MSK Notes

Warren
Legg-Calve-Perthes Disease: presents in 4-8y/o children
Caused by avascular necrosis of femoral head
Presents with limp or hip pain, decreased hip mobility (if there is fluid in
the joint), check all joints

Slipped Capital Femoral Epiphysis
Caused by stress fracture of upper femoral growth plate slip of femoral
head over femoral neck limb shortens and externally rotates
Presents during adolescent, limp and hip or groin pain, 30% cases pain at
knee or thigh (bc of referred pain), and hip is flexed and externally rotated

Summary
Developmental Dysplasia Hip
Infant, Female, breech, Ultrasound, Pavlik Harness
Legg-Calve-Perthes
School age male, Hip pain - restriction motion
Slipped Capital Femoral Epiphysis
Obese male, Hip pain - externally rotated

A 13 year old adolescent male presents to the clinic for one week of limping and
knee pain. On the growth curve, it is noted he is in the 95% for his weight. His exam
is remarkable for acanthosis and normal knee exam. His hip examination
demonstrates diminished ability to flex and internally rotate his right femur.
Which of the following is the best next step in management?

a. Instruct the patient to rest and apply ice
b. Prescribe daily nonsteroidal anti-inflammatory drugs until the pain resolves
c. Order MRI of the hip and knee
d. Arrange for an orthopedic consultation

You are evaluating a 3 month old female in the clinic. The parents comment that her
legs appear uneven since birth. Otherwise she has no other symptoms. On physical
exam, the infant is happy and nontoxic appearing. She is asymptomatic except for a
+ Barlow and + Galeazzi sign. Her most likely diagnosis is:
a. developmental dysplasia of the hip
b. tibial bowing
c. septic arthritis
d. Legg-calve-perthes disease

Rega
Bone Growth and Remodeling

Biomechanical terms
Stiff = resists deformation
Strong = resists failure under high load
Brittle = undergoes sudden failure with little deformation
Stress = load/area
Strain = deformation/original length
How stiff is a material?
= stress/strain
= load/deformation

Onset of material failure = YIELD POINT
strain @ yield for bone = 1%
if you increase the strain over 1%, the bone will start failing
compressive yield 170 MPa 1800 kgf/cm or OR 24,700 lbs/in
2

tensile yield 104121 MPa
shear stress yield 51.6 MPa
Plastic deformation = deformation beyond the yield point
Ultimate failure (fracture) point = structural failure
strain @ fracture for bone = 2%, brittle failure occurs at 2%
compressive failure = 220MPa OR 32000 lbs/in
2

Tensile failure 150-200 MPa
Activation depends on osteoblasts
Activated osteoblast bone lining cells produce collagenase
Which digests osteoid on bone surface, exposing mineralized matrix.
Exposed bone matrix is chemotactic for osteoclasts,
Which are activated and migrate to exposed site
Osteoblasts do produce the enzyme that exposes the bone mineral
that are chemotactic for osteoclasts (activating these cells)

Resorption depends on osteoclasts
Osteoclasts . . .
1) form a sequestrum of dead bone
2) secrete lysosomal enzymes, including acid phosphatase and
proteolytic enzymes.
3) Bone mineral dissolved
4) organic matrix phagocytized.

Bisphosphonates and other osteoclast inhibitors can have adverse side effects
(Fosamax, alendronate, zolecronic acid, etc)
Hypocalcemia (parathyroid hormone compensatory)
Osteonecrosis of Jaw

Often the first sign of osteoporosis is fracture presenting as pain after a fall

Dual-energy X-ray absorptiometry
(DXA, previously DEXA ) is a means of measuring bone mineral density (BMD)

Osteoporosis is low overall bone mass and structural deficiency trabecular bone is
affected first so will have a lot of structural deficiency
Affects mineral and osteoid
Rickets Vitamin D3 deficiency and/or calcium deficiency
Mineral deficiency: Osseous symptoms related to mechanical deformation,
structural weakness and impaired growth
Bowing of legs in rickets deformation due to mechanical alteration of bones
during weight bearing; collagen normal, bone mineral deficient, relatively enlarged
and ragged metaphyses
Adult form = osteomalacia

1 year old African American male presents with short stature for age and bilaterally
bowed tibiae. His mother reports that he is exclusively breast fed. They are
northern city dwellers with little outdoor exposure. Radiographic findings include:
enlarged rib ends
widened physes
widened frayed and cupped metaphyses
Mild femoral & tibial bowing
Osteopenia
Deformation of the long bones is due to deficiency of which of the following
elements?
a) Osteoid
b) Type I collagen
c) Type II collagen
d) Hydroxyapatite [Ca10xHx(PO4)6OH2 ]
e) Overall bone mass

Vitamin D3 is critical to bone mineralization and mediated by sun little outdoor
exposure
Breast milk is not high in Vitamin D

Femoral buttressing: osteoarthritis in the hip with accompanying osteopenia
(bone density that is lower than normal)
Will see cortical bone this is very heavily mineralized and thick. Cortex has
been buttressed

Compression fractures through epiphyses

A 29 year old male presents in the ER with closed transverse fractures of the
distal left tibia & fibula with lateral displacement after being struck by a car.
The orthopedic surgeon elects to perform an open surgical reduction with
fixation of the tibia, leaving the fibula alone. How should the subsequent
osseous healing of the tibia differ from the closed reduction fracture healing
process in the fibula?
A. The soft callus will surround the tibial fixation hardware, resulting in a
larger hard callus on the tibia than on the fibula.
B. The tibial soft callus will be less likely to break and cause subsequent hard
callus discontinuity and pseudarthosis than the soft callus of the fibula.
C. The tibia will heal by means of direct remodeling with little callus, while
the fibula will manifest soft and hard callus formation prior to remodeling.
D. The tibial hard callus will be will remodel at a slower rate and remain
more sclerotic than that of the fibula, due to presence of the hardware.
E. The healing in both will be identical.





THE FUNCTIONAL PROPERTIES OF CARTILAGE, INCLUDING STIFFNESS,
DURABILITY, AND DISTRIBUTION OF LOAD, RELY ON THE EXTRACELLULAR
MATRIX.

Cartilage microstructure:
- chondrocytes secrete extracellular matrix (ground substance)
- Long molecules of proteoglycan

Fibrocartilage exists in the glenoid labrum
Elastic cartilage: matrix is pervaded by yellow elastic fibers elastin

Synovial fluid = plasma filtrate (electrolytes + small molecules; fewer proteins).

AC (articular cartilage) initially stiff under loading. With increased duration
of loading, viscous flow increases deformation and relieves stress on the
water.

A 35 year old male presents with arm inability to supinate his right forearm
after failing to lift a truck out of a snow-filled ditch. MRI taken three days
post-injury reveals a complete tear of the distal biceps brachii tendon, with 6
cm gap between the torn ends. What is the primary reason for the extensive
gap?
A. Inflammation of the biceps brachii muscle caused gradual retraction of the
tendon.
B. The ground substance of the biceps tendon has been dissolved by
macrophages in the interval between injury and MRI.
C. The triceps brachii contracted spasmodically, extending the arm and
subluxing the torn biceps tendon ends.
D. Elastic energy stored in the stretched tendon caused it to recoil at the time of
injury.
There is a gap to the elastic recoil
E. Avulsion of bone at the distal tendon insertion initiated osteoclastic
resorption of the tendon ground substance.


Brownell
Muscle fiber = 1 muscle cell
Develop by fusion of myoblasts into multinucleate myotubes, differentiation into
muscle fibers
Fixed number of muscle fibers at birth (100-1000/mf; up to 12 long =~100,000
sacromeres end-to-end)
Hypertrophy of fibers increases muscle size and strength



Terminology:
Muscle fiber = muscle cell (multinucleate)
Sarcolemma = plasma membrane
Sarcoplasmic reticulum = endoplasmic reticulum
Sarcoplasm = cytoplasm

Review
A band is the active band where actin and myosin are overlapping
I band is the inactive band where they are not overlapping each other, clear section
H zone: middle where there has no actin, just myosin
M line: midline


Myosin head motor
Minimum step size = ~10-20 nm
In actuality = ~75nm +/-20nm

CapZ: forms Z disc, binds (+) end of actin
Titin: large elastic protein, connects thick filament to Z disc
Nebulin: large non-elastic protein, binds laterally to thin filament
Thick filament: bundle of ~250 molecules of myosin II
Thin filament: actin polymer
Sarcolemma proteins:
voltage-gated Na
+
channels: propagate action potentials
dihydropyridine (DHP) receptor: voltage gated Ca channel (t-tube)
Na
+
/K
+
antiporter ATPase: maintains ionic gradients
Sarcoplasmic reticulum proteins:
ryanodine receptors: Ca
2+
channels gated by DHP receptors
sarcoplasmic Ca
2+
uniporter ATPase: removes sarcoplasmic Ca
2


Ficks Law of diffusion
Td = (Xd)
2
/ 2D
=time; X=distance; D= diffusion constant for solutes in aqueous solutions (~10
-6

cm
2
/sec)
A useful rule of thumb for small ions/molecules ( glucose) in water:
Xd Td
1 nm 1 nsec
diffusion distance is a rate-limiting factor for most physiological processes

How does muscle move so fast?
T-tubule depolarization triggers Ca
++
release from sarcoplasmic reticulum (coupled
by DHP and RyR)
The need for speed! Note that diffusional distance for Ca++ is minimalized (~1-2
uM) or about 1-5 msec diffusion time
When Ca2+ comes through the DHP receptor, it activates the ryanodine receptor
and then ryanodine receptor releases the Ca2+ which is held by the calsequestrin
protein

Muscle energetics: ATP for muscle contraction is generated from 3 sources
1. Creatine shunt (fast generation)
Store energy as a phosphorylated creatine and can use it to quickly generate ATP
when the muscle contracts, most energy will come from the creatine phosphate
2. Aerobic, oxygen, mitochondria (slow generation)
3. And when that is gone use anaerobic glycolysis and cause generation of lactic acid

Will be tested: obvious question
Muscle fiber types compared

Fast twitch muscle:
Fast, glycolytic, anaerobic ATP synthesis
Susceptible to fatigue (fuel rapidly depleted)
e.g., escape reflex muscles, jumping muscles
"white meat"
Also fast oxidative muscle
Fast twitching, utilizes oxidative phosphorylation (O2 dependent ATP
generation), fatigue resistant
Slow twitch muscle:
Slow, b-oxidative (FA metab), aerobic ATP synthesis
Resistant to fatigue (see below)
e.g., postural muscle (legs, back)
Vascularized ("dark meat = myoglobin abundant)

Skeletal muscle innervation
Consists of many different, independent motor units (e.g., ~ 300 MU for
gastrocnemius)
Motor Unit: one motor neuron and all muscle fibers it innervates (~50 to 500
fibers)

One question on bone histology
Substructure: Epiphysis/epiphysial plate/ diaphysis/periosteum
Compact vs. spongy (=trabecular or cancellous) bone

Osteons: Haversian canal systems with lacunae contain osteocytes

Compact bone has haversian systems called osteons, has one capillary, nerve that
goes up in the center of the haversian system

RANKL: Osteoblasts secrete RANKL which induces osteoclasts to break down bone
until osteoblasts secrete OPG that will inhibit RANKL from stimulating osteoclasts
to break down bone
He will make a doc on what we have to know

Calcitonin and PTH have opposite actions
Calcitonin (from thyroid gland) mobilizes ca2+ into bone, PTH (from parathyroid
gland) mobilizes Ca2+ into the blood
Ca2+ concentrations are kept at 2.5mM

Follicle Stimulating Hormone (FSH) and Estrogens effect on bone
Estrogen works on both pre-osteoblasts and RANK-L signaling system to block pre-
osteoclast formation
In the absence of estrogen, that block is no longer on, the pre-osteoclast
formation is not blocked and it differentiates into osteoclast
Reduction in estrogen in postmenstrual women stimulates breakdown of bone,
stimulates osteoclasts
Lack of estrogen stimulates the breakdown of bone

Labs for bone disease know


Synthesis of collagen
Starts off as an single alpha helix self assemble into a 3 part secreted from cell
and reassemble to form a collagen fibril

Collagens
Major ECM protein
Triple helix structure with modified amino acids
Defects in collagen or tenascin X: Ehlers-Danlos syndrome
Lack of proline/lysine hydroxylation: scurvy
Elastins and fibrillin
Major constituents of arteries. Tissue elasticity; Marfan syndrome
Fibronectin
Important adapter molecule linking different ECM proteins and cells
(via integrins)

Basal lamina is an omnipresent net like acellular structure associated with all
epithelia. Structural integrity. Permeability to ions and small molecules
special type of collagen called type 4 collagen that forms sheets
Forms sheets, forms nets, permeability to all small molecules
Perlecan and laminin are attached to the basal lamina, these are all capable of being
defective and affect the basal lamina

Lin

A 15y/o girl visited the clinic because of a recent fracture of the left femur. Pertinent
findings during a physical examination included precocious puberty and serpiginous
pigmentation.

Young individual with a fractured femur, pigments Fibrous dysplasia
Fibrou dysplasia typically occurs in children and most often involves the long bones.
X-ray shows expanding radiolucent lesion with sclerotic areas. Microscopically,
there is replacement of bone by fibrous tissue containing interspersed areas new
bone formation.

A 23 y/o male notes some minor discomfort over the lateral aspect of his right knee
after a day working in a cramped cubicle (because IT put the desktop workstation
on the floor). On physical examination, he has a palpable bump in this region. A
radiograph on the knee reveals a lateral bony projection from the lower femoral
metaphysis. There is no adjacent soft tissue swelling. The lesion is excised and is
composed of a 3-cm stalk of bony cortex capped by cartilage. Which of the following
is the most likely diagnosis? Osteochondroma

Osteochondromas are not true neoplasms but an exaggeration of the growth plate.
They are benign and slow-growing. They may cause discomfort because the project
outward from the bone.


A 30y/o man has pain about his left knee that he says has been worsening for
weeks. On physical examination, the left knee appears larger than the right, and
there is tenderness to palpation. A radiograph revels a 7-cm lytic lesion involving
the epiphyseal region of the distal femur with a soap bubble appearance. The
lesion is curetted, and histologically there are numerous multinucleated cells in a
stroma with plump to spindle shaped mononuclear cells. Which of the following is
the most likely diagnosis? Giant cell tumor

A giant cell tumor of bone typically arises in the epiphysis.

A 16y/o boy noted pain in his left knee after each hockey practice session for the
last past month. One examination, there is tenderness to palpation of his left knee,
with reduced range of motion. A plain film radiograph of the left leg reveals a mass
of the proximal tibial metaphysis that erodes the bone cortex, lifting up the
periosteum where reactive new bone is apparent. The mass does not extend into
the epiphyseal region. A biopsy is performed and microscopic examination shows
atypical, elongated cells with hyperchromatic nuclei in an osteoid stroma. Which of
the following neoplasms is the most likely diagnosis? Osteosarcoma

Osteoid production is characteristic for osteosarcoma. The location about the knee
is common. Most arise in the metaphyseal region. Overall, malignancies are
uncommon in children, but bone tumors are one of the most common malignancies
at this age.


Yasmer
Salter Harris Fracture: 10 year old male with hand trauma. A fracture through the
physis extends to the metaphysis, making this a Salter Harris type 2 fracture.



Type 1: there is a gap, cracked all the way through
Type 5: crush injury

Osteoarthritis: would not be erosions, probably would see it in bigger weight
bearing joints

Rheumatoid arthritis: would be erosions

Always start off with plain x-rays

Osteoarthritis
Large weight bearing joints
Joint space narrowing
Osteophyte formation
Subchondral sclerosis
Erosions are not a typical feature
Ankylosis is rare

Rheumatoid arthritis
Affects smaller non-weight bearing joints
Joint space narrowing
Erosions
Periarticular osteopenia
Findings are bilaterally symmetric
Osteophyte formation is not characteristic
Ankylosis is rare
Ewing Sarcoma
Most common primary bone neoplasm in first decade of life
Permeative lytic lesion
Cortical destruction
Aggressive periosteal reaction
Associated soft tissue mass
Diaphyseal or metadiaphyseal location
Centrally located
Brodies abscess
Subacute-chronic osteomyelitis
Usually found in the metaphysis (occasionally in epiphysis)
Geographic, lytic lesion with well defined margin
Non-aggressive in appearance
May or may not have fever and elevated ESR
Ankylosing Spondylitis
Males more often than females (4:1 to 10:1)
Mixed erosive and productive changes
Predominantly affects the axial skeleton and large proximal joints
Bilateral sacroiliac joint erosions that progress to ankylosis
Syndesmophytes (not osteophytes) that progress to bamboo spine
Fractures at C-T and T-L junction with pseudoarthrosis

Pumerantz


Monoticular arthritis or bone infection?
If it is a bone infection, has nothing to do with the vertebral column
What does a bone infection look like in a long bone?
Differentiate between the different syndromes
What causes what syndrome

Moellmer

Intoeing
Tibial Torsion (bicondylar axis of knee vs. tanslmalleolar axis)
Tibial Torsion Birth 0 but tibia increases lateral rotation to ~18 in adult
Tibial torsion is the number one cause of intoeing
Metatarsus adductus is most common congenital deformity that causes intoeing

Diagnostic testing: weight bearing xray

Ottawa ankle rules
Order ankle radiographs if:
Pain in malleolar region
Bone tenderness at tip or posterior edge of either malleolus
Unable to bear weight 4 steps



Parsa

Muscle Pathology

Normally, muscles are arranged in a checkerboard pattern with Type 1 and 2 fibers
dispersed evenly
When there is a neurogenic pathology, there is a loss of innervation to the
muscle fibers and there will be outbranching from other motor neurons causing
grouping of muscle types to occur, losing the checkerboard pattern

When there is a myopathic pathology, there does not need to be reinnervation
of muscle, so the muscle types will not change


Muscular Dystrophy
Pseudohypertrophy is due to deposition of fat
Muscle fibers will show abnormalities: central nuclei enlargment, fibrosis due to
replacement of fat
Dystrophin immunohistochemistry completely absent DMD
BMD: diminished dystrophin

Dermatomyositis: (autoimmune) Membrane attack complex visible in
immunofluorescence studies
Perimysium inflamed and peripheral fibers atrophied due to perivascular
perfusion
o Perimysium: is a sheath of connective tissue that groups muscle fibers into
bundles

Polymyositis: (autoimmune) CD8+ lymphocytes and other lymphoid cells
surround and invade healthy muscle fibers expressing HLA classes I and II


Inclusion myositis (degenerative): vacuoles of beta-amyloid and tau protein
inclusions

Ryanodine receptor mutations
In the common, well-described congenital myopathies, mutations have been
identified in genes that encode for muscle proteins. The loss or dysfunction of these
proteins presumably leads to the specific morphological feature on muscle biopsy
samples and to the clinical muscle disease.
Nemaline (rod) myopathy: Nemaline myopathy can be caused by mutations
in at least 7 different genes (e.g., -tropomyosin, nebulin, -actin, troponin,
etc. derived from Z-band material ). May be autosomal dominant or recessive
Central-core disease; autosomal dominant: due to a mutation in the
ryanodine receptor (RYR1) associated with malignant hyperthermia risk.
Myotubular (centronuclear) myopathy: varied hereditary patterns due to
different mutations including myotubularin, dynamin-2, etc.


Mitochondrial diseases
Anytime you have a young patient presenting with stroke or muscle weakness, think
mitochondrial disease, biopsy can be confirmatory

Becker muscular dystrophy: CTG repeats, frontal balding, weakness, genetics
would be very helpful

Lambert-Eaton syndrome: paraneoplastic syndrome, presynaptic antibodies
against calcium channels disrupting release of ACh, small cell lung carcinoma

Malignancies of the muscle fibers rhabdomyosarcoma
Embryonal rhabdomyosarcoma is more common in the head and neck regions of
children. One variant, sarcoma botryoides, usually presents as a soft, multilobular,
polypoid mass develops in the walls of hollow, mucosal-lined structures

Alveolar rhabdomyosarcoma develops in early to middle adolescence, commonly
arises in the deep musculature of the extremities.

Pleomorphic rhabdomyosarcoma tends to occur in individuals over the age of 45


Katsaros

Osteoarthritis
A 78 year-old female with pain at her thumb base, hips, and knees for the past 10
years presents to clinic for relief of her pain. The pain is worse with standing for
prolonged period of time and worse with walking. She has a strongly positive
rheumatoid factor and her knees have swelling but no warmth.
What is the more likely diagnosis?
A. OA
B. RA

OA is joint failure, not an autoimmune disease (unlike RA)
It is defined by hyaline cartilage loss and sclerosis of the bony end plate.
Osteophyte formation of the joint and joint capsule stretching
Mild synovial swelling can be seen (unlike the robust swelling seen in RA)
Weakness of the muscles

Charcot joint: When you lose nerves to that joint, do not have sense and more likely
to hurt that joint
seen in diabetes, syphillis


Finley

Arthralgia vs Arthritis
Arthralgia: Joint pain (there may not be any inflammation)
Arthritis: Inflammation of the Joint
- Pain
- Redness
- Swelling
- Increased warmth
- Fluid accumulation (synovial effusion)
- Stiffness (especially in the AM)
loss of function

Rheumatoid Arthritis
Anti cyclic citrullinated peptide (Anti CCP)

Criteria for RA
4 parts of criteria
How many joints are involved
Serology: RF and CCP
Symptom duration: greater or less than 6 weeks
Acute phase reactants: normal or abnormal CRP/ESR

Score greater than 6 is definite RA



Faerber

Steinmann

Lumbar Spinal Stenosis: lumbar spine has narrowed, nerve roots have become
ischemic esp when standing, when these patients stand it squishes the nerves and
prevents circulation, relieved by bending forward or sitting down
Neurogenic claudication: pain comes from movement, bending forward
Vascular claudication: pain while standing
Whats the typical neuro exam findings? Normal
There is no ischemia to the nerves, theyre normal

Weakness with elbow flexion, xrays are negative, what is the next most appropriate
imaging studies?
CT, MRI
CT will tell bone injuries and MRI will be for neuro and soft tissue images
Neurological deficit MRI scan

Pain hurt while walking and pain better while sitting lumbar spinal stenosis

19 y/o line man lower back pain, pain on and off past year, hamstring tightness,
increased pain while standing spondolisthesis

on exam, peroneal sensation, foot drop, sensory loss caudate equina syndrome
loses bladder control emergency discectomy

criteria for diagnosing scoliosis (minimum degree)
Kisby
Train-of-Four (TOF) Stimuli (4 pulses - 0.5 sec apart):
- Number of responses (e.g., twitches) indicate
degree of NM blockade:
4 twitches - 0-75% ACh receptors blocked
3 twitches - at least 75% blocked
2 twitches - 80% blocked
1 twitch - 90% blocked
0 twitches - 100% blocked

In green: target for surgical procedures

Succinyl CoA
dibucaine number test ability of patients to metabolize succinylcholine
Patients with atypical cholinesterase -- RESISTANT to DIBUCAINE BINDING
(20-50% vs 80% normal)

Non-depolarizing blockers are competitive antagonists
Depolarizing blockers bind to same site of Ach and are agonists desensitizes
Phase 1
Mechanism of Action:
Prolonged cholinergic depolarization FLACCID PARALYSIS -- Divided into two
phases - - Phase I and Phase II Block
Phase I block: Depolarization Block --fasciculations, with continued
depolarization -- flaccid
paralysis
-- Potentiated by AChE
Inhibitors -- Ach
Phase 2
Phase II block: Desensitization Block
With continued exposure to
succinylcholine, repolarization occurs
and membrane is NOT easily depolarized again; resistant to ACh

Closely resembles a non-depolarizing block (= CURARE)
Adverse effect
HYPERKALEMIA can be life-threatening (cardiac arrest); Cause: K
+
-LOSS
from MUSCLE; CAUTION: patients with various diseases or conditions in
which
co-morbidity due to Ach receptors

Malignant Hyperthermia life-threatening
CAUSE: genetic defect of SR causes sudden & prolonged Ca
2+
release with
massive muscle contraction & temp
HIGHEST INCIDENCE
Succinylcholine + Halothane.
TREATMENT: Cooling, OXYGEN,
DANTROLENE IV

Spasmolytic Drug
Baclofen
3MOAs
Agonist at GABA B receptors on spinal motor neurons (MNs)
Postsynaptic inhibition --- Hyperpolarization
by K
+
conductance ( GABA inhibition)
Presynaptic inhibition -- Ca
++
influx -- release of excitatory NT (e.g.,
glutamate)
Reduces Pain by release of substance P (neurokinin-1) in the spinal cord
MNs.

Cyclobenzaprine
has strong anti-muscarinic effects
Sedation, dry mouth, blurred vision, urinary retention, tachycardia.
Confusion, visual hallucination
-- CAUTION: Glaucoma, Urinary Retention

Fraix
Spondylolysis:
Fracture of the pars interarticularis scottie dog
Hyperextension of the spine

Spondylosis: arthritis of the spine

Spondylothesis: vertebral slipping

DMD: proximal muscle weakness, gowers movement bc of proximal girdle muscle
weakness