MSK Week 3 Objective 16

- Thin trabeculae
- 2D appearance of isolated islands (not connecting to network of trabeculae)
- +/- cortex with large osteons

- unmineralized osteoid
- increased # osteoclasts
- "swiss cheese" cortex
- trabecular cutting cones
- peritrabecular fibrosis

- thick later of unmineralized osteoid on trabeculae
- centres still mineralized
- Cortex thin but thick layer of periosteal osteoblasts
- Rickets: widened growth plate

1. Osteolytic (osteoclasts, howship lacunae, thin trabeculae)
2. Mixed (osteo clasts and blats, fibrovascular tissue, some woven bone)
3. Osteosclerotic (osteoblasts, mosaic lamellar bone)

- marrow replaced by sheets of plasma cells
- +/- amyloid deposition

- high grade malignant cells
- production of atypical osteoid
- +/- admixed chondroid and fibrous areas

Softening of bone due to loss of minerals (demineralization), most notably calcium from bone. Osteomalacia may be caused by poor dietary intake of calcium, or by poor absorption of calcium and other minerals needed to harden bones. Osteomalacia is a characteristic feature of vitamin D deficiency in adults (Rickets disease in children).

High levels of PTH lead to increased bone resorption, leading to Osteitis fibrosa cystica. OFC can show extremely thin bones, bowing of those bones, fractures, and cysts.

- Primary hyperPTH (tumors)
- Secondary hyperPTH (renal)

Renal osteodystrophy is thought to be the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcaemia, both of which are due to decreased excretion of phosphate by the damaged kidney. Low activated vitamin D3 levels are a result of the damaged kidneys' inability to convert vitamin D3 into its active form, calcitriol, and result in further hypocalcaemia and hyperphosphatemia.

Loss of control and coupling of osteoclast and osteoblast activity. It is a chronic disorder that typically results in enlarged and deformed bones.

Plasma cell myeloma (aka mutiple myeloma)

Osteosarcoma (aka osteogenic sarcoma)