Key Terminology & Definitions - Musculoskeletal Flashcards
Axial skeleton
Head, vertebrae, ribs and sternum
Appendicular skeleton
Thoracic and pelvic limbs
Achondroplasia
Absence of cartilage development
Chondrodysplasia
Disorder of cartilage development
Skeletal dysplasia
Disorder of skeletal development - no further specification of structure or location
Brachycephalic
Shortening of head
Brachygnatia
Shortening of jaw
Palatoschisis
Cleft palate - partial/complete
Prognathia
Abnormal projection of jaw (mandible)
Pectus excavatum
Concavity of the sternum - reduced thorax w/ reduced dimensions
Kyphosis
Abnormal dorsal curvature of spinal column
Lordosis
Abnormal ventral curvature of spinal column
Scoliosis
Lateral deviation of spinal column
Block vertebrae
Failure of two vertebral bodies to separate
Butterfly/hemivertebrae
Failure of two halves of vertebral body to fuse
Spina bifida
Failure of dorsal midline closure (bone often involved) - failure of fusion of neural arches, some degree of exposure of underlying spinal cord
Amelia
Absence of one of more limbs
Hemimelia
Absence of the distal part of the limb
Micromelia
Presence of abnormally of small limbs
Notomelia
Accessory limb attached to the back
Peromelia
Congenital deformity of the limbs
Phocomelia
Absence of proximal portion of one or more limbs
Adactyly
Absence of a digit
Dactylomegaly
Abnormally large digits
Ectrodactyly
Partial or complete absence of a digit
Polymelia
Presence of multiple limbs
Polydactyly
Presence of supernumerary digits
Polypodia
Presence of supernumerary feet
Syndactyly
Fusion of digits
Hyperphalangia (Hyperphalangy)
Inc in no. phalanxes (normal trait of dolphins, flipper)
Osteogenesis imperfecta
Genetic defect in type 1 collagen (mutation in COL1A1 and COL1A2 genes) formation characterised by osteopenia and excessive bone fragility
Histo - no primary lesions on growth plate as collagen II not affected, trabecular bone - reduced, no fibrous tissue proliferation, osteoblasts normal or small, evidence of FXs (including in utero with calluses present at birth), cortical bone - delayed compaction, cortices may be formed of woven bone -> osteopenia
Osteopetrosis
Persistence of primary and/or secondary spongiosa caused by a defect in osteoclastic resorption/in utero, BVD/FeLV infection, avian leucosis virus -> pathological FXs, trabecular bone in epiphyses, metaphyses and diaphysis, dec in cortical bone quality and quantity (failure of remodelling), affected animals often stillborn
Histo - GP = no primary lesions, T bone - numerous dysfunctional osteoclasts, cones of primary trabeculae (calcified cartilage) extend into medullary cavity, C bone - too thin to inadequately compacted
Skeletal dysplasia
Disordered skeletal development
Congenital cortical hyperostosis
Disorder of bone modelling, one or multiple limbs - abnormal radial periosteal bone formation (long bones) (front more prone - radius + ulna), autosomal recessive in newborn pigs
Histo: GP not involved, T bone - not involved, Cortical bone - superiosteal cortex normal, trabeculae of woven bone oriented perpendicular to long axis of the cortex radiate outwards from its periphery, from the cambium (osteogenic) layer of the periosteum
Craniomandibular oesteopathy
‘Lion jaw’ - disorder of bone modelling, Westies - autosomal recessive, bilaterally symmetrical lesions, diffuse, irregular thickening of the mandibles, occipital and temporal bones (occasionally nasal, maxillary and appendicular bones), tympanic bullae often severely affected
Histo: GP not involved, T bone - medullary cavities become osteosclerotic (proliferation of endosteal woven bone, modelling and remodelling), C bone - thickened by proliferation of periosteal woven bone, rapid, disorganised modelling and remodelling, regions of lamellar bone next to woven bone
Campylognathia
Harelip
Chondrodysplasias
Disorders of endochondral ossification (bone growth) due to primary lesions in growth cartilage, affects growth plate and articular epiphyseal cartilage complex -> disproportionate dwarfism (short-legged, normal-sized head as from intramembranous ossification)
Histo: GP width normal or reduced, chondrocytes arranged in columns or disorganised, matrix normal or rarefied, T bone - thickened or irregular, lateral bridging between trabeculae, retained cartilage cores, C bone - normal histo, grossly variable in shape or size of bones (Spider lamb syndrome)
FGFR
Fibroblast growth factor receptor
Mutations in: FGFR3 = spider lamb chondroplasia, FGFR4 = dachshund, Pekingese, basset hounds
AECC
Articular epiphyseal cartilage complex
Osteochondrosis
Developmental disease of joints - disorder of endochondral ossification, involving growth cartilage in young animals, focal or multifocal failure or delay of endochondral ossification at growth plate/physis of AECC, focal retention of growth cartilage because of failure to become calcified and replaced by bone, in AECC becomes an area of necrosis of epiphyseal cartilage, trauma most common cause
Histo: focal or multifocal failure of endochondral ossification, T bone - in laterns, normal; manifesta + dissescans - contact with subchondral bone, proliferation of woven bone and fibrotic change, C bone not involved in most cases
Osteochondrosis latens
Lesion confined to epiphyseal - well-demarcated area of necrosis of cartilage, only visible microscopically (no clinical signs)
Osteochondrosis manifesta
Lesion accompanied by delay in endochondral ossification - visible grossly and radiographically, larger lesions than latens
Osteochondrosis dissecans
If traumatic clefting through the area of necrosis occurs, fragments of cartilage can break off (forming ‘joint mice’), may resolve without clefting, most severe lesion
Facet
Flat bone surface
Cervical vertebral myelopathy
‘Wobbler syndrome’ - disorder of endochondral ossification, neurological disease secondary to compression of spinal cord by abnormally developed cervical vertebrae or junctions between them, osteochondrosis can cause abnormal and asymmetrical development of the articular facets or abnormally large cranial vertebral epiphysis - horses, large dog breeds, Komodo dragons
Static vertebral myelopathy
Constant compression due to anatomic stenosis of spinal canal (no movement) = cervical vertebral static stenosis (CVS), C5-C6/C6-7 in older horses, dogs affected
Histo: GP - +/- oesteochondrosis, T bone normal, C bone - histologically normal but overall bone shape wrong
Dynamic vertebral myelopathy
Compression only during movement (flexion most prominent) = cervical vertebral instability, C3-4/C4-C5 in younger horses
Osteoporosis
(Metabolic disease) Reduced bone mass, porous, thin and fragile bones due to protein calorie malnutrition, immobilisation, dietary calcium, vit C or copper deficiency, oestrogen/androgen deficiency (menopause), advanced age
Histo: GP - not affected (unless due to pituitary dysfunction or calorie restriction during growth, then small physes), T bone - thinner, loss of trabecular continuity (weaker), form transverse reinforcement bars in metaphysis, C bone - thin (osteopenia) due to osteoclastic resorption on endosteal surface, may resemble T bone w/ chronicity
Infraction
Incomplete fragmented fractions without displacement/collapse/fracture of trabeculae but no bone deformation
Rachitic rosary
Prominent nodular thickening of costochondral junctions
Rickets and osteomalacia
(Metabolic disease) Failure of bone mineralisation with subsequent deformities and fractures in growing skeleton (rickets)/adult (osteomalacia), soft bones, accumulation of osteoid (not mineralised), thickened hypertrophic zone of growth plate (failure of endochondral ossification), rachitic rosary, due to vit D deficiency, phosphorus deficiency
Histo: GP - diffusely, irregularly thickened, failure of endochondral ossification, T bone - appear flared due to failure of removal of cartilage and bone, C bone - can appear normal or softened, deformed by weight bearing
Fibrous osteodystrophy
Decreased bone mass, increased pliability due to replacement by fibro-osseous tissue, ‘rubber jaw’, due to hyperparathyroidism - 1^y = functional chief cell adenoma, 2^y - nutritional low Ca^2+, high PO4^3-, renal failure - kidney fails to secrete PO4^3-, paraneoplastic - PTH related peptide released from tumours
Histo: GP - not involved, T bone - replaced by irregular spicules of woven bone separated by fibrous connective tissue, C bone - resoprtion and replacement by fibrous tissue, can become exuberant
Exostosis
Nodular, benign, bony growth projecting from a bone’s articular surface
Enostosis
Bony growth within the medullary cavity, usually from the endosteal surface
Osteophyte
Nodular, benign bony growth at the margins of a diathrodial joint
Enthesophyte
Ossification of a tendon or ligament (forming bony projections) at the point of insertion in the bone (nodular)
Hyperostosis
Diameter of the bone has increased (uniformly rather than nodular)
Hypertrophic osteopathy
Hypertrophic pulmonary osteopathy (proliferation of connective tissue and periosteum) - progressive, often bilateral, periosteal new bone formation in diaphysis and metaphysis, especially affects distal limbs, may progress up the leg, more common in forelimbs, long bones, occurs as a secondary reaction to space-occupying lesion in thorax
Osteochondromas
Multiple cartilaginous exostoses - defect in skeletal development, project from bony surfaces as eccentric masses adjacent to physes, outercap of hyaline cartilage, undergo orderly endochondral ossification to give rise to trabecular bone at the base of lesion
Bony cysts
Appear radiographically as well-demarcated, lucent areas without aggressive growth (resembles a bubble/hole)
Subchondral cyst
Sequelae to osteochondrosis and degenerative joint disease
Simple cyst
Contain clear, colourless, serum-like or serosanguinous fluid, wall of fibrous or woven to lamellar bone, unknown cause
Aneurysmal cyst
Filled with blood or serosanguinous fluid, not lined by endothelium, cause unknown
Compound fracture
At least one of the fracture fragments is visible externally, perforates muscle fascia, subcutaneous + skin depending on location
Transverse fracture
Perpendicular to long axis of bone
Linear fracture
Parallel to long axis
Oblique non-displaced fracture
Tangential (along diagonal) axis - remain relatively aligned
Oblique displaced fracture
Diagonal complete displacement (bones completely separated)
Spiral fracture
3D - twisting motion
Greenstick fracture
Cortical bone, minimal involvement of underlying trabecular bone
Comminuted fracture
Involves 3+ diff fractures, very severe forces shatter fracture fragments
Haematoma
Bleeding from damaged vessels - many erythrocytes and inflammatory cells (neutrophils)
Rigid fracture repair
Surgical intervention, application of devices - fractured ends nearly touching each other -> direct osteonal bridging of the fracture site, osetoclasts form channels for new osteons will cross the fracture line and the new osteons will unite the bone without formation of callus
Small gap rigid fracture repair
< 1 mm - bone cells will migrate from the fracture ends and from the lamellar bone at a right angle to the fracture line -> osteonal bone parallel to the long axis of the bone
Larger gap rigid fracture repair
> 1 mm - woven bone fills the gap and must be modelled into osteonal bone
Pseudoarthrosis
False joint - non-functional area of conflict for locomotion
Epiphysiolysis
Separation of epiphysis from the metaphysis (“slipped epiphysis”), forms a horizontal fissure through normal or abnormal physis (SH Type I), dogs - anconeal process of ulna (ununited anconeal process), cats - physeal dysplasia w/ slipped capital femoral physis, livestock - femoral head + ischial tuberosity (muscle insertion site), normal physes FXs can occur in areas of shear force during weight-bearing, can also be caused by trauma, infection/inflammation of growth plate
Histo: GP - horizontal FX w/ complete or partial separation from metaphysics (hypertrophic zone more susceptible), T-bone - reaction to trauma (myelofibrosis, proliferation of reactive woven bone, variable amounts of haemorrhage + fibrin), C-bone - no primary lesions, secondary changes due to altered mechanical use
Valgus deformity
Deviation of the limb laterally, damage occurred on the lateral aspect of the physis
Varus deformity
Deviation of the limb medially, damage occurred on the medial aspect of the physis
Osteitis
Non-specific inflammation of bone
Periostitis
Inflammation of the bone and periosteum
Osteomyelitis
Involvement of the medullary cavity and bone marrow
Diskospondylitis
Inflammation of the intervertebral disc and osteomyelitis of the vertebrae
Splendore-Hoeppli phenomenon
Intense focal eosinophilic material admixed with bacteria and neutrophils on histo - suggestive of inflammatory disease
Metaphyseal osteopathy
Hypertrophic osteodystrophy - disease of young, growing, large breed dogs, severe pain localised to metaphyses of long bones, distal radius and ulna mostly affected, initial lesion suppurative and fibrinous osteomyelitis of trabecular bone, infractions, chronic lesion has exacerbations over weeks-months, most resolved with pain management
Panosteitis
Disease of growing large breed dogs, shifting lameness (due to pressure on nerves by proliferating tissue) and limb pain - increased density of medullary cavity in diaphysis, usually near nutrient foramen, can also be in periosteum, proliferation of well-differentiated woven bone and fibrous tissue, NO INFLAMMATION, resolves spontaneously if pain managed
Aseptic necrosis
Caused by intramedullary neoplasms (especially lymphoma), lesions causing dec venous outflow from bone and inc BM pressure, ischaemia leads to infarction (bone necrosis), young small and miniature dog breeds, aseptic necrosis of femoral head associated with collapse of articular cartilage clinical signs
Cachexia
Insufficient dietary energy/improper processing
Whorled and ring fibres
Morphological muscle cell change - whorls/rings of cytoplasm with internally located nuclei (change of direction of sarcomere) = chronic myopathic change
Chronic myopathic change
Excessive fibre size (diameter) variation, internal nuclei, fibrosis, fat infiltration, accompanies a variety of myopathic and neuropathic changes
Global necrosis
E.g. Affecting entire muscle fibre
Segmental necrosis
Segmental hypercontraction (large dark fibres), fibres become homogenous and eosinophilic (due to hyaline degeneration), loss of striation and their nuclei Sarcoplasm begins to fragment, fragmented sarcoplasm may mineralise, circulating monocytes infiltrate and mature to macrophages, these cross the cell mem and clear debris (other inflammatory cells may also be recruited), satellite cells are activated to become myoblasts and start the regenerative process
Muscular dystrophy
Dogs (Golden Retriever, Rottweiler, sporadic in others, X-linked defect in dystrophin gene allows gaps in sarcoplasm (Ca^2+ enters) -> repeated necrosis and regeneration -> progressive cardiomyopathy + skeletal muscle wasting
Myotonia (channelopathies)
Inability of skeletal muscle to relax resulting in spasmodic contraction; most related to heritable defects causing abnormal ion channel func e.g. hyperkalaemic periodic paralysis in quarter horses (Na^+ channel defect), fainting goats (Cl^- channel defect)
Metabolic myopathies
Inherited disorders of muscle metabolism, seven types of glycogen storage diseases in animals
Malignant hyperthermia
Defective ryanodine receptor characterised by unregulated release of Ca^2+ from sarcoplasmic reticulum -> excessive myofibre contraction generates heat -> hyperthermia (then proteins coagulate).
Humans, pigs (porcine stress syndrome), horses, dogs, fatal, produces pale, soft ‘parboiled’ looking muscle, triggered by anaesthesia halothane, stress
Polysaccharide storage myopathy
Carbohydrate metabolic defect, horses - especially draft and quarter horse-related breeds, glycogen synthase 1 (GYS1) gene affected
X-linked muscular dystrophy
Muscular dystrophy - various dog breeds, DSH cats, dystrophin gene affected (cohesive protein located between the sarcolemma and the outermost layer of myofilaments in the muscle fibre (myofibre))
Double muscling
Muscular hyperplasia - various beef breeds, whippets, myostatin gene affected (myokine, a protein produced and released by myocytes that acts on muscle cells to inhibit muscle cell growth)
Porcine stress syndrome
Malignant hyperthermia - various pig breeds, ryanodine gene receptor (Ca^2+ release inc)
Degenerative myopathies
Segmental/global myofibre necrosis where inflammatory cells are not the cause of damage - sequelae for myocyte degeneration + necrosis
Disturbance of circulation
Includes occlusion of major artery e.g. aortoiliac thrombosis; widespread vascular damage e.g. vasculitis; inc intramuscular pressure - prolonged recumbency
Nutritional deficiency
High metabolic activity of muscle makes it sensitive to free radical damage, need antioxidants as defence mechanism, selenium and vit E, selenium most commonly deficient, nutritional myopathy common in livestock, horses and camelids -> pale muscle = ‘white muscle disease’
Toxic myopathy
Causes monophasic or polyphasic necrosis, livestock prone to ingesting myotoxins in plants e.g. sycamore tree (equine atypical myopathy), box elder tree (equine pasture-associated myopathy), white snakeroot, cottonseed products, coffee senna, coyotilloIo
Ionophore toxicity
Antibiotics used as feed additives -> toxic myopathy, e.g. monensin, lasalocid, maduramicin, narasin, horses especially sensitive to toxicity
Exertional myopathy
Ionic and physical events associated with myofibre contraction leading to myofibre necrosis in certain conditions, often have pre-existing conditions e.g. selenium deficiency, called ‘capture myopathy’ in wild animals, in horses related to equine polysaccharide storage myopathy and/or abnormal calcium homeostasis w/ other factors, sled dogs and greyhounds
Myositis ossificans
Abnormal response to localised tissue trauma -> focal zone of fibrosis with osseous metaplasia, central proliferating undifferentiated cells, middle zone of osteoblasts producing osteoid, outer trabecular bone, surgical excision curative, dogs, humans, horses (NOT INFLAMMATORY)
Bacterial myositis
Bacterial emboli that reach muscle from direct penetration, haematogenous, nearby inflammation, common in livestock, supportive and necrotising, supportive and fibrosing, haemorrhagic, granulomatous
Pyogenic bacteria - bacterial myositis
Localised suppurative and necrotising myositis, may resolve completely or become an abscess, sometimes spreads alone fascial planes
Granulomatous myositis
Mycobacteria - bovis, tuberculosis etc
Fibrosing and granulomatous myositis
Splendore-Hoeppli reaction, encapsulated lesions (fibrosing), actinobacillus lignieresii (G -ive = wooden tongue in cattle), actinomyces bovis (G +ive, lumpy jaw in cattle), staphylococcus aureus (G +ive), botryomycosis in horses + pigs (not fungus)
Porcine encephalomyelitis
Enterovirus, Picornaviridae
FMDV
Aphthovirus, Picornaviridae
Bluetongue virus
Orbivirus, Reoviridae
Akabane disease
Akabane virus, Bunyaviridae
Sarcocystis spp.
Protozoan, horses, ruminants, pigs
Trichinella spirali
Nematode, pigs
Neospora caninum
Protozoan, dogs, cattle foetuses
Trypanosoma cruzi
Protozoan, dogs
Cysticercus spp.
Cestode (larval form), ruminants, pigs
Nematode larval migrans
Dogs
Hepatozoon americanum
Protozoan, dogs
Immune-mediated myositis
Most common in dogs, cytotoxic T lymphocytes damage myofibres, mixture of lymphocyte types in infiltrate + interstitial and perivascular patterns of infiltration
Polymyositis
Inflammation and degeneration of skeletal muscle throughout the body (wasting)
Masticatory myositis
Wasting, pain opening mouth
Extraocular muscle myositis
Sunken eyes
Purpura haemorrhagica
In horses - immune-mediated vasculitis associated with bacterial infection e.g. Streptococcus equi spp. equi -> muscle injury
Endocrine diseases
Can lead to type 2 myofibre atrophy, can cause neuropathy and denervation atrophy (with resulting altered fibre type pattern), hypothyroidism (dogs), hypercortisolism + hyperadrenocorticism (dogs), PPID (horses)
Electrolyte abnormalitis
Can cause profound weakness, sometimes myofibre necrosis e.g. hypokalaemia (cattle, cats), hypophosphataemia (cattle), hypernatraemia (cats), hypocalcaemia (Cattle)
Osteopenia
Reduced bone density
Joint mice
Fragments of cartilage breaking off + embedded in other areas of the joint
Exuberant
Excessive proliferation of tissue
Porphyria
Deficiency (inherited or acquired) of the enzymes that transform porphyrins -> abnormally high levels (bone liver, RBC), become bright red-pink fluorescence on exposure to UV light in a dark room
Arthrogryposis
Ruminants - in utero infection (e.g. Schmallenberg virus) or toxicity causes failure of skeletal muscle innervation + muscle hypoplasia
‘Double muscling’
Congenital muscle hyperplasia due to inc no. myofibres, defect in myostatin gene (Belgian blue cattle, ‘bully’ whippets)
‘Splay leg’
Pigs - myofibrillar hypoplasia, myofibrils fail to develop
