X-Ray Dx 9/22/98
Bone Metabolism
-enchondral-uses a cartilage matrix/precursor (matrix not seen on plain film)
-adds length to bones
-intramembranous-adds bone as you go
-flat bones (face)
-parts of some long bones (ex. clavicle)
-adds width to bone (thickness)
-no matrix
-mechanism for repairing fractures
-directly apply calcium to surace
Epiphysis
-covered by articular cartilage
-near ends of bone
-responsible for production and support of articular cartilage
-subchondral bone mediates its blood supply
-subject to maldevelopment
-arthritis, ischemia, tumors can affect it
-are at proximal and distal ends of bones
-physis=epiphyseal plate=growth plate=growing/maturingenchondral
part
-most mature part of physis is next to metaphysis, least mature part is next
to epiphysis
Apophysis
-greater trochanter
-not covered by cartilage
-attachment site for ligaments and tendons
-initially-region of uncalcified matrix then matures
Young child/fetus
-shaft is dense in middle of 2nd trimester
-epiphysis shows up as a big gap (not radiographically evident)
ZPC-Zone of Provisional Calcification
-most immature part of metaphysis
-most mature part of physis
Physis
-affected by trauma, hormonal, and vascular changes (until it closes)
-once it closes, no more length
Can do surgical limb-lengthening procedures
-peel back periosteum
-slice diaphysis
-periosteum repairs as you separate pieces slowly
-useful in shattered limbs repaired short if grew unevenly
Metaphysis
-most metabolically active part of bone
-most common site for osteomyelitis
-most common site for a variety of tumors
-frequent site for ischemic injury
-starts of ZPC
Diaphysis
-child-lot of red marrow
-adult-conversion to fatty/yellow marrow
-trabecular fiber and cortex (mechanical strength)
-can be attacked at marrow
-multiple myeloma, Ewing’s, may see infection
-cortex-dense, strong, compact
-outer-periosteum-osteoblasts and clasts
-osteoblasts-can only add Ca to bone
-osteoclasts-can only recover Ca from bone
-pos. Ca balance until skeletally mature
-21-35-stable
-after 35-lose bone density (.3%/yr in men) at menopause for
for women 3-5%/yr for about 10 yrs.
-inner-endosteum
Growing bone only connected to periosteum at ends
-periosteum attached via Sharpey fibers
-easy to separate young bone from periosteum
-don’t like to see separation of periosteum in adult (means infection or tumor)
-95% of people reach bone maturity by age 21
Bone metabolism (esp. Ca and P)
-Ca:P is 2:1 usually in serum
-Ca used for:
-muscle function, nerve function, hemostatic pathway (clotting)
-skeleton stores Ca for body
-can enhance Ca uptake from GI tract
-<1% of available Ca circulates in serum but can get more quickly
-issues:
-dietary Ca
-stress on bone (thicker subchondral bone)
-Vit D influences Ca uptake
-PTH affects serum Ca balance
-alkaline phosphatase (seen with osteoblastic activity)
-from thyroid
-controls Ca in serum
-if serum Ca is low PTH levels inc.
-improved solubility of Ca at bone matrix so osteoclasts can pull
it out easier
-acts at renal tubules (inc. recovery from urine)
-stimulation of 1,25-dihydroxycalciferol
-if PTH inc., should inc. serum Ca due to
-inc. GI resorption
-inc. reuptake from renal tubules
-improving work of osteoclasts
-Calcitonin
-opposes work of PTH
-if inc. calcitonin:
-dec. reuptake of Ca
-dec. recovery from GI
-dec. osteoclast activity
-reduces serum Ca
-P acts as exchange molecule
-allows Ca to precipitate out of solution and be integrated into bone
-also involved in extraction of Ca from bone
Estrogen and androgens
-stimulate bone production by inc. anabolic activity
-affect longitudinal growth (enchondral)
Growth Hormone
-affects chondrocytes
-if skeletally immature:
-inc. GH=giants
-dec. GH=dwarfs
-if skeletally mature:
-inc. GH=acromegaly (can see a slight inc. in height)
Glucocorticoids
-induces protein catabolism
Know about bone metabolism for tests
Ch. 7 Table 7.2 (Bone Disease)
-VICTANE
Predictor Variables
-skeletal location (some processes only like certain places)
-position within bone
-site of origin
-shape
-size
-margination
-cortical integrity
-behavior of lesion
-matrix
-larger lesions are more agressive
Preliminary analysis
-age, sex, race, history
-# lesions, symmetry of lesion , systems involved
Supplementary exams
-CT, bone scan, MR
-lab exams
-biopsy (for tumors)
Benign
123
Primary
1234567
Secondary
4567
+
+++
+++
+
+++
+
+++
++
+++
+++
Benign
Primary
Secondary
+++
++
++
+
++
+++
++
+
+
+++
-
+
+++
+++
+++
+++
+++
+++
-
+
+++
++
+++
-
+
+++
+
-
Age (decades)
Size
0-6 cm
+++
6+ cm
+
Monostotic
+++
Polyostotic
+
Cortical Destruction -=absent, +=occasional, +++=more so
plyostotic-arises in multiple sites
Periosteal Rx
solid
laminated
spiculated
Codman’s
Destruction
geographic
motheaten
permeative
Margins
sharp
imperceptible
Matrix
ST mass
Joint Space
Know this table
Table 7.5-monostotic vs. polyostotic
Table 7.9-lesion matrix (radiologic)
Osteolytic Behavior
Geographic Lesion
solitary
Greater than 1 cm
Sharp Margins
Motheaten Lesion
Multiple
2-5mm
Ragged margins and coalescence
Imperceptible transition
Permeative Lesion
Multiple
Less than 1mm
Imperceptible transition
Osteoblastic Behavior
Diffuse Lesion
Homogeneously sclerotic ("ivory")
Obliterated corticomedullary junction
Localized Lesion
Single or multiple
Irregular, hazy border
Asymmetrical
Mixed Behavior
Both osteolytic and osteoblastic features
-osseous-great ability to pick up Ca
-floccules-”popcorn”
-stipples-polka dots
-Lipoma
-often cleared out regions in bone
-central spot of calcification
-4 tissue types in table
-osseous>cartilage>fat>fibrous
Table 7.10 Periosteal response
-spicules-like a porcupine
-Codman’s-tattered ends
-benign pattern is solid