What is TR (time repition) in MRI pulse sequence?
Time between each RF pulse, varies from 500msec to 4000msec
What is TE (time echo)?
Time each RF to listening for signal generated by patient varies from < 40msec to 100msec>
What determine the type of image created?
TR and TE times
T1 in MRI (Time 1) main characteristics
- Weighted image with short TR (500msec) and short TE (40msec)
- Water is dark (CSF, edema, synovial fluid - NOT water in fat)
What does the pathology look like on a T1 film?
Usually dark on T1 due to edema (most pathologies have edema with water)
T2 MRI main characteristics:`
Weighted image - long TR (1500-4000msec)
- Long TE (80-100msec)
- Water is BRIGHT
T2 allows what?
System to go back to neutral state
- Listened long enough for echo signal, so now we see water that looks brighter, and can now see edema
what color is bone marrow on T2 MRI?
What does fat look like on MRI?
It re-aligns quickly and appears as bright white on MRI
- Fatty tumors, subcutaneous fat, yellow marrow
Contrast in MRI (signal intensity) is related to ____ ?
How tightly bound water is to time
Describe the Hydrogen properties in MRI contrast formation?
Hydrogen is more loosely bound in fat than water substance like CSF; re-aligns faster in fat than CSF
Spin-echo flip angle?
Gradient echo flip angle:
< 90 degrees
SE T1: (Fat color)
- Fat image
- Structures containing fat appear brighter/whiter (bone marrow, subcutaneous fat);
SE T1: (Water containing) -
- Edema, neoplasm, inflammation, CSF, large amounts of Fe) appears DARK
* long TR, short TE
SE T1 is standard or not?
SE T2 first echo:
Proton density, good anatomical detail, has properties of both T1 and T2
- Not done anymore
SE T2 second echo water image (loosely bound)?
Loosely bound water (neoplasms, edema, inflammation, healthy nucleus puposus, CSF) appear bright/white
What is the appearance/what does it detect of tightly bound or low water content on SE T2 second echo?
Ligaments, menisci, tendons, calcium, sclerosis, cortical bone or large amounts of Fe appear dark/black
Main charac. of SE T2 second echo?
- Classic Image
- MRI is the ONLY one that can see water in an IVD
FSE, fast spin echo:
Multiple echoes/TR, faster exam time, good in neuroimaging especially spine myelographic images
- Very sensitive to EDEMA
Fast MRI using short TR and TE with (flip angle)
- >90 degrees
- Provides a T2 image in less time, but does sacrifice some signal
- Terms: GRE, GRASS, FLASH, FISP, MPGR, SPGR
Technique that suppresses signal from fat, making small areas of pathology (often appearing bright because of edema) more evident and increasing the overall sensitivity of the exam, usually accomplished
- VERY SENSITIVE TO WATER
Techniques providing function information:
Kinematic (kMRI) functional joint movement
MRA is used to ____ ?
image VASCULAR flow
Diffusion MRI does what?
Reveals disturbances of fluid restriction as seen in stroke
MR spectroscopy can display what?
Concentration of biochemical metabolites
Functional MRI (fMRI) does what?
Displays changes in oxygen concentration associated with neural activation, and provides high resolution imaging of the brain
What can upright MRI reveal?
Weight bearing (kMRI) can reveal pathologies that may be missed (canal stenosis, transitional motion, & disc lesion)
WHat is the most important clinical indication to use an MRI?
Suspicion of C, T, or L spine disc disease
*** MRI IS THE GOLD STANDARD OF DISC PATHOLOGY*
- IS THERE A MASS?
Suspicion of what would be a good reason to send out for an MRI?
Central canal, foramina, or lateral recess stenosis
SPinal CORD pathology - MYELOMALACIA
What is a congenital disorder that would be of good use for an MRI?
Arnold Chiarimalformation (herniation of cerebellum through foramen magnum) syringomyelia
What would be some good things to evaluate using MRI?
- Bone marrow infiltration
- Primary bone neoplasms (benign and malignant)
- Suspected failed back syndrome - Gd DTPA
What is a red flag, and would suggest getting an MRI?
FAILURE TO IMPROVE with TREATMENT
Persistent bone pain with malignant history
SHould a patient have painful scoliosis?
80% is not painful
What’s the biggest MRI contraindication?
1st trimester pregnancy
What is something in the body that would cause a contraindication of MRI?
- aneurysm clips, intraocular foreign bodies (welders), permanent eyeliner, subcutaneous metal shards and shrapnel
Cardiac Pacemakers/defibrallators/implanted neurotransmitters (TENS) unit would mark a red flag for what?
WHen does bone marrow change on bone pathology?
STIR VS FAT SUPRESSION
MRI cervical spine, sagittal T1 and T2
pic of herniated discs
disc herniations can be:
Soft discs, herniation without surrounding osteophytosis, can be acute, subacute or chronic
Contained central protrusion
What would Cauda Equina Syndrome present as?
- _Saddle Parestesia or anesthesia**_
- _Bowel and Bladder distrubances**_
- Lower extremity motor weakness and sensory deficits
- Reduced or absent lower external reflexes
- Low back pain
- Uni or bi lateral sciatica
What is this?
What are characteristics of synovial cyst?
Can have them with no symptoms, no way to see on plain film, and complication of facet DJD
What are the main points of an annular tear?
- POSTERIOR anular fibers
- clincially significant
- Pain generator due to nociceptors
- CAN MANAGE chiropractically
Clinical Significance of Modic Changes:
Type 1: Represents marrow edema. Painful! Associated with an acute process. Converts to
Type 2: Represents fatty degneration of subchondral marrow. Associated with a chronic process
Type 3: Correlate with extensive bony sclerosis on plain radiographs
Describe fatty infiltration of spinal musculature:
- Semispinalis cervicis or lumbar multifidus
- Strongly associated with LBP
- Is an indicator for spine stabilization exercises
- Responds favorably to neuromusculoskeletal rehab and therapy exercises
WHat is Tarlov’s Cyst?
- Perineural cyst - fluid filled meningeal dilation of the nerve root sheath
- up to 9% of pop.
- Usually asymptomatic
- 20% do have symptoms –> if it expands
- May need drainage
Convex Left > 15 degrees may indicate interspinal pathology
What is pictured?
What is a descriptive term for decreased bone density?
Is, “osteopenia” a precise diagnosis?
When does osteopenia occur?
When bone resporption exceeds bone formation regardless of specific pathogenesis
What are the major causes of diffuse osteopenia:
What is an osteoprogenitor cell?
Originates from the marrow stem cells, develop into osteoblasts
What is an osteoblast?
Produces osteoid (soft material) 90-95% collagen, remainder is ground substance (mucopolysaccharides); numerous and large in growing skeleton
- Decrease in # and size at maturity
What is an osteocyte?
Arise from osteoblasts that become entrapped in their own osteoid, maintain the integrity of the bone around them
MATURE BONE CELLS
What are inactive cells?
What are osteoclasts?
Bone resorptive cells, derived from hematopoetic monocyte lineage
for normal bone density, Osteoblastic activity should =
what is the process in getting to a mature Osteocyte?
- Marrow stem cell
- Osteoblast - produces osteoid
- Osteoid is mineralized by Calcium Hydroxyapatite
- Osteocyte is formed
Water is responsible for _____ % of wet weight of bone?
Cellular components make up a ____ fraction of bone weight?
What is the remaining organic matrix/osteoid?
- (90% collagen) and 10% mucopolysaccharides account for 30% by dry weight
- The inorganic material accounts for 70% of osseous tissue by dry weight
Bone quality ratio aka
*MATRIX vs. MINERAL RATIO****
Organic matrix/osteoid is _____ , remaining _______ is what?
- 90% collagen
- Remaining 10% is mucopolysaccharide material (ground substance)
Inorganic material exists as what?
- It is destributed regularly along the length of collagen fibrils surrounded by ground substance
What does the skeleton do in relation to calcium?
Contains 99% of the body’s calcium and serves as the reservoir for maintenance of serum calcium; normally 10mg/dL ****
70% of plasma calcium is believed to be maintained by?
A continuous exchange of calcium ions between bone and extracellular fluid
What is defined as producing an inward flux of calcium from extracellular fluid?
if 70% of plasma calcium is an exchange between bone and ECF, whats the remaining 30%?
Mediated by the actions of the parathyroid hormone and other hormones
The process of resorption and formation occur ______ ?
Continuosuly in normal bone and are related to the function of osteoclasts and osteoblasts, whose function must remain in balance
Osteoclasts exists where?
In pits on bone surface called resorption bays or Howship’s lacuae
What are the osteoclasts main function?
Secrete acid to breakdown hydroxyapatite, and collagenase to break down osteoid
- May secrete substances to attract and promote function of osteoblasts
What is the key production of osteoblasts?
Produce osteoid/matrix which is then mineralized by calcium hydroxyapatite
- Scurvy can actually impede the osteoblasts ability to produce osteoid/matrix
What is the substance capable of directly or indirectly stimulating osteoclasts or increasing formation of new osteoclasts?
PTH, active metabolites of Vit. D, Prostaglandin E2, Thyroid hormone, Heparin
Is calcitonin inhibiting or excitatory when it comes to osteoclasts?
What is osteoporosis characterized as?
Qualitatively normal, but quantitatively deficient bone
What is the MOST FREQUENT BONE DISEASE IN HUMANS?
What is associated with decreasing osteoblastic function with age?
When is osteoporosis radiographically significant?
when 30-50% bone loss (spine closer to 50)
Where is osteoporosis predominant?
Is osteoporosis bone softening?
What is Osteomalacia defined as?
Pathology, inadequate mineralization of osteoid
Immature cortical and spongy bone (osteomalacia) and interruption of orderly development and mineralization of physis (rickets)
What is related to the deficiency of calcium, Vit D, or phosphorus?
Is Osteomalacia a quality or quantity problem?
Quality, its bone SOFTENING
pic of Vit D process in body
What are the deficiencies of osteomalacia related to?
- Liver Disease
- GI disease
- RENAL DISEASE*** (with loss of phosphorus)
- Sunlight def.
Osteoid is a soft material and gains it’s hardness by adding what?
Calcium and minerals
Hyperparathyroidism accelerates what?
Describe primary HPT:
Increased production of parathormone by glands, usually benign adenoma = HYPERCALCEMIA
Describe Secondary HPT:
Abnormal stimulation of glands by sustained hypocalcemia: Chronic renal disease, GI malsorption,
- serum calcium - low, low normal and phosphorus is elevated
Describe Tertiary HPT:
In long standing HPT, parathyroid function may become autonomous, can be related to ectopic tissue, paraneoplastic syndrome, may have hypercalcemia
- Can be from external stimulus, ext production of parathyroid hormone via tumor
What is the parathormone function (main):
ULTIMATELY INCREASE SERUM CALCIUM
Osteoblastic inhibition would be a characteristic of what?
If serum calcium drops, what does parathormone do?
Parathyroid hormone increases serum calcium, it is a positive feedback
What are the 3 features in regards to the function of Parathyroid hormone function?
- Renal Conservation of calcium and inhibiton of phosphate resorption
- Renal stimulation of 1-alpha-hydroxylase causing increase formation of 1,25 Vit. D
- Indirect effect on GI absorption of calcium
What is calcitonin secreted by?
The human parafollicular or C cells of the the human thyroid gland
What is calcitonin controlled by?
Serum calcium levels
What does calcitonin inhibit?
Bone calcium resorption by decreasing osteoclastic function and may lead to hypocalcemia and hypophosphatemia
- also inhibits GI calcium abosorption
What does calcitonin stimulate?
In regards to the kidney, what does calcitonin inhibit?
Renal tubular cell reabsorption of calcium
What is used to treat pagets disease?
Calcitonin, inhibits clastic activity
Where is osteoporosis most prevelant?
- Vertebral column
What is the major cause of osteoporosis?
AGE RELATED CONDITIONS: Senile and postmenopausal states (by far most common and most often seen in clinical practice)
Describe the role of medications in regards to Osteoporosis:
Steroids (many pts; chronic use end up w/bone density issues), heparin
What are some endocrine states that would affect osteoporosis?
HPT, hyperthyroidism, Cushing’s, acromegaly, pregnancy, diabetes mellitus, hypogonadism
What are some deficiency states that could affect osteoporosis?
SCURVY***, malnutrition, calcium deficiency
Major causes of generalized osteoporosis:
- Age related
- endocrine states
- deficiency states
- chronic liver disease
- anemic states
- osteogenesis imperfecta
- idiopathic condition
What would be the reason for localized osteoporosis?
Immobilization and disuse (fracture healing)
- Some degree of bone atrophy occurs; sustained Hyperemia in bone (too much blood flow in bone marrow) overstimulates osteoclasts
What is a VERY important reason for localized osteoporosis?
_Complex regional pain syndrome ***_
Sympathetically mediated pain syndrome, RSDS
had FOOSH injury 3-4 months ago
What is a type of osteoporosis that would cause pain?
Transient regional (localized) osteoporosis
- Transient (temporary) osteoporosis of the hip (TOH)
- Commonly seen in men
- Regional Migratory Osteoporosis
what is pictured?
Complex Regional Pain Syndrome (CRPS) /Sympathetic Mediated Pain Syndrome (SMPS)
Describe the key points of Complex Regional Pain Syndrome (CRPS) / Sympathetic Mediated Pain Syndrome (SMPS):
- Typically follows trauma
- VERY PAINFUL (suicidal type of pain)
- Just around joints (r wrist; can also be rheumatoid, lupus, scleroderma, etc)
*** Common in WRIST
Transient Osteoporosis of the hip usually involves?
Healthy middle aged men, rarely women, but almost exclusively during the 3rd trimester of pregnancy or the immediate postpartum period
- Usually SINGLE HIP
Transient Osteoporosis of the hip is characterized by what?
Acute disabling pain in the hip and functional disability without a history of previous trauma
Histological exam of transient osteoporosis of the hip reveals what?
Focal areas of thin and disconnected bone trabeculae covered by osteoid and active osteoblasts, active osteocytes in the lacunae
what is this
Transient osteoporosis of the hip
- should clear up on its own
What are the key features of regional migratory osteoporosis?
RMO was discovered by Duncan et al
- Occurs in 5-41%
- It may occur in different or same joint in an unpredictable time interval after the onset of the first symptoms
- Can stay in left knee, jump to R knee, or diff joint
- The joint nearest to the diseased one is the next to be involved
RMO of the ankle
What is general slowing down of osteoblastic activity?
What is the etiology of osteoporosis?
When does the gradual loss of bone occur with osteoporosis?
Beginning in the 5th or 6th decade in men and 4th decade in women
- 40’s and 50’s in men
- 30’s in women
> 50 y/o men lose bone at ______ ?
.4 % a year
> 35 y.o. women lose at _________ ?
.75-1% increasing to 2-3% post menopause
There is a significant loss of ____ bone in women who have osteoporosis?
What disease may cause “fish vertebrae”?
Pic of osteoporosis byproducts
What type of bone is lost in osteoporosis?
When does the anterior wedge of osteoporosis normally occur?
Post Traumatic - Typically get with axial load trauma on normal bone. Edge anterior b/c vertebrae posterior is stronger
What is the worst sign when dealing with osteoporosis?
Losing posterior and ant. body height, commonly via Mets and Mult Myeloma
- MOST COMMON PATHOLOGICAL COLLAPSE
What can cause fish vertebrae?
Biconcave (both endplate compression)
- Mult Myeloma
where are common fracture sites of osteoporosis?
what could this be?
Osteoporosis, but could be multiple myeloma or Mets
- Normally would have white cortex, grey medullary cavity, and very gray soft tissue
what is this?
Hemangioma is what?
Benign bone tumor
Percutaneous Verebroplasty fixes what? (pic)
Due to percutaneous vertebroplasty, ant. wedge fracture possibly
(liquid cement shows up extremely white on X ray)
When does an insufficiency fracture occur?
When the elastic strength of the bones is not sufficient to withstand normal physiologic stress (type of stress fracture)
Simplistic def. of insufficiency fracture?
normal stress on abnormal bone
What is a major cause of an insufficiency fx?
Characteristically, what does an insufficiency fracture involve?
Weight-bearing bones of the lower extremity, often bilateral
What are 2 main places of insuf. fx?
Sacrum and Pubic Rami
(MICRO fractures in trabeculae)
Insufficiency fx. (associated with osteoporosis)
What are the osteoporosis risk factors?
Osteoporosis is not _____
a direct calcium deficiency, but an osteoblastic deficiency
Calcium deficiency =
What is the most sensitive meausure of bone mineral density?
DEXA/DXA Scan is dual ______
X-ray Absorptiometry (DEXA/DXA)
What is the MAJOR feature of a DEXA/DXA scan?
Very sensitive scan to detect early bone (mineral) density loss (only thing we need to know about DEXA)
What is an aka for Hypovitaminosis C?
What is Hypovitaminosis C associated with?
Long term deficiency of Vit C, seen predominantly in infants
- Children have specific and unique findings
- 90-95% of osteoid is collagen
- If it can’t produce, they slow down bone production
What is Vit C essential for?
The formation of collagen, osteoid and endothelial linings - bleeding gums, muscles, soft tissues, cutaneous petechiae and hematuria
What is the main “Hallmark” in regards to hypovitaminosis (Scurvy/Barlow’s disease)?
Spontaneous hemorrhage due to capillary fragility - bleeding in subperiosteum: Bone PAIN
Osteopenia is defined as:
Decreased osteoblastic function
T/F, you will have osteopenia with Hypovitaminosis C?
An adult with Hypovitaminosis will present as similar to what disease?
What is subject to bleeding in Hypovitaminosis C?
Capillary Fragility is why you are susceptible to bleeding
Is Scurvy a mineralization disorder?
What is the major sign in kids in regards to Scurvy
Trummerfield sign, band of radiolucency
Major radiographic signs of Scurvy?
What is a dense bright Zone of provisional mineralization (ZPM)?
White line of Frankel
What is a dense cortical margin of epiphysis with radiolucent center?
What is an irregular metaphyseal margin?
Corner (angle sign)
What is a Pelken’s sign?
Bony protuberances at margin of ZPM
_What is Trummerfield/Scorbutic zone? ***_
Radiolucent metaphyseal band directly beneath ZPM, due to defective bone formation –> LEUKEMIA LINES
- failure of normal bone formation
3 big signs of Scurvy in CHILDREN?
- Subperiosteal Hemorrhage
Define the name of Hypovitaminosis in adults and kids -
Kid = “Rickets”
Adult = “Osteomalacia”
What is the major takeaway from Osteomalacia?
It is based on a QUALITY deficiency, and there is an abundance of unmineralized osteoid, thus causing BONE SOFTENING
How does osteomalacia clinically present itself?
Muscle weakness and bone pain on palation
- Deformities - Pelvis (sacrum could sink down into pelvis), femur (bows laterally), tibia, and spine (prone to compression fractures or scoliosis)
What are the main bone softening disorders?
Osteomalacia, Paget’s, and Fibrous Dysplasia
Describe the bone ratio in osteomalacia :
The ratio of mineral to osteoid is defective; not enough mineral to put on osteoid; Too much unmineralized osteoid; BONE SOFTENING = bowing deformities
Osteomalacia can a lot of times occur due to:
Hypophasphotemia (renal disease), but can also be due to not enough Ca+
What are the radiographic features of Osteomalacia?
- Coarsened Trabecular pattern
- Loss of cortical definition
Describe pseudofractures and their importance in bone softening disorders:
First described by Looser in 1930 and later by Milkman in 1934, they are defined as
- Little band of unmineralized osteoid
Pseudo fracures are only seen when?
BONE SOFTENING DISEASES
What are deformities of Osteomalacia?
Weight bearing bones; triradiate pelvis, acetabular protrusion, femoral and tibial bowing, kyphoscoliosis and endplate concavity, bell-shaped thorax
what are common locations for osteomalacia?
Femur, ribs, and pelvic rami
What is a seam of unmineralized osteoid?
Where do pseudofractures occur?
Happens in ribs, boney pelvis, femur, but NOT SPINE
Pseudofractures almost always ____ ?
Perpendicular to cortex
Describe polyostotic Fibrous Dysplasia:
Not monostotic –> polyostotic = multiple bones
What are the akas of Pseudofractures?
Looser’s lines, Milkman’s syndrome, increment fractures, osteoid seams, umbauzonen ***
What is pediatric osteomalacia with same etiologies, may begin as early as 6-12 months?
What is rickets defined as?
Renal tubular loss of phosphorus, not cured by administration of Vit D (resistant/refractory rickets) aka renal rickets (kidney losing phosphorus)
Renal Rickets + Secondary HPT =
What does Rickets clinically present with?
Muscle tetany, irritability, weakness, delayed bone development, small stature and bone deformities/bowing
- Enlargement around growth plates (trumpeting) and rib ends (rachitic rosary)
What is the most common cause of Rickets/Osteomalacia?****
Rickets presents with loss of _____ ?
Zone of Proliferative Mineralization
Describe the mineral process of Rickets:
There is a mineral deficiency (calcium or phosphorus) - loss of ZPM & cant make bone after it
- BONE SOFTENS
- CANT MAKE NEW BONE IF YOU DONT HAVE A ZONE
What is the “hallmark” finding of Rickets?
Loss of ZPM (easier to see in big bones)
Trumpeting, associated with Rickets
What is X linked Hypophosphatemia?
Genetically transmitted, X linked dominant trait
- Renal tubular loss of phosphate, part of Fanconi Syndrome –> Resistant to Vit D administration (Not lack of Vit D intake)
What develops from X-linked Hypophosphatemia?
Childhood rickets develops, and patients are short, bowlegged and stocky
What happens in the adult skeleton from X-linked Hypophosphatemia?
Develops osteosclerosis and enthesopathic paravertebral ligament. Ossification may resemble AS or DISH
What is a clinical finding of X-linked Hypophosphatemia?
Decreased pedicle length, lumbar spinal stenosis
X-linked Hypophosphatemia is a type of ____
X-linked Hypophosphatemia is a ______ of Osteomalacia?
Subtype (the phosphorus side of it)
What is Hypophosphatasia?
Rare genetic disorder related to low serum alkaline phosphatase production by osteoblasts
- This helps link collagen to osteoid (linkage disorder)
What “resembles rickets”?
What are some clinical findings of Hypophosphatasia?
Peculiar radiolucent metaphyseal defects extending from the growth plate into the metaphysis
What are some changes that occur due to Hyperparathyroidism HPT?
Histopathologic changes consist of osteoclastic and osteocytic bone resporption with fibrous tissue replacement (osteoitis fibrosa cystica, Recklinghausen’s disease of bone)
What are some major bone changes that occur from Hyperparathyroidism?******
Osteopenia, accentuated trabecular pattern, loss of cortical definition, brown tumors and the radiographic/pathologic hallmark - subperiosteal bone resporption
- Classic HPT finding = Pathognomonic
What body part do we need to see if we suspect HPT?
is HPT a bone softening disorder?
What is actually occuring in HPT?
Clasts are working faster than blasts, the clasts take away both calcium and phosphorus (QUALITY prob.)
3:1 female:male, and
typical patient is 30-50 y.o.
Symptoms are usually related to ______ during HPT?
bone, renal, or GI
Physical indicators of HPT?
Weakness (hypercalcemia), lethargy, polydipsia, polyuria, renal calculi, and bone tenderness
Kidney loses calcium on a ______ in HPT?
Parathyroid Hormone general overview:
- Osteoclastic and osteocytic stimulation –> Increase calcium from bone
- Osteoblastic inhibition
- Renal Conservation of calcium and inhibition of Phosphate resorption
- Renal stimulation of 1-a-hydroxylase causing increase formation of 1,25 Vit D
- Indirect effect on GI absorption of calcium
Parathyroid hormone increases what?
Calcium and phosphorus out of the bone
Describe Primary HPT:
Direct gland involvment: adenoma 90%, carcinoma, hyperplasia, or ectopic tumors (3o).
- Renal function = Normal –> HYPERCALCEMIA and HYPOPHOSPHATEMIA
Describe secondary HPT:
Sustained gland function from persistant hypocalcemia predominantly from RENAL DISEASE with loss of calcium and decrease Vit. D formation,
- less likely GI malsorption –> low normal or HYPOCALCEMIA & HYPERPHOSPHATEMIA.
In Secondary HPT, renal disease with hypocalcemia is associated with:
Soft tissue and vascular calcification and osteomalacia - Renal Osteodystrophy/uremic osteopathy (not rare)
In secondary HPT, renal disease + Hypocalcemia =
Soft tissue & Vascular Calcification & Osteomalacia**
Describe Tertiary HPT:
With chronic renal failure or malabsorption and long standing 2o who develop autonomous pathological function and HYPERCALCEMIA & HYPOPHOSPHATEMIA
- “can be due to corrected secondary HPT”
HPT bone changes:
Diffuse Osteopenia and Localized Bone Resorption
In HPT, Subperiosteal Bone Resorption can be _____ ?
Seen in many locations but hand, middle phalanges radial aspect 2nd-4th digits pathognomonic ***** TEST
What happens with cortical bone during HPT?
Intracortical bone resorption within Haversion Canals linear striations
Describe Endosteal bone resorption within HPT?
Typically hands and other findings (know endosteal bone resorption happens with HPT)
Describe Subchondral bone resorption when it comes to HPT:
Common, SI, SC, AC, SP (symphysis pubis), and DV junction, can mimic inflammatory joint disease. SI joint sacroiliitis
DRA (dialysis related arthropathy)
DRSA (dialysis related spondyloarthropathy)
* Typically related to secondary HPT
Describe Trabecular bone resorption in HPT bone changes:
Diffuse in skeleton, very prominent in cranium, causes very granular appearance of diploic space “salt and pepper” or “pepper pot skull”
Describe Subligamentous Bone resorption of HPT bone changes:
At entheses; trochanters, ischial and humeral tuberosities, elbow, calcaneus, inferior distal end of clavicle
Describe brown tumor/osteoclastoma/Giant cell tumor in regards to HPT bone changes:
Localized cyst like bone resorption containing fibrous tissue, giant cells and hemorrhages, “brown” color Histopathologic
Describe Acro-osteolysis in regards to HPT bone changes:
Distal tuft resorption, seen with many other conditions
Subperiosteal bone resorption associated with HPT
- Acro-osteolysis –> TUFTS (tuft resorption)
Subperiosteal bone resorption
NOT pathognomonic in this location
Salt and pepper skull
What is common in Primary HPT?
Brown Tumor and Chondrocalcinosis
What is rare in primary HPT?
Osteosclerosis and Periostitis
What is common in Secondary HPT?
Osteosclerosis and Periostitis
What is rare in Secondary HPT?
Brown tumor and Chondrocalcinosis
Additional findings of renal osteodystrophy are observed _____ ?
In association with Secondary HPT, including rickets, osteomalacia, and soft tissue and vascular calcification
What is renal osteodystrophy?
Renal disease leading to secondary HPT will push patient into rickets/osteomalacia if hypocalcemic
- Renal Disease + Secondary HPT = RICKETS
What is termed renal osteodystrophy/uremic osteopathy?
Comibnation of secondary HPT + osteomalacia + soft tissue and vascular calcification
Osteosclerosis is more commonly seen in _____ ?
RO and predominates in the axial skeleton (rugger jersey spine)
Dialysis Related Spondylo-Arthropathy
Renal failure patients treated with hemodialysis will have _____
Resolution of RO bone changes
Dialysis resolves what?
RO bone changes
Normally after 3-5 years of dialysis, what happens?
Cervical spine involved is MC
What occurs during DRSA?
Narrowing of disc height, subchondral cysts, endplate erosions, collapse, erosions of contiguous vertebral bodies, facet erosion, spondylolisthesis, peridiscal calcification****
- Calcification in subcutaneous regions
Hypoparathyroidism is acquired or genetic?
Deficiency of Parathyroid hormone is most commonly from what?
Excision or trauma to the parathyroid gland during thyroidectomies
What are the 2 main things that occur during Hypoparathyroidism?
HYPOCALCEMIA & HYPERPHOSPHATEMIA
What are some underlying physical changes of Hypoparathyroidism?
Bone osteosclerosis (mc), thickening of cranial vault bones, calcification of basal ganglia, rarely choroid plexus and cerebellum***
What is happneing within the spine during Hypoparathyroidism?
Rare spine changes of pain, stiffness with calcification of ALL and posterior spinal ligaments, resembling DISH
Is hypoparathyroidism acquired? expand on it:
YES it is acquired
- Has Ca and P levels like Secondary HPT
- Osteosclerosis like Secondary HPT
PHP stands for what?
PHP is an ___
End - organ resistance to parathormone
PHP main features:
X-linked dominant and more common in females
- MAJOR DIFFERENCE:Genetic, unlike hypoparathyroidism (which is acquired)
- End/Target-Organ restance to PTH
In PHP, what conditions would you see?
Hypocalcemia, hyperphosphatemia and basal ganglia & soft tissue calcification
What is another major difference between PHP and HPT (hypo)?
Short stature, obesity, round face, and brachydactyly (short fingers and toes)
- Tend to be mentally challenged
*** all above is PHP
What does PPHP stand for?
Normocalcemic form of PHP, same somatotype
- Also GENETIC
- Do not have a problem with PTH –> “false PHP”
What is the major difference between PHP and PPHP?
PPHP is NORMOCALCEMIA & NORMOPHOSPHATEMIA
- Also has Basal Ganglia & Soft tissue calcification
- Both may occur in the same family –> STOP PROCREATING
Neoplasm is described as what?
Widespread marrow infiltration with cancer cells (inhibits osteoblastic activity) and results in loss of bone density
Neoplasm is often accompanied with what?
Other radiographic or clinical findings (punched out)
Patients will be ____ in regards to a neoplasm?
What is associated with Neoplasm?
Multiple Myeloma, leukemia in children, and lymphoma (non-Hodgkins) can cause diffuse osteopenia
Reduced bone mass of normal quality; related to imbalance between osteoclastic and osteoblastic activity favoring osteoclastic resorption; serum calcium, phosphorus and alkaline phosphatase typically normal; generalized osteopenia with fractures frequent
Related to deficiency of calcium, Vit D or phosphorus with multitude of causes including dietary deficiency, malabsorption, liver disease and renal disease; abundance of unmineralized osteoid resulting in bone softening disease and osteopenia including pseudofractures; rickets in the child with radiographic findings including loss of zone of provisional calcification
Renal disease acquired or genetic resulting in Ph deficiency and leading to osteomalacia/rickets (Vit D resistant osteomalacia/rickets)
- Primary - Related to parathyroid tumor or hyperplasia
- Secondary - Related to renal disease or GI malabsorption
- Tertiary - Related to ectopic autonomous functioning tissue or chronic secondary HPT
Radiographic findings of HPT related to increased osteoclastic activity with localized resorption including subperiosteal at middle phalanges pathognomonic
Acquired related to accidental removal/damge to parathyroid glands during thyroid surgery, radiation, infection, carcinoma; hypocalcemia and hyperphosphatemia; radiographic finding is osteosclerosis as well as calvarial thickening and hypoplastic dentition, may be associated with extensive calcification of spinal ligaments and basal ganglia calcification
Pseudohypoparathyroidism PHP review:
PHP is a genetic disorder related to end organ resistance to parathyroid hromone with normal parathyroid hormone production; characteristic somatotype of short stature, obesity, round face, brachydactyly, abnormal dentition and mental retardation;
Radiographic findings: similar to hypoparathyroidism; hypocalcemia and hyperphosphatemia
Pseudopseudohypoparathyroidism PPHP review:
Genetic disorder similar to PHP and frequently a sibling of; is the normal calcium and phosphorus version of PHP; produce and respond to parathyroid hormone; same somatotype and radiographic findings
Congenital abnormality related to decreased alkaline phosphatase production by osteoblasts resulting in findings similar to rickets; radiolucent metaphyseal defects
Hypovitaminosis C Scurvy review:
Deficiency of Vit C resulting in decreased abilitiy to produce collagen with inadequate osteoid formation; is a form of osteoporosis; adult form identical to adult osteoporosis; childhood form changes at the bone and are characteristic with proper names
Arthritic disorder affects 1 in ____
What are the most prevelant types of arthritis:
- SLE = systemic lupus
- PA = psoriatic arthritis
- AS = Ankylosing spondylitis
- JRA = Juvenile rheumatoid arthritis
- PSS = Progressive Systemic Sclerosis (scleroderma)
What remains the primary method of initial imaging in arthritic disorder?
The noncontrast radiograph
What are synovial joints characterized by?
- 2 layers: Outer fibrous & Inner Synovial
- Articular/Hyaline cartilage, synovial membrane, synovial fluid, (anatomical) joint space (not radiographic space)
Describe the synovial membrane:
Loose vascular connective tissue - secretes synovial fluid (blood plasma and mucoid substance) lubrication and nutrition; “bare area” –> major role in inflammatory
(no role in degnerative)
Describe the articular cartilage:
Hyaline is most common intraarticular cartilage and consists of chondrocytes embedded in a matrix of collagen fibrils and ground substance (mucopolysaccharide chondroitin sulfate concentrated in water)
Describe the subchondral bone plate:
Thin cortex and underlying cancellous trabeculae, abundant blood supply
What is the bare area?
NO periosteum, no articular cartilage; btwn end of synovial membrane & articular cartilage
What are the 2 branches of arthritis?
Mono and Poly arthritis
What are the categories under monarthritis?
- Crystal induced (gout and psedo gout)
What are the 4 categories under polyarthritis?
- Inflammatory Joint Disease
- Degenerative Joint Disease
- Metabolic Deposition Disease
- Hematological Disease
What is under inflammatory Joint disease?
Painful Soft tissue swelling of joints
What are the 2 subtypes of Inflammatory joint disease?
What are under Rheumatoid types?
What are under Rheumatoid Variants?
What is under DJD?
What goes under Metabolic Deposition disease?
What goes under Hematological?
Describe the Important Arthritis Chart as best you can:
What are the only 2 types of arthritis in human beings?
Mechanical or Inflammatory
Mechanical arthritis =
Inflammatory arthritis =
All arthritis destroys what?
Gout starts where?
Single joint, nomally the big toe
Metabolic Deposition Disease =
Accumulation of normal or abnormal metabolic biproducts in or around the joint
Trauma: Bleed into joint —>
Describe the Rheumatoid factor in Polyarthritis:
IgM is reactive to IgG (serological blood test)
- Rheumatoid types are autoimmune diseases, antigen-antibody reactions, IgM reacting to altered IgG
What is the major key point of Rheumatoid?***
It is the ONLY one that is PRIMARY to the JOINT –> Main target is SYNOVIAL MEMBRANE —> Worst of the group
HLA-B27 (+) / Rheumatoid (-) —>
Rheumatoid Variants (P.A.I.R)
HLA-B27 (-) / Rheumatoid (+) –>
Rheumatoid Types (R.S.P.D.T/V.)
In lupus, what is the “Secondary” target?
What is Reiter’s Syndrome aka?
Reactive Arthritis Syndrome
Describe Psoriatic Arthritis:
Very Specific and common inflammatory, non-rheumatoid arthritis
What can IBD patients develop?
Ankylosing Spondylitis that can act like rheumatoid arthritis
What is “Primary” DJD?
(common joints; Spine) nothing else has happened to the joint
What is the secondary DJD?
Joints involved where we don’t expect to see it, unpredictable joints (uncommon joints, any joint), and clinically we know something else has happened to that joint
Bony enlargements come from _____ ?
Bony enlargements from DJD come from osteophytes
Describe Metabolic Deposition Disease:
Accumulation of normal (uric acid –> Gout) or abnormal (amyloids –> amyloidosis)
Metabolic byproducts –> Creating “lumps and bumps” around a joint
What is amyloid?
Abnormal Proteinacious material/metabolic byproduct
In Metabolic Deposition Disease, describe uric acid:
Normal metabolic byproduct
MBB has amyloid and uric acid : gout
All arthritis _______
Enlarges the joint
THERE ARE ONLY 2 TYPES of ARTHRITIS IN HUMANS:
Joint Degenerates or Joint is INFLAMED
What are the 4 things that inflame joints?
- Immune complexes
- Metabolic Byproducts
- Blood (Toxic/Inflammatory if outside of vascular system)
All arthritis does one thing, what is it?
Desroys articular cartilage and narrows radiographic joint space
- Radiographic joint space = bone-bone
DJD is _______ whereas Inflammatory is _______?
DJD is mechanical stress across a joint (macro/microtrauma) and Inflammatory is chemical (typical lytic enzymes, collagenase –> Produced by synovial membrane due to being inflammed)
Inflammation is to ______ what _______ are to Degeneration ? *****
Relative frequency of arthritis, Weekly:
Relative frequency of Arthritis, Monthly:
CPPD, RA, AS, PA, SCM (Joint mice)- Synovial Chondrometaplasia, DISH, OCI (OsteitisCondens)
Relative Frequency of Arthritis, Yearly:
Gout, Infection RAS, Lupus, PSS (scleroderma)
What are the ABCS of Anatomic - Radiographic Correlation?
- A - Articular Alignment, adjacent bony relationships across the joint
- B - Bone, for joint evaluation, focus on the subchondral bone
- C - Cartilage, not visible but the space occupied is
- All arthritic diseases destroy articular cartilage and narrow the radiographic joint space
- S - Soft Tissues, periarticular soft tissues often enlarged by bone or soft tissue swelling
- Progressive, non-inflammatory joint disease characterized by degenerative pathologic changes to articular cartilage and its related components
- Non-Uniform loss of joint space, Asymmetrical, Osteophytes, Mechanical Problem
What are some findings of DJD?
Small joints of hands and feet as well as large weight bearing joint typically involved (spine also involved)
Describe the etiology of DJD:
Exact etiology unkown, although pathologic sequence of change is well known
What is the most common encountered Joint Disorder?
Describe X ray findings and clinical findings:
- Great disparity between radiographic findings and clinical presentation in any given patient
- Just because X ray looks bad, it doesn’t mean the patient has symptoms
Describe the symptoms of DJD:
- Onset insidious with episodic moderate aching pain, stiffness and periarticular soft tissue swelling
- Can be via inflammatory around joint, but NOT IN THE JOINT
Stifness with prolonged inactivity, gradually decreasing with activity and returning with fatigue describes symptoms of ____
Repetitive movements or recurrent chronic injury, first thoughts would be ____
What lab values would DJD present with?
NORMAL LABS, no inflammatory or serological markers
Periarticular swelling, soft tissue inflammatory episode (increase pain) -
Once DJD is initiated it is :
IRREVERSIBLE (can be slowed down though)
what is the actual process of DJD ?
“Trigger” is likely from abnormal mechanical forces across the joint that injure or kill chondrocytes with resulting loss of the surrounding matrix/chondroitin sulfate and destruction of collagen fibers
- Rep. microtrauma
Where does DJD begin?
At cartilage surface and extends toward subchondral bone - progressive asymmetrical joint space narrowing **
Describe the subchondral findings of DJD:
- Subchondral new bone due to cartilage loss (OSTEOPHYTES), subchondral synovial fluid intrusion - GEODES (subchondral cysts –> related to arthritic disease –> classic in DJD)
- Subchondral Sclerosis (ONLY DJD, NOT in inflammatory)
WHat is a hole in a rock?
What are osteophytes?
The classic radiographic finding and lead to bony enlargement of the joint - visible in superficial joints
** CLASSIC finding in DJD
How do osteophytes develop?
From the articular margin due to combination of cartilage metaplasia and increase capsular insertion stress
Osteophytes are bony with ____ ,
- Cortex, and unattached margin is capped with layer of cartilage
- Osteophytes have cartilage caps
- Doesn’t make a difference in extremities (hip, joint, knee, PIP, etc.)
- Makes a big difference in spine
Osteophytes only occur in _____
DJD is symmetrical or Asymmetric?
Inflammatory is almost always _____ ?
4 main DJD radiographic findings: ****
- Non uniform loss of joint space - fundamental
- Osteophyte formation - Classic finding
- Subchondral sclerosis/eburnation - variable
- Subchondral cysts/geodes - variable
* Hips will have larger geodes than smaller joints
Intra articular loose bodies are found in what disease? WHat are they?
Joint Mice, found in DJD, loose ossicles in the joint, SCM (synvoial chondrometaplasia) –> Cartilage pieces produced by synovial membrane)
Geodes can weaken _____
What is an articular deformity and what is it associated with?
Collapse of subchondral bone associated with DJD –> linked with Geodes
Heberdene’s Nodes (DIP)
Boucharde’s Nodes (PIP)
DJD primary joints in hand:
- DIP, PIP & 1st MCP occ. Scaphotrapezium
- Not primary in MCP
- Writst: Radioscaphoid = primary; Radiolunate = SECONDARY
DJD Primary Joints, Shoulder:
What are common PRIMARY areas of DJD?
- FOOT - DIP, PIP and 1st MTP
What are secondary DJD?
** MOST COMMONLY SEEN IN POST MENOPAUSAL WOMEN
What is CPPD?
Calcium Pyrophosphate Deposition DIsease
- Common Metabolic Disease
- Causes Pseudogout
The bigger the joint,
The smaller the osteophytic bone
If we see a geode, how do we differentiate this?
- Is it next to a DJD (asymetrical joint space)
- Is it up against the subchondral bone plate
What is the #1 cause of secondary DJD, and also common to cause primary?
Avascular Necrosis AVN
Probably due to AVN in DJD
Patella femoral DJD