what is intramembranous ossification? where does it begin and where does it occur?
Definition: bone forms without a cartilage model.
It begins with mesenchymal (stem) cells which differentiate into osteoblasts within embryonic or fibrous connective tissue
Occurs in deeper layers of the dermis
what is the name of bones that form without a cartilage model? can you give examples?
Bones called dermal bones or membrane bones AKA ones that go under intramembranous ossificaiton
examples:
- skull roofing bones
mandible(lower jaw)
clavicle
sesamoid bones (patella)
explain step 1 of intramembrous ossification
- Mesenchymal cells closure
- These differentiate into osteoblasts
- Osteoblasts secrete osteoid (unmineralized mix)
- Osteoid mineralize to form the bone matrix
Location: ossification center
explain step 2 of intramembrous ossification
Step 2 - Bone Spicules Form
- Bone grows outward as spicules (small struts)
- Osteoblasts become trapped into pockets and then turn to osteocytes
- Mesenchymal cells produce more osteoblasts
explain step 3 of intramembrous ossification
Step 3 - Vascularization
1. Blood vessels invade area
2. Spicules fuse
3. Blood vessels become trapped inside developing bone
explain step 4 of intramembrous ossification
Step 4 - Spongy Bone Formation
1. Osteoblasts continue to deposit bone close to the blood vessel
2. This results in spongy bone with interwoven blood vessels
explain step 5 of intramembrous ossification
Step 5 - compact bone + periosteum
1. Remodeling around blood vessels produce osteons of compact bone
2. Connective tissue around bone organizes into fibrous layer of periosteum
3. Osteoblasts near the bone surface remain as the cellular layer of the periosteum
explain step 6 - the devellopment timeline of intramembranous ossification
Step 6 - development timeline
1. Begins roughly at week 8 of embryonic development
2. Ossification centers are visible at 10 weeks
3. By 16 weeks, most bones are identifiable
what are the two disorders that cause short bones?
- pituitary growth failure and
- Achondroplasia
EXPLAIN why pituitary growth failure occurs and if its common today or not
- The growth hormone (GH) is inadequate in production
- There is low epiphyseal cartilage activity, causing abnormally short bones
- Rare today due to the synthetic GH therapy
explain achondroplasia and the results of it
Epiphyseal cartilage grows VERY slowly causing it to be replaced by bone early in life
The results are:
- Short, stocky limbs
- Trunk being normal in size
- Normal mental + sexual development
what are disorders that cause LONG bones
- marfan syndrome and
- gigantism
explain what marfan syndrome is and its results
Genetic connective tissue disorder/inherited metabolic condition
Excess cartilage formation at the growth plates/epiphyseal cartilages
Results:
Very tall, long slender limbs
Affects other connective tissues throughout the body and can cause cardiovascular problems
explain gigantism and its treatments
Gigantism
- EXCESS GH before puberty
- Long bones keep growing, often due to a pituitary tumor (much like achondroplasia)
- Can reach 2.7 meters/8 feet 11 inches
Treated by surgery, radiation, and GH suppression medicaiton
what are other skeletal abnormalities?
clubfoot (talipes equinovarus), Fibrodysplasia ossificans progressiva (FOP) and Acromegaly
explain clubfoot (talipes equinovarus) and who it affects as wel as what its treated with
- Inherited developmental abnormality
- Feet turn inward/inverted
- Affects 2 in 1000 births, boys roughly twice as often as girls
- This occurs due to abnormal muscle development and distorts growing bones
- Treated with casts or supports
explain fibrodysplasia ossificans progessiva
- Gene mutation that causes bone deposition around skeletal muscles) (bones form in soft tissues and unusual places)
- Called heterotopic (hetero, place) or ectopic (ektos, outside) bones
- No effective treatment
explain acromegaly and what it does
acromegaly causes overproduction of GH after epiphyseal cartilage/growth plates close
- Bones become thicker, not longer
- Affects the face, jaws, and hands
- Also soft tissue enlargement/alterations changes physical structures
whats the main difference between gigantism and acromegaly
Gigantism = length increase
Acromegaly = thickness increase
tell me about calcium in the body, its fucntions, and importance
Calcium facts:
Most abundant mineral in the body
1-2kg total
99% stored in skeleton
Functions:
Muscle contraction
Blood clotting
Nerve impulses
Important:
Large calcium changes (greater than 30-35 percent)→ affect neurons and muscles
Also, Normal daily fluctuations are less than 10 percent
name the minerals and vitamins that are nutritional factors for bone growth and explain what each do
Minerals:
Calcium + phosphate → hydroxyapatite crystals (Ca₁₀(PO₄)₆(OH)₂) and theres major salt found (phosphate salts)
Vitamins:
Vitamin A → stimulates osteoblast activity
Vitamin B12 and K → required for protein synthesis
Vitamin C → required for key enzymatic reactions in collagen synthesis and stimulates osteoblast differentiation
Vitamin D/cholecalcitriol
- Vitamin D3 is a precursor cell
- Calcitriol hormone is synthesized in the kidney
Its function is essential for normal calcium and phosphate ion absorption in the digestive tract
- Can be synthesized in the skin or absorbed in diet
- Vitamin D3 deficiency leads to rickets in children and osteomalacia in adults
what are factors that increase blood calcium levels, what secretes it, and whats the response
Factors that increase blood calcium levels
– Parathyroid hormone (PTH)
▪ Secreted from parathyroid glands
▪ Responses
– In bones:
* Osteoclasts stimulated to erode matrix, releasing stored calcium
explain the effects when calcium is low (below 8.5mg/dl) in bone, intestine and kidneys
PTH – raises Blood Calcium
PTH releases when calcium is LOW (below 8.5mg/dl)
Effects:
Bone:
Stimulates osteoclasts which allow for bone resorption and Ca is released (since osteoclasts don’t have PTH receptors, so the PTH binds to the adjacent osteoblasts, which causes them to release hormone RANKL which stimulates immature osteoclasts to differentiate into mature osteoclasts and then erode the bone matrix, releasing stored calcium ions)
Intestine:
Enhances the calcium absorbing effects of calcitriol – > calcium absorption increased
Kidney:
More calcitriol production, more calcium reabsorption, and allows for more calcium absorption in the intestines (PTH increases renal production of the calcitriol hormone. Normal circumstances means a low level of calcitriol is present because its being continuously secreted by the kidneys)
this all increases blood Ca
what are factors that DECREASE blood calcium levels, what secretes it, and where is it found and whats its response
- Factors that decrease blood calcium levels
– Calcitonin
– Secreted from C cells in the thyroid gland
– Responses
▪ In bones:
– Osteoclast activity inhibited; calcium deposited in bone matrix
▪ In intestines:
– Calcium absorption decreased with decreasing PTH and calcitriol
▪ In kidneys:
– Inhibits calcitriol release and calcium reabsorption
