Musculoskeletal Pathology

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

PART III MUSCLE

Unit 7 Normal structure/function and response to injury…………. page 15
Unit 8 Degenerative myopathies………………………………….. page 17
Unit 9 Inflammatory myopathies (myositis)………………………. page 19

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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.

We all know that bone is HARD. What makes it that way?

The osteoblasts make a kind of matrix, mostly collagen, but some other things too.
Minerals get embedded into the matrix, primarily calcium and phosphorous, and before
you know it, that matrix has become HARD.

 Cortical bone tends to be very SOLID

and is what makes up the TUBE part of
the bone.

 Cancellous bone is a three-

dimensional lattice arrangement that
makes up the INSIDE part of bone.

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.)

Various terms to describe fractures:

 Simple – clean break separating bone into two parts
 Communited – bone breaks into multiple parts
 Compound – break in overlying skin as well as in bone
 Transverse – broken straight across
 Spiral – pattern of break is spiral
 Greenstick – periosteum remains intact and holds the ends of bone in place
 Pathologic – fracture that occurs not because of unusual trauma, but because bone
was previously weakened by some other disease

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:

The inflammatory phase - 0-7 days

Rupture of blood vessels in the periosteum causes hemorrhage. Then other cells move in
to start the healing. Some of these cells will mature into osteoblasts. Take a look below –

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    
Inflammatory phase (0-7 days)

The reparative phase - 1-12 weeks

This extends for months and involves both fibroblasts and osteoblasts. A callus made of
woven bone bridges the fracture site and stabilizes the area. Excessive movement and
tension favor the development of fibrous tissue, which does not stabilize the fracture very
well. The woven bone gets replaced by lamellar bone eventually. See below:

   
Reparative phase (1-12 weeks)

The remodeling phase - 12 weeks – 6 months or so

Several weeks after the fracture, the ingrowth of callus has sealed the bone ends.
Remodeling then begins. But the bone is weak for months until normal strength is re-
established.

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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.

Avoiding nutritional osteodystrophy requires adequate amounts and ratios of calcium,

phosphorous and Vitamin D. When the body senses low calcium in the blood, there is
increased production of parathyroid hormone (PTH), which signals to intestine and b to
bring more caldium into the blood.

So…… what can go wrong?

What if there is not enough calcium in the diet?

Oh dear, not enough calcium in the food, so the animal has to get calcium from its own
bones! The result is a reduction in bone density. This is called OSTEOPOROSIS. In
reality, osteoporosis is rarely due to a simple dietary deficiency of calcium, but is almost
always a result of deficient calcium combined with overall insufficient nutrition.

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.

Fibrous Osteodystrophy (a.k.a. osteodystrophia fibrosa, osteitis fibrosis cystica)s

term describes the skeletal lesions that are the result of increased widespread osteoclastic
resorption of bone and its replacement by fibrous tissue. The direct cause is always too
much parathyroid hormone.

Fibrous osteodystrophy happens because of too much phosphorous (either due to

kidney problems which decrease excretion of phosphorous, or a diet that has too much
phosphorous). In either case, the parathyroid hormone gets elevated and calcium is pulled
out of bones and the hard matrix is replaced by fibrous tissue. As a result, the bones
BEND.

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 BONE - Unit 3
Inflammation of Bone

Inflammation of bone is designated osteitis, but almost always there is inflammation of

the bone in the marrow as well, so it is called osteomyelitis.

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.

Osteomyelitis is difficult to diagnose and also difficult to treat.

There are several possible sequelae to infection of bone –

 It can spread to the joint and cause arthritis.
 It can stay in the bone for a long time and just slowly destroy the bone.

Vertebral osteomyelitis is perhaps recognized more often than hematogenous

osteomyelitis of other parts of the skeleton because of its effect on the nervous system.
Vertebral osteomyelitis often leads to pathologic fracture and collapse of the vertebrae,
followed by dorsal displacement of one or both fragments and compression of the spinal
cord. Which leads to paralysis.

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)

This disease of cattle is caused by Actinomyces bovis. A. bovis is a soil-borne, gram-

positive filamentous bacterium. Trauma to the oral mucosa and eruption of teeth allow
the organism to enter the osseous tissues of the mandible, where chronic
pyogranulomatous inflammation develops.

The classic lesion in cattle is “lumpy

jaw”, a mandibular osteomyelitis. The
osteomyelitis follows direct extension
of the infection from the gums and
periosteum. Basically the lesion
consists of granulation and suppurative
tracts. Periosteal proliferation is
excessive, and the bone may become
enormously enlarged.

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 Bones - Unit 4
Tumors of Bone

 Most tumors of bone are malignant. 

 Osteosarcomas
Osteosarcomas are the most common skeletal neoplasms in dogs and cats, composing
about 80% and 50% of skeletal tumors, respectively. Most osteosarcomas
metastasize to the lungs, often before the primary tumor is diagnosed. Affected
animals are usually mature males of the large and especially giant breeds.

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.

The synovial joint is composed of

articular cartilage, synovial
membrane, synovial fluid, and joint
(fibrous) capsule.

The articular cartilage protects the

bone and is very smooth, allowing
for easy joint motion.

Synovial membranes, whether

lining articular cavities, bursas, or
tendon sheaths, are all biologically
similar. They make and absorb the
fluid within the cavity.

Normal synovial fluid is viscous, clear, colorless, or slightly yellow. It has two
functions: the lubrication of the joint, and nourishment of articular plates.

REACTION OF JOINT TO INJURY

Below are depicted the series of events in serious articular injury. The chrondrocytes die,
the cartilage cracks, and fibrocartilage comes in to do the repair. Sometimes the
subchondral bone is exposed. Joint injuries are usually quite painful.

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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.

Infectious arthritis usually starts as serous, fibrinous, or purulent. In serous arthritis,

there is increased production of synovial fluid, resulting in a “puffy” swelling. With
continued presence of intraarticular organisms, fibrin also exudes and if pyogenic
organisms are the culprit, there will be pus has well. In all, the joints are painful so the
animal is lame. If not treated, there can be permanent damage to the cartilage and the
animal will never walk normally again.

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.

In horses, noninfectious arthritis often happens due to

DEGENERATIVE problems - Ringbone, Spavin, and Navicular Disease
Ringbone is a bony outgrowth (exostosis) arising on the second or first phalanx. It
causes serious and painful periarthritis. This disorder typically is bilateral and affects
mainly the forelimbs:

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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.

Navicular disease is a biomechanically

induced, degenerative disease involving the
distal half of the flexor surface of the
navicular bones (sesamoid) of the forelegs of
mature horses.

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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.

Parallel bundles of myofibers

(fascicles) within a muscle belly
are surrounded by perimysium,
which appears as a thin
collagenous septum in histologic
sections. As a whole, muscle
bellies are enveloped by
connective tissue, the
epimysium.

The functional-anatomic relationships among neuron, axon, and myofibers is known as a

motor unit. The axon of a single motor anterior horn cell by repeated branching
terminates on a group of 10 to 1000 muscle fibers.

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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.

Muscle Atrophy: A reduction in myofiber diameter due to loss of organelles including

myofilaments.

 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).

• Common examples of denervation atrophy in veterinary medicine include the

following:
1. Laryngeal hemiplegia in the horse due to injury to the left recurrent
laryngeal nerve. This disease results in atrophy of the cricoarytenoideus
dorsalis muscle and the clinical syndrome of “roarers”.
2. Sweeny in work horses is characterized by atrophy of the supraspinatus
and infraspinatus muscles due to damage to the suprascapular nerve.
Pressure from work collars is responsible.

 Atrophy of disuse or starvation

If the muscle does not get used enough or if the animal is starving and can’t
supply nutrients to the muscle, it will become very small (atrophy).

Necrosis/Degeneration

 Causes of degeneration and necrosis of muscle include: ischemia, trauma, nutritional

deficiencies (white muscle disease), metabolic abnormalities (exertional myopathy),
some toxins, and some infections.

 Gross changes: Acutely degenerate or necrotic muscle usually has distinct or

poorly-demarcated areas of pale yellowish to gray-white discoloration. If vascular
integrity is compromised, the affected area may be red. Necrotic muscle is readily
mineralized, in which case the gross lesions are white, somewhat shiny, possibly
swollen, and possibly gritty.

 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 of injury: The muscle damage in white muscle disease is an example

of free radical (oxidative) cell injury, associated with deficiency of free radical
scavenger molecules such as vitamin E (alpha-tocopherol) and/or
selenium-containing enzymes of the glutathione system. In the absence of
sufficient protection, myocyte membranes and proteins are damaged by free
radicals and there is massive intracellular accumulation of calcium.

Clinical signs may involve stiffness, dyspnea, and acute death.

Gross lesions are usually marked by mineralization of skeletal and/or cardiac

muscle. Affected muscles usually have pale, sometimes white, streaks and may be
gritty when cut.

Ischemic Myopathy (Downer Syndrome)

Cause: Ischemic myopathy is initiated by external pressure on the muscle by

objects or by the weight of the body.

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.

Gross lesions: Skeletal muscular edema, pale streaks in muscle, and

possibly mineralization and myoglobinuria may be observed. The heart is
sometimes affected.

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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.

• Malignant Edema, Gas Gangrene

 General comments: Malignant edema and gas gangrene are clostridial wound
infection characterized by local spreading, edematous, and crepitant subcutaneous
swellings. The two terms are often used interchangeably.
 Cause, signalment, and clinical signs: Malignant edema is a complication of
clostridial infection of wounds and infected animals develop fever and die
rapidly. The disease is seen principally in cattle and sheep, but is also described in
horses.
 Gross lesions: Hyperemia, swelling due to severe serosanguinous exudate that
follows subcutaneous and intermuscular tissue planes, and crepitus (gas bubbles),
are present in lesions. ME is more often a cellulitis than a myositis, but
muscles can be affected in sites of severe cellulitis.

• 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.

Parasitic diseases of muscle

• Sarcocystosis: Sarcocystis sp. are protozoal parasites that infect muscle of animals
that are usually serving as an intermediate host.

Sporozoites from sporocysts invade

vascular endothelium. Schizogony takes
place, schizonts are released and develop in
striated muscle as thin-walled cysts initially
containing metrocytes and then
banana-shaped bradyzoites. The cysts
persist in muscle for prolonged periods of
time. Muscle degeneration is usually
minimal.

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.

• Neosporosis: Neospora caninum was previously confused with toxoplasmosis.

Neosporosis can cause a very severe diffuse myositis in dogs and abortions in cattle.
When the protozoal meronts leave the myofiber they cause muscle necrosis and
severe inflammatory response.

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