Musculoskeletal 1, 2 and 3

Question 1

Name an example of a flat and long bone

Answer 1

Flat- skull

Long- humerus

Question 2

Describe the following long bone anatomical features:

• Epiphysis
• Dyaphysis
• Periosteum
  *

Answer 2

Epipyhsis- top and bottom

Dyaphisis- middle

Periosteum- fibrous capsule of the bone

Question 3

Where is compact and spongy bone found?

What is a physis and a metaphysis?

What is the difference between lamellar bone and woven bone?

Answer 3

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

Question 4

What is cancellous bone?

What is its role?

Answer 4

Interconnected fenestrated plates of bone

Porous and low density- shock absorber

Question 5

Embryology- what are the three primary germ layers?

What does the skeleton develop from?

Answer 5

Ecoderm- skin and appendages

Mesoderm- skeleton, connective tissue, vascular tissue, linings of thorax and abdomen/pelvis

Ectoderm- pharynx, respiratory, GI system, bladder, urethrea

Question 6

What is intramembranous ossification?

Where does membranous ossification occur?

Answer 6

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

Question 7

Describe endochondral ossification

Where does it occur?

Answer 7

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

Question 8

Describe how joints form by cystic degeneration

Answer 8

• 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

Question 9

By what processes do long bones grow in width and length

Describe what happens at a growth plate

Answer 9

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

Question 10

What is primary spongiosa and secondary spongiosa?

Answer 10

Primary- bone spicules with cartilage core

Secondary- bone spicules without cartilage core

Question 11

What procues osteoid?

When is it converted to bone?

Answer 11

Oestoblasts produce osteoid- 90% collagen type 1

Following 10 days- primary mineralisation 70-75%

Several months- secondary mineralisation

Question 12

What is the difference between type 1 and 2 cartilage?

Answer 12

Type 1- cartilage in bone

Type 2- in cartilage- high water

Question 13

What are osteoid and the osteoid seam?

Answer 13

Osteoid- unmineralized bone matrix initially deposited by a later of osteoblasts

Osteoid seam- name of the later of superficial non-mineralised osteoid

Question 14

What are osteoclasts and osteoblasts?

Answer 14

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

Question 15

How are peritrabecular stromal cells connected to osteoblasts?

When do they become osteoblasts?

What are the 4 roles of peritrabecular stromal cells?

Answer 15

Peritrabecular stroll cells of bone marrow connect to osteoblasts by cellular junctions and become osteoblasts during bone deposition

1. Produce haematopoietic growth factors- erythropoietin
2. Progenitor cells of the osteoblasts- provide vertical orientation, establishment of that canlicular-lancunar system
3. Reach to parathyroid hormone stimulation- attract and stimulate osteoclasts to remove bone, proliferate and form fibro-osseous matrix
4. Act as strain gauges and active bone remodelling

Question 16

Describe the process of modelling and reabsorption?

Answer 16

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

Question 17

Describe how bone modelling and reabsorption is regulated?

Answer 17

• 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

Question 18

What are resting lines and reversal lines?

Answer 18

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

Question 19

What can cause abnormalities of skeletal development?

Answer 19

Genetic

Sometimes viral

Question 20

What do the following terms mean for skeletal development?

• Brachygnathia inferior/superior
• Bovine serienomelia
• Dicephalic
• Diprosopus
• Palatoschisis
• Abrachia
• Peromelia
• Micromelia
• Amelia
• Mondactilia
• Polydactilia

Answer 20

• 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

Question 21

What are the following conditions of skeletal abnormalities?

• Canine spina bifida
• Vertebral column distorsion-
  
  • kyphosis
  • scoliosis
  • kyphoscoliosis
  • lordosis

Answer 21

• Canine spina bifida
• Scoliosis- lateral
• Kypohosis- dorsal
• Kyphoscoliosis- dorso-lateral
• Lordosis- ventral

Question 22

What are chondrodysplasias?

Describe its pathology
What is its aetiology?

What is a bull dog calf, a telemark lethal and a ‘Snorter’?

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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?

Answer 24

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

Question 25

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?

Answer 25

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

Question 27

What is congenital hyperostosis? What species does it affect? How does it appear grossly and histologically?

Answer 27

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

Question 28

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?

Answer 28

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

Question 29

What is the alternative name for Marie's disease? What is the aetiology? What species are affected? How does it appear grossly and histologically?

Answer 29

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

Question 30

What are the 4 different bone pigmentations?

Answer 30

Icterus- accumulation of endogenous pigments- periosteum Porphyria- pink tooth disease Melanosis- periosteal melanosis- generalised, calf- melanosis maculosa Tetracycline- selective uptake in growing bone/dentin

Question 31

What is the pathophysiology of pink tooth disease? How does it appear grossly? What are the associated conditions?

Answer 31

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

Question 32

What are some causes of osteonecrosis?

Answer 32

Trauma Inflammation Neoplasia Thromboembolism Vasoconstriction

Question 33

Describe the pathology of bone necrosis How does it appear grossly and histologically?

Answer 33

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

Question 34

What causes 'creepy subsitution'?

Answer 34

Large necrosis- granulation tissue is deposited leading to sequestrum Small necrosis- heals

Question 35

What is Legg-calve Perthes disease

Answer 35

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

Question 36

What causes metabolic osteodystrophies- bone disease? How are they classified?

Answer 36

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

Question 37

Describe the metabolism of bone regulation

Answer 37

* 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

Question 38

What can cause osteoporosis? Describe its pathogenesis How does it appear grossly and histologically? Sequalae?

Answer 38

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

Question 39

Describe how parasitism causes osteoporosis

Answer 39

* 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

Question 40

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?

Answer 40

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

Question 41

What can cause fibrous osteodystrophy How does it appear grossly and histological? What are the associated conditions?

Answer 41

* 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

Question 42

Explain the disease process of fibrous osteodystrophy for primary and secondary hyperparathyroidism

Answer 42

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

Question 43

What do fractures lead to?

Answer 43

1. Haemorrhage 2. Haematoma 3. Proliferating collagen 4. Ossification/chondrification 5. Remodelling/endochondral ossification

Question 44

How are fractures classified?

Answer 44

Physiological- impact- overwhelmed Pathological- no impact- weakened bone Displaced/undisplaced Simple- line Complex- several pieces Articular- eg condyle Dyaphiseal Epiphyseal

Question 45

What happens to fractures with the following scenarios? Inadequate blood supply Instability Infection

Answer 45

Inadequate blood- necrosis Instability- non-union therefore pseudoarthrosis Infection- osteomyelitis

Question 46

What can cause bone inflammation? Where are these inflammations? Periosteitis Osteitis Osteomyelitis Panosteitis

Answer 46

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

Question 47

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?

Answer 47

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

Question 48

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?

Answer 48

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

Question 49

What breeds does canine panosteitis affect? How does it appear grossly, histologically? What are associated conditions?

Answer 49

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

Question 50

What benign and malignant neoplasms can occur in the bone?

Answer 50

Benign- osteoma, ossifying fibroma, fibrous dysplasia Malignant- osteosarcoma, chondrosarcoma

Question 51

What is some common tumour like lesions of bones?

Answer 51

Aneurysmal bone cysts Exuberant fracture callus

Question 52

What species do chondrosarcoma and osteosarcoma affect? How do they appear grossly and histologically?

Answer 52

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