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 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 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 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 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
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
