Musculoskeletal Pathology

melian.yates
Mind Map by , created almost 6 years ago

Doctorate Pathology (Systems Pathology) Mind Map on Musculoskeletal Pathology, created by melian.yates on 27/11/2013.

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melian.yates
Created by melian.yates almost 6 years ago
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Musculoskeletal Pathology
1 Skeletal Muscle
1.1 Muscles of posture, movement & respiration
1.2 Response of Muscle to Injury
1.2.1 Degeneration/ Necrosis
1.2.1.1 Tends to be segmental
1.2.1.1.1 (Necrosis of entire myofibre is uncommon => crush injury or widespread ischaemia resulting from pressure on a large artery)
1.2.1.2 Lots of causes
1.2.1.3 Common triggering factor is increase in Ca2+ w/in the cell
1.2.1.3.1 Allows muscle contraction
1.2.1.3.1.1 Ca-dependent enzymes & lysosomal enzymes increase => myofibre destruction
1.2.1.4 Muscle cell contents may leak into blood if the cell membrane is damaged
1.2.1.4.1 Creatine kinase (CK) is an enzyme which leaks following injury & is commonly used to measure the extent of muscle damage
1.2.2 Regeneration
1.2.2.1 Requirements:
1.2.2.1.1 Intact basal lamina (Sarcolemmal tube)
1.2.2.1.1.1 Blood supply => macrophages to clear up debris
1.2.2.1.1.1.1 Viable satellite cells (act as progenitor cells for new sarcoplasm production)
1.2.2.1.2 If not met, fibrosis will occur
1.2.2.2 Skeletal muscle myofibres have substantial regenerative ability
1.2.3 Atrophy
1.2.3.1 Entire muscle or individual myofibres within are reduced in diameter
1.2.3.2 Causes:
1.2.3.2.1 Disuse (Ex. fracture, failure to use limb, recumbancy)
1.2.3.2.1.1 Cachexia, old age, malnutrition
1.2.3.2.1.1.1 Denervation (nerve provides trophic factors: any interference or damage => muscle atrophy)
1.2.3.2.1.1.1.1 Endocrine disease
1.2.3.2.1.1.1.2 Ex. Equine "roarers" - Laryngeal hemiplegia (Damage to left recurrent laryngeal nerve)
1.2.3.2.1.1.1.3 Can be rapid - over 50% of muscle mass lost in a few weeks
1.2.4 Hypertrophy
1.2.4.1 Entire muscle or individual myofibre diameter increases in size
1.2.4.2 Causes:
1.2.4.2.1 Increased work load
1.2.4.2.1.1 Compensatory
1.2.4.2.1.1.1 Ex. COPD heaves lines
1.2.4.2.1.2 Physiological
1.2.5 Innumerable factors can induce these changes (Trauma, toxins, infectious agents, nutritional deficiencies, Ischaemia, Hereditary disease)
1.2.5.1 => Specific Dx is NOT POSSSIBLE based on morphological or histological features alone
1.3 Muscle Diseases
1.3.1 Inflammation: Myositis
1.3.1.1 Infectious
1.3.1.1.1 Bacteria
1.3.1.1.1.1 Gain entry via direct penetration, haematogenously or extension (Ex. from an infected joint)
1.3.1.1.1.2 Disease or manifestation
1.3.1.1.1.2.1 Abscesses
1.3.1.1.1.2.1.1 Arcanobacterium pyogenes (Bovine, Pigs)
1.3.1.1.1.2.1.2 Streptococcus equi (Equine)
1.3.1.1.1.2.1.3 Corynebacterium pseudotuberculosis (Sheep, Goats, Equine)
1.3.1.1.1.2.2 Black leg
1.3.1.1.1.2.2.1 Clostridium chauvoei ( Bovine, Sheep)
1.3.1.1.1.2.2.2 Activation of latent spores
1.3.1.1.1.2.3 Gas gangrene
1.3.1.1.1.2.3.1 Clostridium septicum & C. novyi (Sheep, Bovine, Equine), C. perfringens & C. sordelli (Pigs)
1.3.1.1.1.2.3.2 Penetrating wounds
1.3.1.1.1.2.4 Wooden tongue
1.3.1.1.1.2.4.1 Actinobacillus lignieresii (Bovine)
1.3.1.1.2 Viruses (Rare)
1.3.1.1.3 Parasites
1.3.1.1.3.1 Nematodes
1.3.1.1.3.1.1 Trichinella, Ancylostoma & Ascarid larvae
1.3.1.1.3.1.2 Cestodes
1.3.1.1.3.1.2.1 Taenia solium (cysticercosis in swine & humans). T.ovis (cystercercosis in sheep)
1.3.1.1.3.1.2.2 Protozoa
1.3.1.1.3.1.2.2.1 Toxoplasma gondii, Neospora caninum, Sarcocystis
1.3.1.2 Immune mediated
1.3.1.2.1 Canine Masticatory Muscle Myositis (MMM)
1.3.1.2.1.1 Autoantibodies SELECTIVELY attack muscle of mastication (Type IIM fibres)
1.3.1.2.1.1.1 Manifests in the masseter & temporalis muscles (Bilateral)
1.3.1.2.1.1.1.1 Acute stage: Eosinophillic myositis
1.3.1.2.1.1.1.1.1 Chronic stage: Atrophic myositis
1.3.1.2.2 Extraocular myositis
1.3.1.2.2.1 Autoantibodies selectively target only the muscles around the eye in the Dog
1.3.1.2.3 Canine Polymyositis
1.3.1.2.3.1 Can affect masticatory muscles but Dogs DO NOT have antibodies to type IIM fibres
1.3.1.2.3.2 Generalized inflammatory myopathy
1.3.1.2.3.3 Muscle necrosis, regeneration & fibrosis
1.3.1.2.3.3.1 Muscle enzymes may be increased
1.3.1.2.3.3.1.1 Fever, pain, weakness, resp. distress
1.3.1.2.3.3.1.1.1 T Lymphocytes, plasma cells, granulocytes
1.3.1.2.3.4 Single biopsy may not be enough to make the Dx (it tends to be multifocal & disseminated)
1.3.1.2.3.5 DDx = Toxoplasma gondii, MMM
1.3.1.3 Other
1.3.1.3.1 Paraneoplastic, drug-induced, idiopathic
1.3.2 Congenital
1.3.2.1 Defects in muscular form
1.3.2.1.1 Congenital diaphramatic defects
1.3.2.1.1.1 Myofibrillar hypoplasia (Pigs - splayleg)
1.3.2.1.1.1.1 Can spontaneously resolve, cause unknown, responsible for significant deaths
1.3.2.1.1.1.2 Hyperplasia of muscle fibres (Calves, lambs)
1.3.2.1.1.1.2.1 Double muscling due to increased number of myofibres in affected muscle (thighs, rump, loin) -> Predisposes to dystocia
1.3.2.2 Muscular Dystrophies
1.3.2.2.1 Inherited group (X-linked) of degenerative muscular diseases causing progressive muscle weakness & wasting
1.3.2.2.2 Usually due to a genetic fault leading to a muscular protein deficiency
1.3.2.2.2.1 Ex. Duchenne MD in humans due to dystrophin deficiency
1.3.2.2.2.2 Dystrophin gene mutations reported in the Golden retriever, Rottweiler, Irish terrier, etc.
1.3.2.2.3 Innervation is normal
1.3.2.2.3.1 Muscle biopsy -> confirm lack of dystrophin with IHC
1.3.3 Toxic, Nutritional & Exertional Myopathies
1.3.3.1 Toxic
1.3.3.1.1 Plants
1.3.3.1.1.1 Gossypol, Cassia (coffee senna)
1.3.3.1.2 Drugs
1.3.3.1.2.1 Monensin
1.3.3.1.2.1.1 Coccidiostat
1.3.3.1.2.1.2 Toxic to: Horses, Sheep, Cattle, Dogs, Birds
1.3.3.1.2.1.3 Skeletal & myocardial necrosis
1.3.3.1.2.1.4 Rapid onset recumbancy & potentially death
1.3.3.1.2.1.5 Usually due to mixing errors in feed
1.3.3.1.2.1.6 Ionophore
1.3.3.1.2.1.6.1 Disturbs transport of Na & K across membrane
1.3.3.1.2.1.6.1.1 Increases Ca2+ => Hypercontraction & Degeneration
1.3.3.1.3 Chemicals
1.3.3.1.3.1 Ex. Fe injections can cause local myonecrosis
1.3.3.1.4 Mycotoxins
1.3.3.2 Endocrine
1.3.3.2.1 Hyperadrenocorticism & Hypothyroidism => Muscle atrophy
1.3.3.3 Nutritional
1.3.3.3.1 White Muscle Disease
1.3.3.3.1.1 Economic importance in young Cattle, Sheep & Pigs (also foals)
1.3.3.3.1.2 Se &/or Vit. E deficiency
1.3.3.3.1.3 Grossly:
1.3.3.3.1.3.1 Lesions are bilaterally symmetrical (hard working muscles)
1.3.3.3.1.3.1.1 Pigs: lesions in heart & liver
1.3.3.3.1.4 Pathogenesis:
1.3.3.3.1.4.1 Oxygen free radicals (OFR) can damage cell membranes
1.3.3.3.1.4.1.1 Vit. E involved in binding OFR & Glutathione peroxidase (includes Se) => Neutralizes effects of OFR
1.3.3.3.1.4.1.2 If Vit. E & Se deficient: Balance shifts to membrane damage => Ca2+ entry & mitochondrial damage => cell swells & dies
1.3.3.4 Exertional
1.3.3.4.1 Caused by intensive & exhaustive activity of major muscle masses
1.3.3.4.2 Classically occurs in the Horse after unaccustomed exercise
1.3.3.4.3 Equine exertional rhabdomyolysis
1.3.3.4.3.1 Dissolution of striped (skeletal) muscle
1.3.3.4.3.1.1 Membrane damage & leakage of myoglobin
1.3.3.4.3.1.1.1 Myoglobinura = rhabdomyolysis
1.3.3.4.4 Azoturia
1.3.3.4.4.1 Exercise following prolonged period of rest
1.3.3.4.4.2 Unable to move, sweating, tremors
1.3.3.4.4.3 Myoglobin leaks from muscle cells -> leaks into urine -> urine is dark red/brown (myoglobinuria) -> damages renal tubules
1.3.3.4.5 Tying-up (similar to Azoturia, but milder)
1.3.3.4.6 Linked to polysaccharide storage myopathy (many breeds)
1.3.3.4.6.1 Ex. Equine polysaccharide storage myopathy (EPSM)
1.3.3.4.7 Capture myopathy, Porcine stress syndrome
1.3.4 Neuromuscular Junction
1.3.4.1 Myasthenia gravis (MG)
1.3.4.1.1 1) Acquired
1.3.4.1.1.1 Autoimmune disease: Abs directed against acetyl choline receptors
1.3.4.1.1.2 Associated w/ thymomas, megaoesophagus & hypothyroidism (Dogs)
1.3.4.1.2 2) Congenital
1.3.4.1.2.1 Inherited deficiency in acetyl choline receptors (Rare)
1.3.4.1.2.2 No Abs against acetyl choline receptors in serum
1.3.4.1.3 Both forms manifest as weakness which worsens on exercise
1.3.4.2 Botulism
1.3.4.2.1 Due to ingestion of Clostridium botulinum toxin which inhibits acetyl choline release
1.3.4.2.2 Dx: Demonstrate toxin in faeces, ingested material, serum
1.3.5 Neoplasia
1.3.5.1 Rare in domestic animals
1.3.5.2 Primary benign: Rhabdomyoma
1.3.5.2.1 Primary malignant: Rhabdomyosarcoma
1.3.5.3 Metastases can also occur to skeletal muscle (e.g. carcinoma, haemangiosarcoma)
1.4 Anatomy
1.4.1 Types of Myofibres
2 Bones function, structure & organization
2.1 Bone is a hard, highly specialized connective tissue, comprising interconnected cells embedded in a clacified, collagenous matrix
2.2 A living, dynamic, responsive tissue, growing & remodeling throughout life
2.3 Functions:
2.3.1 Supports movement
2.3.1.1 Protects body
2.3.1.1.1 Storage:
2.3.1.1.1.1 Mineral bank
2.3.1.1.1.1.1 Haematopoietic stem cells
2.3.1.1.1.1.1.1 Fat
2.4 Structure:
2.4.1 Composed of cells & matrix
2.4.2 Cells:
2.4.2.1 Osteoblasts
2.4.2.1.1 Mesenchymal cells of bone marrow stromal origin
2.4.2.1.1.1 Form the bone matrix (Osteoid)
2.4.2.2 Osteoclasts
2.4.2.2.1 Multinucleated cells derived from haematopoietic stem cells
2.4.2.2.1.1 Responsible for bone resorption
2.4.2.3 Osteocytes
2.4.2.3.1 Osteoblasts that have become surrounded by mineralized bone matrix
2.4.2.3.1.1 Occupy cavities called lacunae
2.4.3 Matrix:
2.4.3.1 Composed of type I collagen & mineral
2.4.3.2 Mineral - accounts for 65% of bone (includes: Ca, P, Mg, Mn, Zn, Cu & Na)
2.4.3.3 Ground substance (water, proteoglycans, lipids)
2.4.3.4 Strength
2.5 Bone Organization
2.5.1 Not all bones are organized in the same way
2.5.1.1 Organization dictated by the pattern of collagen deposition
2.5.2 1) Immature (Woven) Bone
2.5.2.1 Collagen is arranged in a "random weave"
2.5.2.1.1 This is only normal in the fetus
2.5.2.1.1.1 In adults: Randomly woven bone => sign of pathological condition (e.g. fracture, inflammation, neoplasia)
2.5.3 2) Mature (Lamellar ) Bone
2.5.3.1 The collagen is arranged in orderly layers which are much stronger than woven bone
2.5.3.2 Two main types:
2.5.3.2.1 Compact or cortical bone
2.5.3.2.1.1 forms the diaphyses of long bones & the shell of all other bones (contains Osteons)
2.5.3.2.2 Cancellous (spongy or trabecular) bone
2.5.3.2.2.1 occurs in vertebrae, flat bones & epiphysyes of long bones (Contains NO Osteons)
2.6 Periosteum
2.6.1 A sheath of connective tissue covering the bone (except at the articular surfaces)
2.6.1.1 The inner layer merges w/ the outer layer of bone & contains osteoblasts & stem cells
2.6.1.1.1 The blood supply to the mature bone enters via the periosteum
2.6.1.1.1.1 Damage to the periosteum triggers a hyperplastic rxn of the inner layer
2.7 Bone Development
2.7.1 2 Main Types:
2.7.1.1 Intramembranous ossification
2.7.1.1.1 Flat bones mainly (e.g. skull)
2.7.1.1.2 Mesenchymal cells differentiate into osteoblasts
2.7.1.1.2.1 There is NO cartilage precursor template
2.7.1.2 Endochondral ossification
2.7.1.2.1 Long bones mainly
2.7.1.2.2 Cartilage model of the bone to be formed is vascularised & replaced by bone
2.8 Physis (Growth plate)
2.8.1 Esentially the remnant of the cartilage model located at the junction of Diaphysis & Epiphysis
2.8.2 Imp. site: Many congenital or nutritional bone diseases in the growing animal manifest here
2.8.3 In neonates & growing animals: Growth plate is "open", i.e. chrondrocyte proliferation balances cell maturation & death
2.8.3.1 The growth plate "closes" & ossifies @ maturity
2.9 Bone Resorption
2.9.1 Mediated by PTH & Calcitonin
2.9.2 Parathyroid Hormone (PTH)
2.9.2.1 Produced by chief cells in the parathyroid glands
2.9.2.1.1 Increases serum Ca2+ levels (released in response to decreased serum Ca2+)
2.9.2.2 STIMULATES Osteoclasts
2.9.3 Calcitonin
2.9.3.1 Produced by C -cells in the thyroid glands
2.9.3.1.1 Decreases serum Ca2+ levels ( released in response to Increased serum Ca2+)
2.9.3.2 INHIBITS Osteoclasts
2.9.4 Low serum Ca2+ -> Induces PTH secretion -> Osteoclasts increase in # -> Attach to bone & resorb mineralized matrix => Serum Ca2+ INCREASES
2.10 Bone Dynamics
2.10.1 Bone growth & maintenance of normal structure are directly related to mechanical forces which generate bioelectrical potentials (piezoelectricity)
2.10.1.1 These potentials strengthen bone while inactivity reduces them, leading to bone loss
2.10.2 Neonates: Bone growth predominates & modeling is Imp.
2.10.2.1 Adults: Formation of bone is balanced by resorption (remodeling)
2.10.3 Bone resorption may exceed formation in pathological stages (Hormonal, trauma, nutritional) or in old age & disuse
3 Pathology of Bone
3.1 Fractures
3.1.1 Traumatic
3.1.1.1 Normal bone broken by excessive force
3.1.2 Pathological
3.1.2.1 Abnormal bone broken by minimal or no trauma
3.1.3 Fracture Repair
3.1.4 Callus
3.1.4.1 Bridges the gap, Encircles fracture site, Stabilizes fracture
3.1.5 Factors which delay healing:
3.1.5.1 Malnutrition
3.1.5.1.1 Inadequate blood supply (leads to hypoxia)
3.1.5.1.1.1 Leads to excess cartilage in Callus
3.1.5.1.1.1.1 Healing can still occur since this can turn to bone
3.1.5.1.1.2 Excess movement
3.1.5.1.1.2.1 Leads to excess fibrous tissue in Callus
3.1.5.1.1.2.1.1 This forms a false joint & can't heal properly
3.1.5.1.1.2.2 Presence of Necrotic bone (may form a sequestrum)
3.1.5.1.1.2.2.1 Bacterial Infection
3.2 Metabolic Bone Diseases
3.2.1 Manifestation of Systemic Disease in the skeleton (Endocrine, Nutritional or Toxic Origin)
3.2.2 Hyperparathyroidism (Fibrous Oesteodystrophy)
3.2.2.1 Bone is resorbed & replaced by Fibrous, "rubbery" connective tissue
3.2.2.1.1 Caused by: Persistently elevated PTH
3.2.2.2 Causes of Increased PTH:
3.2.2.2.1 Primary (Rare)
3.2.2.2.1.1 Increased production of PTH NOT related to Ca2+ or P levels (i.e. autonomous)
3.2.2.2.1.1.1 Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
3.2.2.2.1.1.1.1 Results in => Hypercalcaemia
3.2.2.2.2 Secondary (much more common)
3.2.2.2.2.1 Renal
3.2.2.2.2.1.1 Chronic renal failure (Reduced perfusion)
3.2.2.2.2.1.1.1 => Retention of P ( & inadequate production of Vit. D by kidneys)
3.2.2.2.2.1.1.1.1 Hyperphosphataemia & Hypocalcaemia (High P depresses Ca2+)
3.2.2.2.2.1.1.1.1.1 Low Ca2+ => PTH production => Increased Ca2+ resorption from bone ("Rubber jaw")
3.2.2.2.2.1.1.1.1.2 => Fibrous Osteodystrophy
3.2.2.2.2.2 Nutritional (Poor diet) - "Rubber Jaw"
3.2.2.2.2.2.1 Low Ca2+/ High P diets/ Vit. D deficiency
3.2.2.2.2.2.1.1 Increased Osteoclastic resorption of bone & deposition of fibro-osteoid matrix that fails to mineralize
3.2.2.2.2.2.1.1.1 Flat bones of the skull (Maxillary & Nasal bones) => Swell
3.2.2.2.2.2.1.1.1.1 Long bones become soft w/ thin cortices (fracture easily)
3.2.2.2.2.2.2 Ex: Horses - Grain/corn/bran
3.2.2.2.2.2.2.1 Swine - Fed grain rations
3.2.2.2.2.2.2.1.1 Dogs & Cats - Fed meat only diets
3.2.2.2.2.2.3 More common in young, fast growing animals (w/ exception of horses)
3.2.2.2.2.3 PTH secretion triggered by Decreased plasma Ca2+
3.2.2.2.3 Paraneoplastic
3.2.2.2.3.1 Parathyroid hormone- related protein produced by certain neoplasms
3.2.3 Osteoporosis
3.2.3.1 a LESION, not a distinct disease entity
3.2.3.2 Reduction in bone quantity, not quality
3.2.3.2.1 Bone resorption exceeds formation -> Pathological loss of bone
3.2.3.2.1.1 The bone that remains is normally mineralized (Just not enough of it)
3.2.3.2.1.1.1 => Prone to fractures due to reduced strength
3.2.3.3 Causes:
3.2.3.3.1 Starvation, nutritional deficiency (Ca2+)
3.2.3.3.1.1 Senility
3.2.3.3.1.1.1 Physical inactivity (Disuse)
3.2.3.3.1.2 Farm animals (Most common cause)
3.2.3.3.1.2.1 Calves on indigestible milk replacer
3.2.3.3.1.2.1.1 Cattle on low quality hay in cold climates
3.2.3.4 Localized or general
3.2.3.5 Bone atrophy or osteopaenia
3.2.4 Rickets
3.2.4.1 Disease of the young, fast growing skeleton
3.2.4.2 Pathogenesis:
3.2.4.2.1 Failure of mineralization of Physeal & Epiphyeal cartilage during endochrondral ossification & of newly formed osteoid
3.2.4.3 Due to diets low in Vit. D (or P - less common)
3.2.4.3.1 Vit. D. maintains normal plasma levels of Ca2+ & P (acts on intestines, bones, kidneys)
3.2.4.3.1.1 Calcitriol enhances GI absorption of Ca & P
3.2.4.3.1.1.1 w/o Vit. D, only 10-15% of dietary Ca2+ is absorbed
3.2.4.4 Growth plates are thickened
3.2.4.4.1 As the zone of proliferation does not mineralize & mature => blood vessels & chondroclasts cannot invade so the cartilage is not removed
3.2.4.5 Metaphyses are flared
3.2.4.5.1 Because bone & cartilage cannot be removed (Osteoclasts cannot bind to poorly mineralized bone -> further accentuated by weight bearing)
3.2.4.6 Enlarged costochondral junctions
3.2.5 Osteomalacia
3.2.5.1 Similar to Rickets, except disease of adult skeleton
3.2.5.2 Failure of newly formed osteoid to mineralize
3.2.6 Others
3.2.6.1 Hormone -related (Hormones which directly affect bone growth & resorption - other than PTH & Calcitonin)
3.2.6.1.1 Insulin, Growth hormone (Somatotrophin), Glucocorticoids, Oestrogens, Androgens & Thyroid Hormones
3.2.6.2 Vitamin -Related Conditions
3.2.6.2.1 Vitamin A
3.2.6.2.1.1 Hypervitaminosis A
3.2.6.2.1.1.1 Cats fed liver for prolonged periods
3.2.6.2.1.1.2 Vertebrae fuse (Vertebral ankylosis) with each other due to bone proliferation (esp. in neck)
3.2.6.2.1.1.2.1 Pathogenesis not clear
3.2.6.2.1.1.3 Can also be teratogenic -> Cleft palate
3.2.6.2.1.2 Hypovitaminosis A
3.2.6.2.1.2.1 Due to dietary deficiency in Dam: Can be teratogenic in Pigs & large Cats
3.2.6.2.1.2.2 More commonly, due to dietary deficiency in Neonates (Puppies, Kittens, Calves, Piglets)
3.2.6.2.1.2.3 Deficiency => Failure of osteoclastic remodeling => Bone overgrowth & nerve compression (esp. optic nerves)
3.2.6.2.1.3 Essential for normal bone growth in foetuses & neonates
3.2.6.2.1.3.1 Stimulates osteoclasts
3.2.6.2.2 Hypervitaminosis D
3.2.6.2.2.1 Dietary or iatrogenic origin
3.2.6.2.2.2 Usually chronic
3.2.6.2.2.3 Hypercalcaemia: Metastatic calcification of soft tissues
3.2.6.2.3 Vitamin C (Ascorbic Acid)
3.2.6.2.3.1 Scurvy in Pigs, NHPs
3.2.6.2.3.2 Imp. for collagen formation
3.2.6.2.3.2.1 Haemorrhage
3.2.6.2.3.2.1.1 Fractures
3.3 Inflammation
3.3.1 Causes
3.3.1.1 Bacteria (Most common)
3.3.1.1.1 Viral, Fungal, Protozoal (Less common)
3.3.1.1.2 Staphy, Strep, A. pyogenes, Gram -ve
3.3.2 Routes of Infection
3.3.2.1 Direct Inoculation
3.3.2.1.1 At time of fracture
3.3.2.2 Direct Extension
3.3.2.2.1 From other infected sites (sinuses, middle ear, joints)
3.3.2.2.1.1 Arthritis, synovitis, otitis media, rhinitis, sinusitis, meningitis or tooth root abscess
3.3.2.3 Haematogenous
3.3.2.3.1 Mostly young farm animals
3.3.3 Gross lesions
3.3.3.1 Suppurative exudate (in bacterial infection), Necrosis, Bone proliferation, Pathological fractures
3.3.3.2 Dead bone portions may be separated from blood supply => forming bone sequestra
3.3.4 Consequences
3.3.4.1 Extension to adjacent bone
3.3.4.2 Haematogenous spread to other bones & soft tissue
3.3.4.2.1 Possible consequence of sepsis in young animals
3.3.4.2.1.1 Salmonella dublin, A. pyogenes, Strep
3.3.4.2.1.2 Animal often dies of sepsis prior to bone lesions appearing
3.3.4.3 Pathologic features
3.3.4.3.1 Draining fistulas, necrosis & loss of bone, new bone
3.3.4.4 Sinus tracts to exterior
3.3.5 Metaphyseal Osteopathy
3.3.5.1 Idiopathic/ unknown cause (Infectious aetiology ?)
3.3.5.2 Young, fast growing Dogs (Large or giant breeds)
3.3.5.3 Distal radius & ulna most severely affected: bilaterally symmetrical
3.3.5.4 Swelling in metaphyses of long bones (Neutrophilic infiltrate)
3.3.5.4.1 Fever, lameness, suppurative inflammation & necrosis of metaphyses
3.3.5.5 Most resolve spontaneously, but can progress to periosteal bone proliferation
3.3.5.5.1 May wax & wane
3.4 Neoplastic Bone Diseases
3.4.1 Bone tissue:
3.4.1.1 Osteoma
3.4.1.1.1 Uncommon
3.4.1.1.2 Horses & Cattle
3.4.1.1.3 Flat bones (skull & scapula)
3.4.1.1.4 Disfigurement: Obstruct nasal passages
3.4.1.1.5 Recur if not completely removed
3.4.1.2 Osteosarcoma (OSA)
3.4.1.2.1 Any neoplasm of mesenchymal origin in which the cells produce Osteoid
3.4.1.2.2 Dogs & Cats (Otherwise uncommon)
3.4.1.2.3 Dogs: OSA(80%) > Chrondrosarcoma (10%) > Fibrosarcoma/haemangiosarcoma (7%) > Lymphoid & myeloid tumors of marrow
3.4.1.2.4 Giant breeds of Dog are at massively increased risk
3.4.1.2.5 Strong site preference (Dogs):
3.4.1.2.5.1 Appendicular skeleton 3-4x more frequently involved than axial
3.4.1.2.5.1.1 Proximal humerus, distal radius, proximal tibia & distal femur
3.4.1.2.5.1.1.1 "Away from the elbow - towards the knee"
3.4.1.2.6 Survival time is slightly better for axial than appendicular OSA (Dogs)
3.4.1.2.7 Prognosis is poor due to early metastasis
3.4.1.2.7.1 Pulmonary metastases
3.4.1.2.7.2 Bone metastases
3.4.2 Cartilage:
3.4.2.1 Chondroma
3.4.2.1.1 Benign neoplasm of cartilage
3.4.2.1.2 Rare
3.4.2.1.3 Slow growing, Expansile w/ smooth border
3.4.2.2 Chrondrosarcoma
3.4.2.2.1 Any malignant neoplasm in which mesenchymal cells produce chondroid matrix
3.4.2.2.2 Dogs (most common), Sheep
3.4.2.2.2.1 Flat bones
3.4.2.2.3 Slower growth rate, longer clinical course & later to metastasize than OSA
3.4.2.2.4 Metastatic rate: 20%
3.5 Hyperostotic Bone Diseases
3.5.1 Hypertrophic Pulmonary Osteopathy (HPO)
3.5.1.1 Periosteal proliferation of bone on diaphyses & metaphyses of distal limbs
3.5.1.1.1 Progressive & bilateral
3.5.1.1.1.1 Most cases: Have intrathoracic neoplasm or chronic inflammatory focus
3.5.1.1.1.1.1 Has also been associated w/ intra-abdominal lesions - Ex. Botryoid rhabdomyosarcoma in the canine urinary bladder & ovarian tumors in Horses
3.5.2 Craniomandibular Osteopathy
3.5.2.1 West Highland terriers & Scottish terriers
3.5.2.1.1 Puppies: Arises @ 4 -7 months
3.5.2.2 Bilaterally symmetrical periosteal proliferation of new bone
3.5.2.3 Irregular thickening of rami of mandibles & skull bones (tympanic bullae)
3.6 Developmental Bone Diseases
3.6.1 Primary abnormalities of Bone, Cartilage or Mesenchyme
3.6.2 Hereditary or Environmental
3.6.3 Localized or Generalized
3.6.3.1 Generalized
3.6.3.1.1 Proportionate Dwarfism
3.6.3.1.1.1 Minature breeds: Due to growth factor deficit
3.6.3.1.2 Chondrodysplasia
3.6.3.1.2.1 Abnormal cartilage formation
3.6.3.1.2.2 Cattle, Dogs, Sheep, Pigs & Cats
3.6.3.1.2.2.1 Affects bones which form from a cartilage model (endochondral ossification) - long bones are shorter than normal
3.6.3.1.2.2.1.1 Leads to Disproportionate Dwarfism
3.6.3.1.2.3 Localized forms occur in some Dogs as a breed associated characteristic (e.g. affecting skulls of Pekingnese & Bulldogs or the limbs of Dachshunds & Basset hounds)
3.6.3.1.3 Osteopetrosis (Marble bone disease)
3.6.3.1.3.1 Hyperactive osteoblasts/ Failure of resorption by osteoclasts => Failure of remodeling of cancellous bone
3.6.3.1.3.2 Bones become thickened & dense, but brittle
3.6.3.1.3.3 Associated w/ viral infections (e.g. FeLV, BVD)
3.6.3.2 Localized
3.6.3.2.1 Cervical Vertebral Stenotic Myelopathy (Wobblers)
3.6.3.2.1.1 Equine disease
3.6.3.2.1.2 Narrowing of the vertebral canal due to vertebral malalignment or maldevelopment
3.6.3.2.1.2.1 Fast growing males ranging from 8 months to 4 yrs
3.6.3.2.1.2.1.1 Hind limb ataxia: Due to cord compression
3.6.3.2.1.3 Dogs: Great dane, Doberman
3.6.3.2.1.4 Static: C5-C7 (1-4yrs)
3.6.3.2.1.5 Dynamic: C3 -C5 (1 yr)
3.6.3.2.2 Angular Limb Deformity
3.6.3.2.2.1 Lateral deviation of distal portion of limb (usually)
3.6.3.2.2.1.1 Most common in foals: Congenital or Acquired
3.6.3.2.2.1.1.1 Causes: Malpositioning (in utero), excessive joint laxity, hypothyroidism, trauma, overnutrition, defective endochrondral ossification
3.7 Miscellaneous Bone Lesions
3.7.1 Ossifying Pachymeningitis
3.7.1.1 Plaques of bone form in the Dura of the spinal cord (especially in older dogs)
3.7.1.2 No clinical significance
3.7.2 Heterotopic Bone
3.7.2.1 Spicules of bone form in the lungs of older dogs
3.7.2.2 No clinical significance
3.7.3 Ossifying Epulides
3.7.3.1 Neoplasms of peridontal fibroblast origin
3.7.3.2 Occur in oral cavity (esp. Boxers)
3.7.3.3 Benign -> Complete removal -> Good prognosis