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Musculoskeletal Pathology Notes PDF
Musculoskeletal Pathology Notes PDF
TABLE OF CONTENTS
PART I BONES
Unit 1 Normal structure/function and response to injury…..…….. page 2
Unit 2 Metabolic, nutritional and endocrine diseases of bone......... page 5
Unit 3 Inflammation of bone……………………………………… page 7
Unit 4 Tumors of bone…………………………………………… page 9
PART II JOINTS
Unit 5 Normal structure/function and response to injury…………. page 10
Unit 6 Arthritis………………………………………………..…… page 12
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BONES – Unit 1
Normal structure/function and response to injury
The two main cell types in bone are OSTEOBLASTS and OSTEOCLASTS. The
osteoblasts are constantly making new bone, and the osteoclasts are constantly chewing
away and digesting bone. The balance between these two activities determines how
strong the bone is and helps to maintain the calcium concentration in the body. So our
bones are being constantly remodeled, throughout all of life.
There are two kinds of bone material – lamellar bone, which is normal and found in all
regular bones and then there is woven bone. Woven bone is characterized by the random
orientation of its collagen fibers. It is new bone, laid down rapidly in growth, fracture
repair, and in bone disease. It can be remodeled to form lamellar bone. Woven bone just
isn’t as strong as lamellar bone.
Bone Remodeling
Bone undergoes remodeling during the entire lifetime of an individual. So, your bones
are in fact metabolically active, even though they don’t look like it. In normal
remodeling, bone formation equals resorption, whereas in bone disease a pathologic
imbalance of resorption and formation results in OSTEOPENIA (not enough bone to
support you well).
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Long bones, as well as the tubular bones of
the hands and feet, have a wider portion at
each end (the epiphysis), a cylindrical tube
in the middle (the diaphysis), and a
transition zone between them (the
metaphysis). In a long bone that is
growing, the epiphysis and metaphysis are
separated by the epiphyseal cartilage (the
growth plate or physis), which becomes
entirely ossified after the end of skeletal
growth.
Trauma
Trauma greater than a trivial insult but not capable of breaking of bone usually results in
elevation of the periosteum because of edema and hemorrhage. The PERIOSTEUM is the
membrane on the outside of the bone. It is programmed to proliferate and produce new
bone (exostoses) when irritated.
Fracture
Fracture, which is defined as a discontinuity of the bone, is the most common bone
lesion. There are many words to describe the types of fractures, see below.
(A fractured bone is the same as a broken bone.)
BONE HEALING
Healing of bone is different from healing of any other tissue in the body. It takes much
longer and has distinct phases. It is generally broken down into three phases:
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Inflammatory phase (0-7 days)
Reparative phase (1-12 weeks)
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BONE - Unit 2
Metabolic, nutritional, and endocrine bone diseases
Major causes of metabolic bone disease involve nutritional and/or hormonal processes.
Metabolic bone diseases are often called osteodystrophies. The term “osteodystrophy”
implies defective bone formation. The manifestations of nutritional osteodystrophy are
osteoporosis, rickets, osteomalacia and fibrous osteodystrophy.
Osteoporosis refers to the clinical disease of bone pain and fracture due to a reduction
of bone density/mass. It is a lesion, not a specific disease. It results from an imbalance
between formation and resorption in favor of resorption. The most common cause is not
enough nutrients to create new bone. Osteoporosis is a common lesion, especially in farm
animals, and it is usually nutritional in origin.
The bone remaining is normally mineralized but thinner than normal, so the bones are more
brittle and break easily.
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What if there is not enough Vitamin D?
Vitamin D, which comes from sunlight and food, is very important to help animals be
able to absorb calcium from the intestine. Vitamin D deficiency in a young animal will
cause rickets, the bones are too weak and tend to bow. Vitamin D deficiencies in adult
animals will cause osteomalacia.
Rickets and its adult equivalent, osteomalacia, occur when insufficient calcium is
available for mineralization of newly formed osteoid. Both rickets and osteomalacia are
due to failure to mineralize the newly formed matrix made by osteoblasts.
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BONE - Unit 3
Inflammation of Bone
Bones can only be infected in two ways – by a puncture from the outside, or by
circulating bacteria in the blood, which settle out in bone.
Osteophytes which develop following trauma are examples of local primary periostitis.
Small osteophytes may be resorbed completely, but large ones may be converted from
woven bone to lamellar bone and may persist indefinitely.
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Mandibular Osteomyelitis and Periostitis (Actinomycosis)
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Bones - Unit 4
Tumors of Bone
Osteosarcomas arise most commonly at metaphyses; however, they can occur in ribs,
vertebrae, bones of the head, and various other parts of the skeleton. Neoplastic tissue
tends to fill the medullary cavity locally and can extend proximally and distally.
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JOINTS - Unit 5
Normal structure/function and response to injury
Joints or articulations are structures in which two or more bones or cartilages are united.
The most common type of joint is a SYNOVIAL joint.
Normal synovial fluid is viscous, clear, colorless, or slightly yellow. It has two
functions: the lubrication of the joint, and nourishment of articular plates.
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The synovial membrane
commonly responds to injury by
villous hypertrophy and
hyperplasia. The membrane
produces excess fluid which is
watery, different from normal joint
fluid which is viscous.
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JOINTS – Unit 6
Arthritis
Inflammatory joint disorders in large animals are almost always due to infections. There
are two ways that bacteria can arrive at a joint – either through a puncture, or through the
bloodstream.
In farm animals, most infectious arthritis is polyarticular, hematogenous and affects very
young animals. After bacteria enter through an uncleaned umbilicus, they can circulate
and settle out in multiple joints.
HORSES
Infectious arthritis in foals is most usually due to Actinobacillus equuli, but other
organisms such as Streptococcus sp., Salmonella sp., and E. coli also will cause
polyarthritis.
SHEEP
In lambs, Erysipelothrix can be a problem. Chlamydia psittaci can also be harmful to
lamb joints. Other causes in sheep include Corynebacterium ovis, E. coli, and
Streptococcus sp.
CATTLE
In calves, polyarthritis is very common after a neonatal septicemia and primary causes
are E. coli and Streptococcus sp.
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CAPRINE ARTHRITIS-ENCEPHALITIS
Caprine arthritis encephalitis virus is a lentivirus
that causes arthritis and encephalitis in goats.
Very young animals usually get the encephalitis
form and older goats will have the arthritis form.
In addition to lameness, animals may get carpal
hygromas. Commonly affected joints are carpus,
stifle, and hock. Joints become very large, quite
painful, and inflammation persists for a very
long time.
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Bone spavin is an arthropathy of the tarsus of the
horse and occasionally the cow. Pain is caused by
exostoses on the medial portion of the tarsus.
Although the lesion is small, it is a serious and
stubborn cause of lameness. The major lesions
develop in the medial side of the tarsus, involving
the distal intertarsal joint and less frequently the
tarsometatarsal and proximal intertarsal joints.
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MUSCLE – Unit 7
Normal structure/function and response to injury
MUSCLE is a unique tissue that supplies the labor required to move us around.
Skeletal muscles are formed of parallel bundles of myofibers (or myocytes), which are
long cylindrical multinucleate cells filled with parallel bundles of myofilaments
embedded in a matrix of sarcoplasm (or cytoplasm).
During muscle contraction the actin filaments slide over the myosin filaments and they
hook together to create a shorter muscle.
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Reactions and Lesions Following Muscle Injury
Hypertrophy:
Muscle hypertrophy is an increase in the volume of fibers and may
occur as a consequence of abnormal activity or excessive use. It is
normal in body-builders.
Denervation Atrophy
The muscle must have nerve supply in order to stay alive and healthy. If the
nerves supplying the muscle are damaged, the muscle will become very small
(atrophy).
Necrosis/Degeneration
Regeneration: If the result is not very severe, the basement membrane remains intact
to provide a scaffold for repair. Muscle can regenerate easily, as long as the basement
membrane remains. Insults that disrupt the basement membrane, such as may occur
with a suppurative or granulomatous myositis, do not favor effective regeneration and
result in scarring.
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MUSCLE – UNIT 8
Degenerative myopathies
Nutritional Myopathy Vitamin E-Selenium Deficiency (White Muscle Disease)
General comments: White muscle disease is a selective, segmental degeneration of
muscle that leaves the sarcolemma, basement membranes and satellite cells intact so that
efficient regeneration can occur.
Signalment: The disease occurs primarily in fetal or neonatal calves and lambs,
but may occur in adults.
Mechanism: The pressure occludes veins, leading to congestion, edema, and even
greater pressure and, when severe, the pressure occludes the arterial supply. Large
muscle masses (hips, thighs, sternum) of large species (cattle and horses) are most
commonly affected.
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Exertional Myopathies - General comments: The exertional myopathies are a group of
diseases in which the acute lesions resemble those of acute nutritional myopathy but for
which a different pathogenic mechanism is confirmed or presumed.
Cause and mechanisms: The initiating factor for these diseases is intensive or
exhaustive activity of the major muscle masses. It is postulated that glycolysis
rapidly produces locally severe heat and lactic acidosis, which modifies and
coagulates contractile proteins. In addition, interstitial edema predisposes to
ischemia and further damage, particularly if moderate muscle movement
continues.
Diseases
1. "Tying Up" and Azoturia
Signalment: Draft horses, riding horses, and racing horses following
exertion. Lesions and outcome depend on the severity. Usually, brief rest
results in recovery with few consequences.
Gross lesions other than myoglobinuria are rarely identified
2. Capture Myopathy
Cause, signalment, and clinical signs: This is an acute myopathy often
associated with death following a chase, struggle, or transport of wild
animals and birds. Clinically there is acidosis, dyspnea, weakness, muscle
tremors or rigidity, hyperthermia, collapse and sometimes death.
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MUSCLE – UNIT 9
Inflammatory myopathies (myositis)
Bacterial diseases of skeletal muscle
• Suppurative myositis
Causes and signalment: Development of abscesses in skeletal muscles (as well
as lesions elsewhere) is caused by Actinomyces pyogenes infections in ruminants,
Streptococcus equi in horses, and other streptococci in a variety of other species.
Involvement of skeletal muscles may occur as a manifestation of septicemia or by
invasion of muscle following wound contamination.
Gross lesions may include abscesses, which may rupture to drain to the surface or
become encapsulated by fibrous connective tissue, or a diffuse interstitial
myositis.
• Blackleg
Cause, signalment, and clinical signs: Blackleg is an acute, noncontagious
infectious disease, principally of cattle, caused by the spore-forming bacillus
Clostridium chauvoei. Ingested spores, which are ubiquitous in the environment,
are absorbed from the intestinal tract and disseminated via the bloodstream to the
skeletal musculature and other tissues. In tissues the spores remain latent but can
begin to proliferate if a bruise or other process causes the local microenvironment
to become favorable for vegetative growth. The disease follows activation of
latent infections.
Gross lesions: Crepitant swellings may be present over the thighs, rump, back,
and shoulders, with major lesions in the underlying muscles. Small lesions may be
present in other muscles including the masseter, intercostal, and psoas muscles,
tongue, diaphragm, and/or heart. In affected areas, yellow gelatinous exudate,
blood and gas bubbles are present in the subcutaneous and intermuscular
connective tissues. Affected muscles are swollen, dark red to black and typically
are porous, spongy, and dry (hemorrhagic necrosis). A characteristic odor is
described as similar to rancid butter. Additional gross lesions include fibrinous
epicarditis, pericarditis, and pleuritis with serosanguinous effusions.
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• Actinobacillosis
Cause and signalment: Actinobacillus lignieresii is the cause of "wooden
tongue" in cattle.
Gross lesions: The organism produces small pyogranulomas in the tongue and
soft tissues of the head and neck of cattle and other species. Lesions may occur in
other soft tissues such as gut, udder, lung, skin and lymph nodes., There is
extensive proliferation of connective tissue in the tongue which causes the tongue
to be enlarged, hard and partially immobilized.
Septic tenosynovitis
Septic tenosynovitis results from contamination of the synovial tendon sheath from
penetrating wounds or as an extension from septic arthritis. Purulent and fibrinous
exudate accumulates within the synovium. This is a serious condition and even if
infection can be controlled, adhesions and weakening of the tendon are possible
outcomes.
Cysts are seen most commonly as incidental changes in bovine cardiac and skeletal
muscle, but degenerate cysts may occasionally induce a local minimal granulomatous
reaction.
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