Musculoskeletal 1, 2 and 3 Flashcards
Name an example of a flat and long bone
Flat- skull
Long- humerus
Describe the following long bone anatomical features:
- Epiphysis
- Dyaphysis
- Periosteum
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Epipyhsis- top and bottom
Dyaphisis- middle
Periosteum- fibrous capsule of the bone
Where is compact and spongy bone found?
What is a physis and a metaphysis?
What is the difference between lamellar bone and woven bone?
Compact in the dyaphisis
Spony bone in epiphysis- shock absorbtion
Physis/epiphyseal plate- growth plate
Mataphysis- region between epiphysis and dyaphsis
Lamellar bone- mature- spongy, cancellous, trabecula
Woven- immature
What is cancellous bone?
What is its role?
Interconnected fenestrated plates of bone
Porous and low density- shock absorber
Embryology- what are the three primary germ layers?
What does the skeleton develop from?
Ecoderm- skin and appendages
Mesoderm- skeleton, connective tissue, vascular tissue, linings of thorax and abdomen/pelvis
Ectoderm- pharynx, respiratory, GI system, bladder, urethrea
What is intramembranous ossification?
Where does membranous ossification occur?
IM ossification- flat bones of the face etc- arise in vascularized by mesenchyme at site with high oxygen tension
Primarily with bone blastoma- latter appositional growth
Membranous- flat bones
Describe endochondral ossification
Where does it occur?
Bones and joints of limbs- vertebral colum
- Bones arise in hypoxic mesenchyme that must differentiate into cartilage before being replaced by bone
- Long bones develop from cartilage models within the axis of limbs in absence of capillary bed
- Joint cavities arise by cystic degeneration
Describe how joints form by cystic degeneration
- Cystic degeneration of mesenchyme between ends of bone leads to joint formation, mesenchyme dies back to inner surface of fibrous layer of the joint capsule and cruciate surfaces to form lining
- Articular surfaces and menissci are not covered by synovium
- Surfaces of ligaments covered by synovium
By what processes do long bones grow in width and length
Describe what happens at a growth plate
Width- intramembranous ossification
Length- endochondral ossification
Growth plate in columns
- Arranged into zones- rest to death
- Top is zone of reserve- resting cells to rest
- Below chondrocytes are proliferating and producing molecules to modify the matrix to allow capillary invasion and initiate matrix mineralisation- proliferating
- Below chondrocytes are dying- minerals coming from the vessels calcified trabeculae forms by action of osteoprogenitor cells differentiating in OBs- hypertrophy
What is primary spongiosa and secondary spongiosa?
Primary- bone spicules with cartilage core
Secondary- bone spicules without cartilage core
What procues osteoid?
When is it converted to bone?
Oestoblasts produce osteoid- 90% collagen type 1
Following 10 days- primary mineralisation 70-75%
Several months- secondary mineralisation
What is the difference between type 1 and 2 cartilage?
Type 1- cartilage in bone
Type 2- in cartilage- high water
What are osteoid and the osteoid seam?
Osteoid- unmineralized bone matrix initially deposited by a later of osteoblasts
Osteoid seam- name of the later of superficial non-mineralised osteoid
What are osteoclasts and osteoblasts?
Osteoblasts- arise from mesenchyme adjacent to bone surfaces and bone marrow stromal cells.
Osteoclasts- originate from the fusion of cells of monomyelocytic stem cell origin, both local monocytic cells and those of blood origin
How are peritrabecular stromal cells connected to osteoblasts?
When do they become osteoblasts?
What are the 4 roles of peritrabecular stromal cells?
Peritrabecular stroll cells of bone marrow connect to osteoblasts by cellular junctions and become osteoblasts during bone deposition
- Produce haematopoietic growth factors- erythropoietin
- Progenitor cells of the osteoblasts- provide vertical orientation, establishment of that canlicular-lancunar system
- Reach to parathyroid hormone stimulation- attract and stimulate osteoclasts to remove bone, proliferate and form fibro-osseous matrix
- Act as strain gauges and active bone remodelling
Describe the process of modelling and reabsorption?
Modelling-
- stimulus activates osteoblasts
- start producing osteoid and begins mineralising
- they encapsulate themselves in osteoid
- they become osteoblasts, and oestoid becomes woven to compact
Reabsorption-
- Resting osteoblasts cover the bone- where there isn’t any present the osteoclasts attach and pump acid- dissolve some bone- minerals are reabsorbed
Describe how bone modelling and reabsorption is regulated?
- Osteoblast precursors and resting osteoblasts can produce RANK-L
- RANK-L stimulates osteoblast precursor to active
- Oesteoclasts- bone reabsorb
- Oesteoblast precursors and resting osteoblasts also produce OPG which inhibits activation of oesteoclasts
- Osteocytes control the amount of both depending on mechanical factors- astronauts
- Parathyroid hormone- stimulates production of RANK-L, inhibits differentiation of osteoblasts from resting to active- from decrease in blood Ca2+
- Calcitonin- from increased Ca2+ induces death of oesteoclasts
- Releasing of matrix from reabsorption- the growth factors bound to these stimulate osteoblasts
- Inflammatory GFs- IL1, TNFa- can stimulate osteoclasts
What are resting lines and reversal lines?
Resting lines- longitudinal straight basophilic line within the bone matrix is the evidence for at some point the osteoblasts were resting for a while
Reversal lines- these scalloped lines are the evidence that in the past an osteoclast was actively reabsorbing the bone matrix within the site- you can imagine the shape of an osteoclast sitting in there
What can cause abnormalities of skeletal development?
Genetic
Sometimes viral
What do the following terms mean for skeletal development?
- Brachygnathia inferior/superior
- Bovine serienomelia
- Dicephalic
- Diprosopus
- Palatoschisis
- Abrachia
- Peromelia
- Micromelia
- Amelia
- Mondactilia
- Polydactilia
- Bone brachygnathia inferior- short mandible
- Canine domesticative mutations- short maxilla
- Brachygnathia superior- boxer
- Bovine serienomelia- mermaid- no back legs
- Calf dicephalic- two heads
- Kitten/calf diprosopus- two heads 1 neck
- Palatoschisis- cleft palate
- Abrachia- lack of limbs
- Peromelia- part of limbs
- Micromelia- small limbs
- Amelia- lacking a limb
- Mondactilia- less digits
- polydactylia- extra digits
What are the following conditions of skeletal abnormalities?
- Canine spina bifida
- Vertebral column distorsion-
- kyphosis
- scoliosis
- kyphoscoliosis
- lordosis
- Canine spina bifida
- Scoliosis- lateral
- Kypohosis- dorsal
- Kyphoscoliosis- dorso-lateral
- Lordosis- ventral
What are chondrodysplasias?
Describe its pathology
What is its aetiology?
What is a bull dog calf, a telemark lethal and a ‘Snorter’?
Cartilage/bone defect
Pathology- defect of endochondral ossification, therefore affect mainly long bones at growth plate.
Aetiology- genetic
Bull dog calf- lethal chrondroplaysia in dexter and holstein, born dead, small limbs, brachygnathia, looks like bulldog
Telemark lethal- telemark breed, born alive, dies soon after, similar to bulldog but less severe
‘Snorter’- dwarf, hereford and angus, non-lethal, short legs, board head, prognathic
What is the name of this skeletal disorder?
What is its aetiology?
What is its pathology?
What breeds are affected?
Describe its gross and histological appearance and sequale
Ovine chondrodysplasia- spider lamb
Aetiology- genetic mutation of fibroblast growth factor receptor
Pathology- defect of enchondral ossification- semi-lethal
Breed- Suffolk, Hampshire
Gross- long limbs and neck, shallow body, scoliosis, kyphosis, sternal deformity
Histology- multiple small ossification centres in nodules of hypertrophic cartilage. Chondrocyte columns in growth plates are irregular
Sequale- fractures
What is the aetiology of osteogenesis imperfecta?
What species are affected?
Describe its pathogenesis?
How does it appear grossly and histologically?
What are the associated conditions?
Aetiology- genetic mutations in COL1A1/2
Species- calves, lambs and dogs
Pathogen- quantitative or qualitative defect in type 1 collagen
Gross- bones are brittle, animals exhibit intrauterine fractures, skeletal deformity, bowed limbs
Histology- calcified cartilage spicules in the primary spongiosa lined by a thin, basophilic layer of bone matrix
Ac- opalescent teeth (pink), joint laxity, blue sclera, spontaneous fractures
What is the correct name for marble bone disease?
What is its aetiology?
What species and breeds does it affect?
Describe its pathology?
Describe its gross and histological appearance?
What are its associated conditions?
Osteopetrosis- marble bone disease
Aetiology- genetic
Species- cattle, horses, dogs, cats, deers
Breed- cattle (Angus, Hereford, Simmenthal)
Pathology- defective osteoclastic resorption/remodelling of primary spongiosa
Gross- generalised- long bones shortened and fragile, metaphyses and diaphysis of long bones are filled with dense, unresorbed cored of primary spongiosa- no marrow cavity.
Histology- metaphyses are relatively avascular, and the medulla is occupied by cartilage matrix lines by a thin later of woven bone.
Associated conditions- brachygnathia inferior, protruding tongue, anaemia
What is congenital hyperostosis?
What species does it affect?
How does it appear grossly and histologically?
Suspected autosomal recessive/circulatory disturbance
Species- pig
Grossly- animals stillborn or die within first few days- thickening of the radius and ulna, thick layer of extracortical bone that extends along the diaphysis
Histology- radiating trabeculae of woven bone which extend from cortical bone beneath a thickened periosteum
What is the alternative name for craniomandibular osteopathy?
What breed of dogs are affected?
How does it appear grossly and histologically?
What are its associated conditions?
Lion Jaw
Westies
Gross- bilateral, bones of the head (mandible, temporal) intermittent and progressive. Ankylosis of mandibular process. Tympanic bullae filled with new bone
Histology- intermittent and concurrent bone formation and resorption, woven and lamellar bone together- resting and reversal lines
Ac- masticatory muscle atrophy
What is the alternative name for Marie’s disease?
What is the aetiology?
What species are affected?
How does it appear grossly and histologically?
Hypertrophic osteopathy
Species- dogs most common, horses, bovine, ovine
Pathology- change in circulation to limbs, increase blood flow, increase in periosteal bone production
Gross- diffuse, periosteal new bone formation along the metaphysics and diaphysis of limb bones
Histology- initial hyperaemia and oedema with fibrovascular periosteal proliferation, followed by deposition of perpendicular trabeculae by osteoblasts
What are the 4 different bone pigmentations?
Icterus- accumulation of endogenous pigments- periosteum
Porphyria- pink tooth disease
Melanosis- periosteal melanosis- generalised, calf- melanosis maculosa
Tetracycline- selective uptake in growing bone/dentin
What is the pathophysiology of pink tooth disease?
How does it appear grossly?
What are the associated conditions?
Inherited porphyrin synthesis disorder
Pathology- uroporphyrinogen III synthase decrease- porphyrin accumulation
Gross- brown colouring of bone not cartilage/connective tissue in UV light red fluorescence
Associated conditions- clinically photosensitivity- seen on back of calves
What are some causes of osteonecrosis?
Trauma
Inflammation
Neoplasia
Thromboembolism
Vasoconstriction
Describe the pathology of bone necrosis
How does it appear grossly and histologically?
Pathology- lack of proper blood supply, necrosis of the osteocytes, necrotic bone recognised as foreign body, inflammatory reaction against the dead bone- outcome dependent on size/sepsis
Gross- dry periosteum, tan discolouration of bone
Histology- empty lacunae with no osteocytes, pyknotic nuclei may be present and there is often bone marrow necrosis
What causes ‘creepy subsitution’?
Large necrosis- granulation tissue is deposited leading to sequestrum
Small necrosis- heals
What is Legg-calve Perthes disease
Genetic autosomal recessive disease affecting WHWT, poodles and yorkies
Initiated by ischaemia episodes, delayed incorporation of vessels supplying the femoral head into fibro-osseous canals
Weight-bearing leads to continuous infarcts, necrosis
Gross- fracture and collapse of the necrotic trabecular bone and flattening of the femoral head
What causes metabolic osteodystrophies- bone disease?
How are they classified?
Metabolic oesteodystrophies are the result of disturbed bone growth, modelling or remodelling due to nutrition or hormonal imbalances
- Rickets
- Osteomalacia
- Fibrous osteodystrophy
- Osteoporosis
- It May occur in combination
Describe the metabolism of bone regulation
- Calcitonin- inhibits osteoclasts
- PTH- inhibits osteoblasts and promotes osteoclasts
- PTH- on the kidney increases Ca2+ reabsorption, decreases phosphorus reabsorption and increases Vit D synthesis
- Active Vit D increases calcium and phosphorus absorption from GI and increases osteoclast activity- increased blood Ca2+
- When osteoblasts are active, it uses calcium to reduce blood content which increases PTH
- Active osteoclasts increase blood calcium- increases calcitonin which increases osteoclast apoptosis
What can cause osteoporosis?
Describe its pathogenesis
How does it appear grossly and histologically?
Sequalae?
Cause- senility, calcium deficiency, starvation, GI parasitism, inflammatory, bowel disease, corticosteroids
Path- increased osteoclastic activity
Starvation- reduced apposition of bone
Parasitism- malabsorbtion
Corticosteroid- collagen synthesis inhibition
Disuse- reduced weight-bearing
Gross- reduction in the quantity of bone, the quality of which is normal, narrowed cortices, transverse reinforcement trabeculae and there is increased fragility
Histology- rare and smaller trabeculae- normal calcification
Ac- pathological fracture
Describe how parasitism causes osteoporosis
- Calcium and phosphorus absorbed with active vitamin D, parasites present this
- This decreases Ca2+ causing PTH to increase
- PTH activated osteoclasts and inhibits osteoblasts and increases Vit D synthesis
- Vit D synthesis makes no difference as parasites
- Causes bone thinning
What is the difference between rickets and osteomalacia?
What causes it?
Describe the pathogenesis
How does it grossly and histologically appear?
Explain how Vit D deficiency can cause this?
Rickets- young, Osteomalacia- adults
Hypovitaminosis and Hypophosphatemia
Pathogenesis- defective mineralisation at sites of bone growth (young) or bone remodelling sites (adults), insufficient mineralization of newly formed osteoid
Gross- sites of rapid growth- metaphyseal regions- disorganization of trabeculae in the metaphysis with extensions of cartilage into the metaphysis
Histological- failure of mineralisation of cartilage and osteoid, with persistence and disorganization of hypertrophic chondrocytes at sites of endochondral ossification
Vit D deficiency- causes inhibition of phosphorus reabsorption kidneys, reducing blood phosphorus and therefore cannot create normal osteoid, also increases PTH and causes activation of osteoclasts
What can cause fibrous osteodystrophy
How does it appear grossly and histological?
What are the associated conditions?
- Primary PTH secreting tumour- primary hyperparathyroidism
- Renal failure- secondary hyperparathyroidism
- Low calcium/ high phosphorus diet- horses- nutritional
- A PTH-like secreting tumour (anal sac carcinoma)- dog/cat rare- pseudohypoparathyroidism
Grossly- bone enlargement, tooth loss, fractures, spongy appearance, mandible classical location
Histologically- excessive bone reabsorption increased osteoclast activity, fibrous proliferation- excessive osteocytes
Associated conditions- osteoporosis
Explain the disease process of fibrous osteodystrophy for primary and secondary hyperparathyroidism
Primary hyperparathyroidism
- Increased PTH causes increased Ca reabsorption and inhibiting phosphorus reabsorption
- Also increases osteoclasts activity
- It also indirectly causes osteoblasts to produce collagen
- This leads to increased collagen which cannot be broken down by osteoclasts
Secondary
- Normally phosphorus is filtered and some reabsorbed
- If kidney function is compromised- neoplasm, failiure
- Increases phosphorus there fore PTH which causes calcium mobilisation
- This causes collagen production and bone breakdown
What do fractures lead to?
- Haemorrhage
- Haematoma
- Proliferating collagen
- Ossification/chondrification
- Remodelling/endochondral ossification
How are fractures classified?
Physiological- impact- overwhelmed
Pathological- no impact- weakened bone
Displaced/undisplaced
Simple- line
Complex- several pieces
Articular- eg condyle
Dyaphiseal
Epiphyseal
What happens to fractures with the following scenarios?
Inadequate blood supply
Instability
Infection
Inadequate blood- necrosis
Instability- non-union therefore pseudoarthrosis
Infection- osteomyelitis
What can cause bone inflammation?
Where are these inflammations?
Periosteitis
Osteitis
Osteomyelitis
Panosteitis
Aseptic- traumatic
Bacterial- tuberculosis, yersinosis, salmonellsosis
Mycotic
Viral- distemper
- Periostitis- inflammation of the periosteum
- Osteitis- inflammation of bone
- Osteomyelitis- inflammation of bone and bone marrow
- Panosteitis- inflammation of all bone structures
Where is the predilection site for bacterial osteomyelitis?
What can cause it in foals and calves?
What predisposes to it in calves and foals?
How does it grossly appear?
What are the associated conditions?
Prediction site- capillary loops
Fenestrated, inefficacy of phagocytes, blood flow turbulence
Foals- E. Coli, streptococcus, salmonella, Rhodococcus, klebsiella
Calves- actinobacterium, salmonella
Dogs/cats- secondary to penetrating injury
Predisposes- inadequate passive immune transfer and bacterial septicaemic infection- osteomyelitis
Gross- bone destruction and purulent material, bone fragility
Ac- pathological fracture
What causes ‘lumpy jaw’?
What species does it affect, and what is the causative agent?
Describe the pathogenesis
How does it appear grossly and histologically?
Mandibular osteomyelitis
Actinomyces bovis- cattle
Path- oral injury, penetration of bacteria through mucosa close to the teeth, bone erosion, penetration inside the bone, pyogranulomatous osteomyelitis
Gross- mandible/maxilla swelling, gingival ulceration, displacement of teeth, honeycomb appearance on the cross section
Histology- necrotic bone, purulent exudates, splendorehoeppli figures
What breeds does canine panosteitis affect?
How does it appear grossly, histologically?
What are associated conditions?
Giant breeds of dogs
Aetiology unknown
Grossly- none, X-ray changes- radiodensity after 10 days, medulla close to the nutritional foramen
Histology- expanding areas of fibrovascular tissue, bone marrow cavity which are replaced by woven bone with resting and reversal lines, inflammation is low
Ac- mild to severe lameness which can shift from one leg to another
What benign and malignant neoplasms can occur in the bone?
Benign- osteoma, ossifying fibroma, fibrous dysplasia
Malignant- osteosarcoma, chondrosarcoma
What is some common tumour like lesions of bones?
Aneurysmal bone cysts
Exuberant fracture callus
What species do chondrosarcoma and osteosarcoma affect?
How do they appear grossly and histologically?
Chondrosarcoma-
Dogs, cats, sheep
Gross- nodular expansile lesions- ribs and head
Histology- relatively well-differentiated chondrocytes proliferating with abundant matrix- mitoses rare
Osteosarcoma-
Dogs, cats
Gross- destructive and/or osteoproliferative lesions- weight baring bones
Histology- moderately to poorly differentiates atypical osteoblasts with high mitotic activity, associated with osteoid production
