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51 Cards in this Set

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List & describe the major components of Bone
1. Epiphysis = end of long bone that is originally separated from the main bone by a layer of cartilage but later becomes united to the main bone through ossification

2. Metaphysis = zone of growth between Epiphysis & Diaphysis during development of a bone

3. Diaphysis = shaft of the long bone
-rigid outer shell of compact bone (Cortex) surrounding central Medullary area filled with thin bone trabeculae & hematopoietic marrow
List & describe the major components of Bone
1. Epiphysis = end of long bone that is originally separated from the main bone by a layer of cartilage but later becomes united to the main bone through ossification

2. Metaphysis = zone of growth between Epiphysis & Diaphysis during development of a bone

3. Diaphysis = shaft of the long bone
-rigid outer shell of compact bone (Cortex) surrounding central Medullary area filled with thin bone trabeculae & hematopoietic marrow
Describe the Zones in the Epiphyseal Plate
1. Resting Zone = not much goes on but Chondrocytes are alive
2. Proliferating Zone = where all the cell division occurs in the Growth Plate
3. Hypertrophic Zone = chondrocytes enlarge & secrete EC matrix
-Longitudinal & Transverse Septa
-Longitudinal Septa projects down into the Metaphysis
Cartilage Matrix
-Fibrils = Collage type II
-Proteoglycan granules = black dots b/w the fibrils
What is seen here?
Mineralization occuring almost exclusively in the Longitudinal Septa = deposition of Calcium Hydroxyapatite
What is this picture showing?
Describe the process of Mineralization
In Proliferative Zone there are Matrix Vesicles on the lateral edges of Chondrocytes
-Matrix Vesicles bud off and are distributed into the newly forming matrix; become entrapped between collagen fibrils
-deposition of Calcium Hydroxyapatite
Describe Matrix Vesicles
-On the membrane are lipids & proteins that are Ca+ binding
-once the vesicle gets close to the mineralization front, there is increase in Alkaline Phosphatase = hydrolyzed Phosphate + Ca accumulate in the center of the vesicle -> precipitation of Hydroxyapatite
-Hydroxyapatite Crystals break through the outer membrane of Vesicles & extend into EC space
-exposed crystal grows
What is seen here?
Longitudinal Septum under EM
Edge of Trabeculum of Bone & Marrow (lining it are Osteoblasts
-Green = Calcium
-Red = Osteoid = Type I Collagen -> becomes mineralized by deposition of Calcium Hydroxyapatite
What is this picture showing?
Bone Matrix that has been decalcified -> Collagen I Fibers
What is seen here?
What is the cause of Scurvy?
deficiency of Ascorbic Acid (Vitamin C)
What is the pathogenesis of Vitamin C deficiency?
Vitamin C is necessary for the Hydroxylation of Proline & Lysine in Collagen synthesis
-Hydroxylations sites are anchors for cross-linking of alpha-chains
-deficiency leads to Collagen with reduced tensile strength
What are the clinical manifestations of Scurvy?
1. Swollen gums
2. Subperiosteal hemorrhage
3. bleeding into joint spaces
4. Purpura & petechiae
5. impaired wound healing
Vitamin C deficiency = Scurvy
-weak blood vessels due to Collagen defect
-hemorrhage under the periosteum of the calverium
What would cause this?
-Growth Plate with disordered cellular array = chondrocytes are very close to eachother b/c of deficiency of synthesis & secretion of Collagen Type II
-accumulation of blood vessels underneath the Growth Plate
What is the cause of this?
What is the cause of Rickets & Osteomalacia?
Vitamin D deficiency
What is the pathophysiology of Vitamin D deficiency?
Vitamin D deficiency -> decreased Ca++ absorption in gut -> decreased Calcification of Osteoid matrix
What are the clinical manifestations of Rickets?
Skeletal deformities = due to disruption of mineralization at Epiphyseal plates
-Craniotabes = soft skull bones
-Rachitic Rosary = overgrowth of costochondral joint
-Pigeon breast = outward protrusion of sternum
-Lumbar lordosis = spinal curvature
-Bowing of the legs
List the 3 ways of pathogenesis of Rickets
1. Dietary deficiency of Vitamin D3
2. impaired absorption of Ca+ & PO4
3. impaired tubular reabsorption of PO4

**growing bones can't get enough Ca++ or PO4 to support mineralization -> bones become soft & flexible
Top = Pigeon Breast = Pectus Carinatum
Bottom = Rachitic Rosary = Costochondral thickening due to enlargement of the Growth Plate

Vitamin D deficiency = Rickets
What are the names of these abnormalities & what is the cause?
Section through a Ricketic rib
-Cartilaginous & bony part of the Costochondral junction
-tremendous thickening of the Growth Plate & primarily the Hypertrophic Zone
What is seen here? What is the cause?
Rickets growth plate
-only see the Hypertrophic Zone throughout the entire length of the Growth Plate
Left is normal, what is the right?
List 5 possible causes of Osteomalacia
1. impaired absorption of Vitamin D due to Sprue, persistent mild diarrhea, or inadequate intake
2. dietary deficiency of Ca++ or PO4
3. Hyperphosphaturia in Vitamin D resistant rickets
4. Aluminum toxicity
5. Malignant tumors = Oncogenic Osteomalacia
Diseases characterized by DECREASED MINERALIZATION OF NEWLY FORMED BONE, usually caused by deficiency or abnormal metabolism of Vitamin D
Rickets = in children

Osteomalacia = in adults
-hypomineralization of bones = Osteopenia
What are the typical lab findings in Osteomalacia?
1. normal to low Ca++ & Phosphorus

2. Increased ALK PHOS
-trabeculae have core of calcified bone, but are surrounded by coat of unmineralized osteoid
-Osteoblasts are lining the bone surfaces
-Alkaline Phosphatase is coming from Osteoblasts
What is the picture on the Right showing?
Pseudofractures in Osteomalacia
-not fractures but are translucent, poorly calcified linear zones

Tx = Vitamin D + Calcium
What is seen here? What is the treatment?
What are the clinical manifestations of Osteomalacia?
1. Bone pain

2. fractures of veterbrae, hips, wrist
Decreased bone mass, resulting in thin, fragile bones that are susceptible to fracture
What are the clinical features of Osteoporosis?
1. Compression fractures of Vertebral bodies = shortened stature & kyphosis
2. Bone Pain & fractures
3. Back pain
List the risk factors for developing Osteoporosis
1. Hereditary = defective Vitamin D receptor gene
2. Loss of ovarian endocrine function = Estrogen deficiency
3. Diet deficient in Calcium, Vitamin D
4. Smoking
5. prolonged Steroid therapy
6. inactivity or weightlessness (astronauts)
Why does Estrogen deficiency predispose to Osteoporosis?
Estrogen inhibits production of Osteoclasts; enhances Osteoblasts
Right = Osteoporotic Vertebral body -> leads to compression fracture
What is this picture showing?
What are the lab findings associated with Osteoporosis?
Normal Calcium, Phosphorus, & Alkaline Phosphatase

**compared to Osteomalacia, which has elevated Alk Phos
Osteoporosis = bone trabeculum is thin
What is seen here?
What are treatments for Osteoporosis?
1. Estrogen replacement (still be evaluated)

2. Bisphosphonates = anti-osteoclast agents to inhibit bone resorption

3. Ca & Vitamin D
Localized disorder of bone remodeling, resulting in excessive bone resorption followed by disorganized bone replacement, producing thickened but weak bone that is susceptible to deformity & fracture
Paget's disease
What are the clinical manifestations of Paget's disease?
1. Bone pain

2. Bone growth = increase in hat size
Abnormal bone architecture caused by increase in both Osteoblastic & Osteoclastic activity
Paget's Disease
Paget's disease = Hyperostosis Frontalis Interna
This is the Calverium. What is the disease?
Paget's disease
-increased Alk Phos
-normal Calcium & Phosphorus
Paget's disease
-Osteoclasts are resorbing
-Osteoblasts are putting more Osteoid (red) back in = reason for increased Alk Phos
What is this picture showing?
Paramyxovirus, measles, or RSV infection = Paget's Disease
-Osteoclast is seen that is enlarged with more nuclei than normal
What is the proposed etiology of this disease?
Paget's disease
-tremendous overgrowth of bone with more Osteoid (red) due to Osteoblastic activity
-thickening of bone Trabeculae with reduction in marrow space
What bone condition is seen here?
Mosaic Cement lines = Paget's disease
-mixed osteoblastic & osteoclastic activity leads to new bone formation
What is the name for this? What is the disease?
What are the complications of Paget's Disease?
1. High-output Cardiac Failure = due to increased bone vascularity resulting from numberous AV shunts within the marrow

2. Fractures = although bone is thick, it lacks strength

3. Hearing loss = due to narrowing of the auditory foramen

4. Osteogenic Sarcoma in older age
A 6-year-old girl is brought in complaining of joint pain. Further inspection reveals a thin, malnourished girl with hemarthrosis, multiple purpura, & ginvival swelling & bleeding. Her mother tells you that she has not been eating a well-balanced diet due to financial situations. Dx?
Scurvy = Vitamin C deficiency

results in inability to Hydroxylate Lysine & Proline resides on Collagen (are used for Cross-linking to make fibrils)
A 5-year-old boy is brought in concerned of Skeletal abnormalities: protrusion of the sternum, thinning of the occipital & parietal bones resulting in a squared appearance of the head, & rachitic rosary. Dx?
Rickets = Vitamin D deficiency = decreased Ca+ absorption = decreased calcification of the Osteoid Matrix
A 74-year-old man presents with the following:
-bone pain in left thigh
-bilateral hearing loss
-increase in hat size
-Lab: increased ALP

What 2 things may this put him at risk for?
Paget's disease

High-output cardiac failure