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What is the master transcription factor involved in osteoblast differentiation?

What factors signify that an osteoblast is mature?


High alkaline phosphatase, DMP, SOST (Sclerostin?), DKK1.


What are found in bone canaliculi? What is the major protein involved here?

Canaliculi have cytoplasmic projections between osteocytes which communicate via Connexin-43 gap junctions.


Describe the signaling required for osteoclast maturation.

CSF to stimulate macrophages from bone marrow, then signaling of RANK via RANK-L (opposed by OPG) to promote fusion.


Why is carbonic anhydrase important to osteoclast function?

Bone resorption can only occur under acidic conditions, which is facilitated by the products of carbonic anhydrase (H+, HCO3-).


In a typical long bone, what % of its dry mass is cortical bone?

What is the function served by trabecular bone?

About 80% is cortical.

Metabolic; presumably supports the bone marrow.


How do osteocytes communicate with the bone surface? Why might they do this?

Via cytoplasmic processes & via factors like sclerostin and RANK-L. Osteocytes control bone integrity via osteoblast/clast activation?


What is a Volkmann's canal?

A canal perpendicular to the length of a long bone, which connects parallel haversian canals.


Distinguish between intramembraneous and endochondral ossification.

Intramembranous ossification occurs in development of flat bones, involves direct mesenchymal-to-bone tranformation, and increases thickness(?)

Endochondral ossificaiton involves conversion of a cartilaginous template to bone, occurs in development of long bones, and increases length.


What is the significance of the epiphyseal growth plate?

In long bones, endochondral ossification occurs at the epiphyseal growth plates, resulting in elongation. 

The growth plates seal at particular ages, and so can reveal the "age" of a bone.


Which has a higher rate of turnover: Trabecular or cortical bone?

How are lamellae oriented in each?


In trabecular, lamellae follow the trabecular curvature. In cortical, they are concentric (osteons).


How much of a bone is typically remodeling at any time?

How long does it take to resorb, then rebuild typical cortical bone?


2 weeks to resorb, up to 6mo to rebuild.


Describe the structure of a typical bone remodeling unit (BRU).

Osteoclasts at the tip dig through and resorb bone. They are followed by osteoblasts which replace it.


What is the significance of tetracycline in the context of bone mineralization?

Tetracycline appears to disrupt bone mineralization, leaving a distinctive mark (stain?) when given systemically. This can be measured, I guess.


What causes bones to form in a bent shape?

The constantly remodeling bone responds to mechanical stressors; abnormal, prolonged pressure could cause it, but it is more typical of developmental disorders like Rickets.


Briefly summarize the process of fracture healing.

A hematoma forms around the fracture.

A fibrocartilaginous (primary) callus forms, & neovascularization is abundant.

The primary callus is replaced by a bony one.

The bone continues to heal via remodeling for months or years.


Summarize the structure of collagen. How is it secreted?

3 alpha chains made to form a left-handed helix.

Secreted as procollagen, and must be cleaved in the interstitium.


Explain the signifiance and maturation of collagen cross-linking.

More cross-links means a more robust, stronger matrix.

Links usually form between 2 lysines which undergo an enzymatic reaction to form an aliphatic link, which matures nonenzymatically into an aromatic link.


How do lamellae contribute to bone integrity?

Fractures are less likely to break through a lamellar sheet of bone, since the impact causes fractures along the planes of the lamellae, reducing its energy.


Osteogenesis Imperfecta

What is its cause?

What are its clinical symptoms?

Osteogenesis Imperfecta

Results from a mutation in type I collagen (usually COL1A1 or 1A2).

The result are brittle bones, but any matrix that has collagen type 1 is affected. Often lethal at birth.



What is its cause & pathophysiology?

What are its symptoms?

What is rickets?


Results from one of many possible defects leading to vitamin D deficiency and defective mineralization. Bone growth is severely impacted, but other matrix is healthy.

Bone pain, bone brittleness, abnormal development.

Osteomalacia in children is called "Rickets".



What is the cause & pathophysiology?

What are its symptoms?


Defect in sclerostin results in defective osteocytes, which have abnormally high signaling for bone deposition.

Bone deposition results in nerve entrapment (facial palsy, deafness) and occasionally syndactyly.



What is the cause & pathophysiology?

What are its symptoms?

How might it be treated?


Abnormal osteoclasts cannot cause resorption. Unopposed bone deposition leads to thick (but brittle) bones and marrow crowding.

Anemias, nerve entrapment, frequent fractures.

Bone marrow transplants will provide healthy macrophages (and thus osteoclasts).


Paget's Disease of Bone

What is the cause & pathophysiology?

What are its symptoms?

How is it treated?

Paget's Disease of Bone

Overactivity of both osteoblasts and osteoclasts causes excessive bone resorption.

Pain, neurological symptoms, and bone abnormalities. Increased alkaline phosphatase. 

Bisphosphonates, calcitonin.


What are the 4 phases of Paget's disease?

(not discussed in lecture)

1. Lytic (too much osteoclast)

2. Mixed (osteoblast increases)

3. Sclerotic (osteoclast decreases)

4. Quiescent (osteoblast declines)