) fibrous
2) cartilaginous
3) synovial
Which thoracic vertebra is the anticlinal vertebra
11 - process change orientation
Where is the intervertebral fibrocartilaginous joint
the intervertebral disc comprises a pulpy nucleus within a fibrous ring and lies in the intervertebral space between the bodies of each adjacent vertebra
Where is the costovertebral joint found
there are two
1) between the head of the rib and the costal fovea
2) between the turbercle of the rib and the transverse process of the thoracic vertebra
where is the sternocostal joint found
the joint between the costal cartilage and the sternebra
where is the costochondral joint
the joint between the rib bone and the costal cartilage
on what aspect of the carpus is the carpal seasmoid located
medial palmar
sesamoid bone where form and function
Form within tendons and ligaments
1) increase the compressive strength of these structures
2) reduce the impact of friction as ligaments move across bones
3) increase the mechanical advantage of ligaments
what is the other name for the glenohymeral joint
shoulder joint
what bones make up the pelvic inlet and pelvic outlet
Pelvic inlet: Ilium crest, pubis (cranial), ilium
Pelvic outlet: ischium and caudal pubis
What are the 4 sesamoid bones associated with the stifle
1) patella
2) fabellae - medial and lateral
3) popliteal sesamoid
what does the stifle comprise of
femoropatellar and femorotibial joint
list 3 functions of bone
1) support where rigidity required
- levers for locomotion
- protection
2) houses haemopoietic tissues
3) calcium homeostasis
What are the 3 types of tissue within the bone
1) all bones comprised of combination of: o cortical (= compact) bone o trabecular (= cancellous) bone – porous network 2) periosteum – connective tissue covering outer surface of bone (except at articular surfaces) 3) endosteum – all surfaces inside bone - including all the trabecular
3 regions of the bone
1) diaphysis (shaft - longer) – exclusively cortical bone surrounding marrow cavity
2) epiphysis at each end – mostly trabecular bone surrounded by thin shell of cortical bone
3) metaphysis between diaphysis and epiphyses – transition from mostly cortical to mostly trabecular
List the 3 sources of blood supply for the bone and what occurs in mature bone
1) nutrient artery enters diaphysis to supply marrow and cortical bone
2) metaphyseal arteries
3) epiphyseal arteries
Mature bone -> vessels from different regions anastomose -> no anastomosis between epiphyseal and metaphyseal vessels until skeletal maturity
§ due to cartilaginous growth plate
what is the venous drainage of bone marrow and cortical bone
drainage of bone marrow through veins accompanying nutrient, epiphyseal and metaphyseal arteries
o drainage of cortical bone to venules in periosteum
What is bone, and what is it composed of and what is the two types of bone as it matures
- bone is a connective tissue
• major component is type I collagen
• several additional glycoproteins (many bind calcium)
• hydroxyapatite (mainly calcium and phosphate) - mineralisation gives strength
1) organised in layers (lamellae) in mature (lamellar) bone
2) disorganised in immature (woven) bone (found in developing and healing bone - fast maturation
List the 6 bone cells
1) osteoblasts
2) osteocytes
3) bone lining cells
4) osteoclasts
5) bone marrow cells - haemopoietic and adipose tissue
6) blood vessel cells
Osteoblasts where found, function and what mature to
- round cells found on bone surfaces
- secrete osteoid (mixture of bone matrix proteins) which then becomes mineralized to form rigid bone tissue
○ Mineralisation takes a few days to form - become osteocytes as they are embedded in the matrix they secrete
Osteocytes what look like, what structures do they possess and their function
- small round cells within lacunae surrounded by bone matrix, less cytoplasm than osteoblasts
- possess fine processes extending into canaliculi (fine channels)
- processes form junctions with processes from other osteocytes and osteoblasts
- thought to have a role in sensing of mechanical strain that bones are subjected to
○ Secrete molecules that travel through the canaliculi which send messages to the cells on the surface
○ May stimulate bone formation - too much mechanical strain for the bone at that time
Bone lining cells shape, where found and function
- flattened cells covering resting bone surfaces
- capable of differentiating into osteoblasts
Osteoclasts shape, where found and function - how achieve this
- large multinucleate cells
- sparsely scattered on bone surfaces - small number
- responsible for bone resorption:
○ adhere to bone through sealing zone, creating microenvironment between cell and bone surface
○ secrete hydrogen ions and lysosomal enzymes to degrade bone matrix
Organisation of bone tissue what are the 2 types hw organised and what contain
1) Trabecular bone
• network of bone plates and rods
• interspersed with spaces containing bone marrow and blood vessels
2) Cortical bone
• organised into Haversian systems (osteons):
○ longitudinal cylinders consisting of concentric bone lamellae surrounding a central blood vessel and nerve branches (vasomotor and sensory) within ‘Haversian canal’
• blood vessels within Haversian canals linked to each other through transverse ‘Volkmann’s canals’
Differentiation of bone cells what are the 6 different times this occurs
1) embryonic development
2) growth
3) maintenance
4) response to changing mechanical or metabolic needs
5) repair
6) other types of pathology
mesenchymal stem cells what bone cells do they produce, where located, what other cells produce
- Osteoblasts, bone lining cells and osteocytes
- located in most connective tissues, including bone marrow stroma
- can differentiate into adipocytes and muscle cells
Active osteoblasts what occurs when secretion ceased
become osteocytes or bone lining cells, or undergo apoptosis when secretion has ceased.
Osteoclasts where derived and what become to stimulate bone resorption
- derived from haemopoietic cells of monocyte/macrophage lineage (present in blood and bone marrow).
- initially differentiate into mononuclear preosteoclasts, which fuse with each other to form multinucleate osteoclasts if there is continuing stimulus for bone resorption
Embryonic bone development what are the 2 ways and main difference
1) intramembranous ossification
2) endochondral ossification - requires cartilage
Intramembranous ossification what occurs and in which bones
• condensation of embryonic mesenchyme, followed by differentiation into osteoblasts and secretion of osteoid to form spicules of woven bone,
○ gradually forming a network of trabeculae to extend the bone
-> many of the skull bones
What are the 3 functions of cartilage
1) Support where flexibility required
2) Shock absorption - stifle joint also have menisci that adds in this
3) Smooth articular surface - unlike with bone
Cartilage what is it composed of and are there vessels present?
cells and extracellular matrix
• composition of matrix and ratio of cells/matrix varies with cartilage type
• usually avascular - some cartilage do have a vascular supply, if cartilage is very large chondrocytes cannot get diffusion from circulatory system outside cartilage
What is the only cell type found within cartilage, structure, function and how to know if just divided
Chondrocytes
• encased in lacunae within extracellular matrix
• proliferation results in occasional pairs of chondrocytes within lacunae (‘interstitial growth’)
○ Gradually push away as create extracellular matrix -> therefore in older animals will see chondrocytes fairly separated from each other
Extracellular matrix of cartilage what secreted by, what do the fibers resist and what are the fibers composed of
synthesized and secreted by chondrocytes
• fibres (resist stretching) and amorphous extracellular material (resist compression)
• fibres composed of type II collagen
○ almost exclusive to cartilage - narrower and thinner than bone collagen (collagen type I)
○ not normally visible microscopically
- Determine the shape of the cartilage
amorphous extracellular material of cartilage what are the 2 main materials what do they form and what does this result in
composed of proteoglycans and hyaluronan (shapeless)
○ proteoglycans consist of core protein and sulphated glycosaminoglycan (GAG) side chains (polysaccharides)
○ proteoglycans form large aggregates with hyaluronan (a large non-sulphated GAG - no protein content)
§ GAGs (glycosaminoglycan) have multiple negative charge, therefore strongly hydrophilic - attract water
§ swelling pressure of hydrophilic proteoglycan aggregates counteracted by tension of collagen fibres, resulting in extremely high resistance to compression chondrocyte lacuna
§ Very important in shock absorption
What are the 3 types of cartilage
1) hyaline
2) elastic
3) fibrocartilage
Hyaline cartilage where found, what structure does it contain, appearance, how are cells arranges, and ratio of GAGs/collagen
found in:
○ respiratory tract (nose, larynx, trachea, bronchi)
○ ventral ends of ribs
○ articular cartilage (smooth, resilient, frictionless surface)
○ growth plates of growing long bones
- has a perichondrium (connective tissue structure that is continuous with the cartilage that connects it)
• white glassy appearance grossly
• cells arranged randomly except in growth plate, where arranged in columns
• high ratio of GAGs/collagen
Elastic cartilage where found, how different to hyaline cartilage, what structures within
found in: ○ external ear ○ epiglottis (part of larynx) ○ Arytenoid cartilage • more flexible than hyaline cartilage • elastic fibres in matrix • has perichondrium
Fibrocartilage where found, what structures make it unique and ratio of GAGs/collagen
found in:
○ intervertebral discs
○ Menisci - more flexible - located between two bones to provide additional shock absorption
○ points of attachment of tendons and ligaments to bone
○ cardiac skeleton - structure around the valves
• low ratio of GAGs/collagen
• no perichondrium
• chondrocytes arranged in lines between bundles of fibres perichondrium
Endochondral ossification what does it begin with and the 6 steps
begins with formation of cartilage model, followed by formation of primary centre of ossification
1) Hypertrophy of chondrocytes mid-diaphysis
2) formation of periosteal bone collar from mesenchymal stem cells -> osteoblasts
3) death of hypertrophic chondrocytes
4) invasion of cartilage by osteoclasts and blood vessels
5) resorption of cartilage matrix by osteoclasts
6) deposition of bone on cartilage remnants by osteoblasts
Endochondral ossification what other 6 steps occur after the primary centre of ossification has developed
1) chondrocytes in cartilage are still proliferating at the end of the bone -> formation of epiphysis
2) primary centre of ossification continues to enlarge
3) primary trabeculae in mid-shaft is resorbed to form marrow cavity which grows
4) formation of at least one secondary centre of ossification in epiphyseal cartilage at each end, through process similar to that for primary centre
5) growth continues at the growth plate (b/n primary and secondary center) through proliferation of chondrocytes
6) closure of growth plate following puberty
What are the 3 behaviours of chondrocytes during endochondral ossification and what regulated by
1) proliferation -> stimulated by growth hormone which acts through insulin-like growth factor-1 -> stimulated by locally secreted bone morphogenetic proteins (BMPs)
§ inhibited by signalling through fibroblast growth factor (FGF) receptor 3
2) Cartilage matrix secretion - stimulated by IGF1 and BMPS
3) hypertrophy - bone morphogenetic proteins (BMPs)
§ inhibited by signalling through fibroblast growth factor (FGF) receptor 3
List 3 behaviours of invading cells during endochondral ossification and what regulated by
1) vascular endothelial growth factor (VEGF) stimulates angiogenesis
2) BMPs stimulate osteoblast differentiation from bone marrow stromal cells
3) receptor activator of NFkB ligand (RANKL) stimulates osteoclast differentiation - REQUIRED
What can lead to chondrodysplasia and give an example
Mutations in genes regulating endochondral ossification
Genes encoding for
• cartilage matrix proteins
• hormones or growth factors that regulate endochondral ossification, or:
○ their receptors
○ intracellular mediators of their effects
a mutation in the aggrecan (cartilage proteoglycan) gene responsible for ‘bulldog dwarfism’ (severe chondrodysplasia) in Dexter cattle
What does the timing of ossification and growth plate fusion based on and when for primary and secondary ossification centers in different species
Dependent on the species and the breed
Primary -> of major limb bones form before birth in all domestic mammals
Secondary of major limb bones present at birth in ungulates (hooved - need to have well developed limb bones - need to run from predators) but not in dog and cat
What are the 2 processes involved with shaping of bone during growth and why does this occur
1) formation through osteoblastic activity on selective bone surfaces
2) resorption through osteoclastic activity on other bone surfaces
NEED TO MAKE BONE LARGER BUT NOT THCK
in response to changing mechanical loads or bone injury
What are the 4 general steps in growth of long bones
1) Increase diameter of diaphysis via formation
2) Expand marrow cavity - more room for bone marrow to provide more stem cells and blood cells -> therefore resorb bone within the cavity
3) Retain shape, wide at epiphysis for muscle attachments before narrow at diaphysis so not too heavy -> resorption of periosteal surface
4) growth in length through chondrocyte proliferation in the growth plate
What are the responses to mechanical loading and how do they come about
This is done via production of molecules from osteocytes (detect strain and produce molecules through canaliculi)
1) loading stimulates formation (osteoblasts) and suppresses resorption (osteoclasts), leading to thickening of trabeculae and/or cortex; this may result in a change in shape or volume of bone.
2) unloading stimulates resorption and suppresses formation, leading to thinning of trabeculae and/or cortex.
Remodelling of bone mechanism and what surfaces does this occur on
Mechanism -> within cortical bone, osteoclasts tunnel through bone longitudinally, followed by osteoblasts which deposit concentric lamellae of bone to fill in the tunnel, leaving space for blood vessel, thus forming new osteon.
occurs on periosteal and endosteal surfaces, as well as within cortical bone
List 3 main factors that activate osteoblast activity during bone modelling, remodelling, repair and pathology
1) sex steroid hormones (oestrogen, testosterone), BMPs (bone morphemic proteins), other growth factors
2) mechanical load
3) inflammatory cytokines and prostaglandins
List 3 main factors that activate osteoclast activity during bone modelling, remodelling, repair and pathology and what are these factors mediated by
1) PTH (calcium homeostasis, especially during pregnancy and lactation)
2) mechanical unloading (e.g. rest periods following training – horses)-
3) inflammatory cytokines and prostaglandins
○ most of these effects mediated by osteoblasts – hormones and cytokines stimulate RANKL expression in osteoblasts
What are the 4 main stages during cellular fracture repair and are the stages highly defined
1) inflammation
2) soft callus formation
3) hard callus formation
4) remodelling
- stages are sequential but may be considerable overlap -> no clear differentiation
What are the 4 main stages in inflammation during fracture repair
- Disruption of vascular integrity leads to formation of a haematoma.
- Haematoma contains coagulation factors which attract granulocytes, lymphocytes and macrophages into haematoma.
- Inflammatory cells secrete cytokines including interleukins-1 and -6, and growth factors, BMPs -> recruitment of mesenchymal stem cells
- Granulation tissue formed through:
○ growth of capillaries into haematoma
Soft callus formation what is the result and the 4 stages
This stage, where present, involves formation of a fibrocartilaginous tissue around fracture ends.
1) Mesenchymal stem cells differentiate into:
○ chondrocytes, which proliferate and secrete cartilage matrix
○ fibroblasts, which generate fibrous tissue
2) Cell proliferation and matrix production stimulated by growth factors, including PDGF, FGFs, IGFs and BMPs.
3) Fibrocartilaginous plug forms between fracture fragments, providing some stability - not rigid as isn’t bone
4) Chondrocytes undergo hypertrophy, in preparation for vascular invasion and replacement by bone (endochondral ossification)
Hard callus formation what are the 2 main steps and what is needed
Formation of mineralised bone matrix, either:
1) replacing fibrocartilaginous soft callus, or
2) where no soft callus present, directly within the fracture gap and/or on existing bone surfaces.
• Mesenchymal stem cells differentiate into osteoblasts and secrete bone matrix (usually woven bone), under influence of BMPs.
• High oxygen tension critical for osteoblast differentiation, thus hard callus formation requires adequate vascular supply.
Callus remodelling what occurs and the steps
Remodelling of the woven bone hard callus into original lamellar bone configuration (trabecular and/or cortical)
• Resorption by osteoclasts and replacement by osteoblasts:
○ on periosteal and endosteal surfaces
○ within cortex (osteonal remodelling)
Walk what is the sequence and how many beats
- slow and each limb lands separately in sequence
○ Hind followed by lateral fore followed by contralateral hind etc = walk
○ LH, LF, RH, RF
§ Can hear 4 beats
Trot what is the sequence and how many beats
- can be fast – and diagonal pairs of limbs land together
- Left hindlimb landing and taking off with the right forelimb and vice versa
○ LH & RF, …….. RH & LF, (diagonal pairs) - 2 beats
Pace what is the sequence and how many beats, what occurs with dogs
- can be fast – lateral pairs of limbs land together
- Left hindlimb landing and taking off with the left forelimb and vice versa
○ LH & LF, …….. RH & RF, (lateral pairs) - 2 beats
- Dogs can cross over from pace and trot
Canter how many beats, what are the 2 main types and how differentiate
- has 3 beats and can be either rotational or transverse
1) rotational – one lateral pair of limbs land together - much more stable at the back
2) transverse – one transverse pair of limbs land together - not done unless got strong back, will wobble slightly
Describe the sequence in Left and right lead of transverse cancers
1) Left lead diagonal (transverse)->
□ Right hindlimb, left hindlimb + right forelimb land together, Left forelimb
2) Right lead diagonal (transverse)->
□ Left hindlimb, right hindlimb + left forelimb land together, Right forelimb
Describe the sequence in Left and right lead of rotational cancers
1) Left lead rotatory ->
□ Left hindlimb, right hindlimb + right forelimb, left forelimb
2) Right lead rotatory ->
□ Right hindlimb, left hindlimb + left forelimb, right forelimb
Gallop what is the sequence, the types and number of beats
- is faster than canter and the diagonal or lateral pair land separately in fast succession (hind limb then forelimb) so there are 4 beats instead of 3
○ Therefore there are also the transverse and rotatory gallop - instead of landing together land in quick succession
§ LH, RH, …., LF, RF, ………. (transverse, right lead)
§ LH, RH, …., RF, LF, ………. (rotatory, left lead)
What does each stride consist of
consists of a support phase and a swing phase
What are the 3 main ways to identify the gait
1) Symmetry
1. Symmetrical eg walk, trot, pace, hop movement of limbs are bilaterally symmetrical
2. Asymmetrical eg canter, gallop. movement of limbs are different on left and right sides.
- Speed – asymmetrical generally faster.
2) Rhythm – 1 beat = hop
○ 2 beats = trot or pace
○ 3 beats = canter
○ 4 beats = walk or gallop
3) Fix attention on one limb, then a pair of limbs
- Both diagonals together = trot
- Both laterals together = pace
- Both hind together = hop
What are the 2 main objective analysis for the gait
1) Such as lameness locator -> gives relative movement of the four limbs
§ Can give objective comparisons with the effect of nerve blocks or other treatments on the gait are possible
2) Hoof-mounted device -> gives movements of limbs in real time
§ This allows direct measurement of the effects of methods of hoof preparation and horseshoe design as well as the working surface on the hoof movement.
Muscle damage what could be the cause and how long till occur
- Possible nerve damage if not painful
- This occurs within a short period -> weeks if complete
- If incomplete nerve damage then less obvious muscle damage
AEC what is it, what is it composed of and how two tell the difference between layers
AEC = Articular Epiphyseal Complex is the zone of endochondral ossification beneath the articular cartilage (on the tip of the bone) in growing animals.
- The AEC is composed of a layer of articular cartilage (AC) and a subjacent layer of growth (epiphyseal) cartilage (EC).
The deeper growth cartilage is vascularised unlike the articular cartilage
Chondrodysplasia what is it, where occur, what results in and example
- Defect in the formation of cartilage
- Physis and/or AEC
- Causes often undetermined
- Affected animals generally show disproportionate dwarfism (short legs with normal sized or dome shaped heads)
NOT ALWAYS A DEFECT -> certain breeds
EXAMPLE - bulldog calves - The animals are grotesquely malformed with protruding tongue; thick, rotated and abducted limbs; absent hard palate; and umbilical hernia and protruding viscera.
Osteochondrosis where generally occur what species most likely affected and clinical manifestations
- Focal failure of endochondral ossification
- Articular-epiphyseal complex (AEC) > metaphyseal growth plate
- Most species can be affected -> most likely in pigs, horses and large breed dogs
- Clinically manifestations generally about the effect on joints -> degenerative joint disease
What is the pathogensis of osteochondrosis and what look like grossly
Path
1) necrosis of blood vessels in immature growth cartilage
2) necrosis of cartilage
3) endochondral ossification does not occur focally - leading to a retained core of cartilage within the bone
4) cleft -> cartilage flap -> joint mouse OSTEOCHONDRITIS DISSECANS
Grossly - lesions weel demarcated, thickens, white foci on articular cartilage, large clefts and flaps
Osteogenesis imperfecta what is it, where occur, result in
- Defect in type 1 cartilage -> growth plates no affected as primarily type 2 collagen
- Collection of diseases, result in poor quality collagen or decrease in high quality collagen
- Acute fractures mandibles and major limb bones, fracture callceous can be present at birth
Aetiology of osteochondrosis
Multifactorial
• Genetic predisposition - certain breeds of dogs, often the larger breeds
• Trauma or excessive weight bearing
• Rapid growth - young fast growing animals most susceptible
• Hormonal factors
Osteopetrosis what is it, what are the 2 ways it can occur and typical gross appearance
- defect of osteoclastic function → poor remodelling of the primary spongiosa (mineralised cartilage matrix) → increased bone fragility.
1) Can be inherited:
2) Acquired condition often associated with in utero viral infections that damage osteoclastic precursors, eg canine distemper, BVD, FeLV in cats
Grossly - butterfly shape bone
What are the 3 main metabolic bone diseases and there general causes
- Causes nutritional or hormonal imbalances -> can get multiple diseases in the same animals
1) Fibrousosteodystrophy
2) Osteoporosis
3) Rickets/osteomalacia
Osteoporosis how does it occur, consequences and list the 3 main causes and causes within
- The bone is reduced in amount, but normally mineralised (normal quality)
- Bone resorption > bone formation
- Consequences are secondary fractures and hypocalcaemic crisis
1) Nutritional deficiencies - livestock - copper (lambs and calves) calcium (increases parathyroid or high phosphorus diets)
2) Endocrine disorders - Hyperadrenocorticism - Glucocorticoids inhibit collagen synthesis, osteoblastic differentiation, and stimulate osteoclastic bone resorption
3) Disuse - paralysis, fractures, confinement -> stablised at a lower bone density
Osteoporosis what bones mainly affect and the gross lesions
- portions of bones with large component of cancellous tissue, such as vertebral bodies, flat bones (scapula and ilium), and the metaphysis of long bones.
- bones are light, brittle with thin cortec and large medullary cavity, formation of transverse reinforcement
Rickets/osteomalacia when is which, cause and result in
- Vit. D and/or phosphorus deficiency (mainly pregnant or lactating cattle grazing)
- Young animals -> rickets
- Adults -> osteomalacia
- Defective mineralisation of physeal cartilage at sites of endochondral ossification (rickets) and of osteoid matrix (rickets and osteomalacia)
Vitamin D where get from and the 3 functions
can get from sunlight and diet
Function -
1. Enhances absorption of P and Ca from small intestine
2. Stimulates release of P andCafrombone (resorption)
3. Enhances resorptioncincthe kidney
Rickets/osteomalcia where do the lesions generally occur list 3
Lesions most prominent at sites of rapid growth where cartilage contributes most significantly to skeletal growth (e.g. physis of proximal humerus, distal radius, ribs, femur
1) retained cartilage in trabecular bone -> extends into metaphysis
2) growth plate much thicker -> failure of cartilage to mineralise
3) shape -> shorter, broader, thickened and uneven growth plate
Fibrous osteodystrophy (FOD) what does it occur with and why, what are the 2 types and types within
FOD occurs with hyperparathyroidism due to increased production of parathyroid hormone (PTH).
1) primary hyperparathyroidism - functional parathyroid adenomas and carcinomas
2) secondary hyperparathyrodism
1. nutritional secondary hyperparathyroidism
2. renal secondary hyperparathyroidism
why is hyperparathroidism a problem with bone
Increased PTH secretion → Increase bone resorption and release of calcium and phosphate from the bone.
Effect of PTH on bone: stimulation of bone resorption.
Secondary hyperparathyroidism when common, example and pathogenesis of both types
1) nutritional -> common with young growing animals on low-calcium-high-phosphorus diet
Eg - dog and cat all meat diet
Path - increased PTH -> bone resorption (rubber jaw)
2) Renal
- Skeletal lesions develop secondary to chronic, severe, renal disease; most common in dogs (“rubber jaw”)
Path - decreased GFR -> decrease Ca and P absorption in GIT -> increase PTH etc.
What are the gross result from hyperparathyroidism
BIG HEAD - bilaterally enlarged mandibles
- Increased axillary bones
- Obstruct nasal passages
- Teeth can become loose and partially burried
- trabecular and cortical bone -> rubbery
- dog and cat mainly get rubber jaw
Toxic osteodystrophies what are the main 2 ones
1) flurosis
2) hypervitaminosis A
Flurosis what result in, how occur and how do lesions occur
when fluroide present in chronic excess is capable of inducing characteristic bone and teeth lesions.
cause - ingestion of small amounts of fluoride compounds over long periods
teeth -> Fluoride disrupts ameloblasts→ irregular enamel matrix, rate of formation, and rate of mineralisatio -> oxidation of exposed dentin -> dark discoloration
Bone -> mechanism unknown
Hypervitaminosis A what common cause in cats and lesion can cause, what are the 2 main lesions overall and are they reversible
- generally diets of liver
cats -> fed livers over long period form exostoses, spine may also become fused
1) osteoporosis - reversible if stop feeding high vitamin A foods
2) physeal lesions -> narrowed - irreversible
Osteomyelitis where generally occur and 4 main routes of infection, what result from and main
- There is a strong predilection for sites of active endochondral ossification ○ metaphysis and epiphyses of long bones and vertebrae Routes of infection: 1) Haematogenous MOST IMPORTANT •Bacteremia/septicaemia 2) Direct implantation •Wounds,fractures •Penetrating trauma 3) Local infections •From adjacent tissueseg.arthritis 4) Non-infectious •Local periosteal injury
what is the Pathogenesis of haematogenous osteomyelitis and what are the 3 anatomic factors favouring metaphyseal localisation
Bacterial entry via umbilicus, skin or mucous membrane → septicaemia → bacteria lodge in metaphyseal capillaries → thrombosis → infarction → osteomyelitis
1) Capillaries invading mineralising growth cartilage (primary spongiosa) make sharp loops
2) Capillaries are fenestrated and open into sinusoidal vessels causing sluggish blood flow, thrombosis and necrosis
3) Phagocytosis in sinusoids is inefficient
Mandibular osteomyelitis (lumpy jaw) what is the primary cause in cattle, what type of inflammation and what occurs
- Lumpy jaw is a primary disease of cattle caused by Actinomyces bovis
○ A. bovis is an obligate pathogen of the oral cavity; the surface tissues must be injured (e.g. penetrating trauma) for deeper invasion to occur - Osteomyelitis follow direct extension of the infection from the gums and results in a chronic pyogranulomatous reaction.
- In the bone there are multiple foci of bone resorption -> The periosteal proliferation is excessive therefore the mandibles are enlarged.
List the 4 main primary neoplasms of bone and the cell in which they derive
1) oesteosarcoma - osteoblast
2) Chondrosarcoma - chondrocytes
3) lymphoma
4) multiple myeloma - plasma cells
What are the 4 common sites for oesteosarcoma and the general rule
Most common sites - Distal radius - Proximal tibia - Distal femur - Proximal humerus Generally away from the elbow towards the knee
Oesteosarcoma when common, what lead to, does it metastasise and prognosis
- Rare in other species apart from cats and dogs where most common - accounts for 80% of all primary bone tumours in dogs
○ Most common in large breed dogs - Generally middle aged to older dogs -> can occur in smaller dogs
- Most combination of production and lysis of bone
- Early metastases to the lungs generally and to other organs -> Poor prognosis even with treatment
Oesteosarcoma what look like grossly, histologically and what predispose to
Grossly
- Haemorrhages
- Can totally destroy the bone
Histological
- Proliferation of neoplastic osteoblasts
- Normal bone formation can occur
- Production of osteoid (eosinophilic material) needs to be present
- Osteoclasts, spindle cell population that produce osteoid
Predispose to pathological bone fractures
Painful
Chondrosarcoma what type of tumour, where occur, difference from oestosarcoma, treatment and gross appearance
- Malignant tumour in which cells produce neoplastic chondroid and fibrillar matrix but never directly produce osteoid or bone
- Flat bones, ribs and sternum
- Can cross joint spaces UNLIKE OESTOSARCOMA
- Treatment -> more likely to be successful as metastasise later and generally if occur to the lungs
Grossly - Waxy/gelatinous appearance
- White/grey
- Large size and lobulated
Lymphoma cause, what lead to, what other organs commonly involved
- Multicentric causes generally
- Eccentric bone infarction from the lymphoma due to ischemia secondary to infiltration of the marrow cavity
- Calves generally get sporadic lymphoma, can also get involved of liver, spleen
- Lysis of bone
Multiple myeloma what occurs, where main place and what can lead to
- Plasma cells replacing existing bone marrow cells
- Lysis of bone
- Most commonly occurs spinal column, ribs, skull and long bones
- Can lead to patholgoical fractures
Secondary tumours how occur and what are the common ones
- Direct extension or metastasis
- Carcinomas generally metastasise to bones more commonly
- Osteosarcomas can metastasise to other bones
Hypertrophic (pulmonary) osteopathy - Marie’s disease what does it result in, cause, common bones affected and gross lesions
- Results in new bone formation
Cause - is a space occupying lesion in the thorax (tumours, large abscesses or granulomas) - Dogs - neoplasm, horses - granulomatous disease
- Common bones affected are: radius and ulnar, metacarpals, tibia and metatarsals
Gross lesions - will continue to progress if mass lesion isn’t removed, if it is removed than will regress
