Pathophysiology - Exam V: Osteoporosis and Osteomalacia

what types of cells are in the bone marrow? (2)

mesenchymal stem cells

hematopoietic stem cells

what do mesenchymal stem cells mature into?

osteoprogenitor → osteoblasts

what do hematopoietic stem cells mature into?

monocyte precusor → (needs RANKL) → osteoclast

what are the two parts of an osteon?

haversain canal (contains blood vessels and nerves)

lammellae (made of collagen and hydroxyapatite (Ca2+ phosphate matrix)

Explain the physiology of bone remodeling

1. osteoblast recognizes damage

2. osteoblast secretes RANKL which binds to monocyte precursor

3. monocyte precursor cell differentiates into osteoclast

4. osteoclas secretes collagenase (breaks down collagen) and HCl (breaks down hydroxyapatite and Ca2+ enters the blood stream

5. osteoblast secretes osteoprotegerin which binds to RANKL to prevent RAKL signal to monocyte precursor cell

6. osteoclasts go through apoptosis

7. osteoblasts secrete osteoid seam (mainly made of collagen)

8. calcium and phosphate stick to osteoid seam reforming hydroxyapatite

Parathyroid Hormone (PTH)

parathyroid recognizes low Ca2+ levels in blood, secretes PTH which stimulates RANKL secretion, causing more bone consumption via osteoclast

Calcitonin

thyroid recognizes high Ca2+ levels in blood, secretes calcitonin, causing decreased activity of osteoclast, therefore less Ca2+ enters blood stream

Vitamin D

increases Ca2+ absorption in intestines, therefore more Ca2+ absorption in intestines, therefore more Ca2+ in blood, meaning less of a need for PTH

estrogen

inhibits osteoclast activity

osteoporosis

decrease in bone mass density due to imbalance of ostoclast/osteoblast activity

both lead to widening of haversian canal and less trabeculae

postmenopausal osteoporosis

due to low level of estrogen, there is an increase in osteoclast activity

senile osteoporosis

due to aging, hypothesized that osteoblasts lose their ability to reform bone

osteomalacia

inability for body to mineralize bone (soft bone disease)

due to lack of calcium, phosphate, and/or vitamin D

less minerals in the blood which leads to inability of hydroxyapatite to form properly