Bones and joints Flashcards

1
Q

What is the composition of bone

A

Non-cellular matrix:
ECM: type 1Collagen associated with calcium hydroxyapatite , regulatory proteins & growth factors

Cellular matrix:
- Osteoblasts, osteocytes, osteoclasts

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2
Q

What is the function of bone?

A

-Protection
-Haematopoesis
- support
-Lipid and mineral storage

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3
Q

What is the function of osteoblasts

A

Secrete uncalcified/ unmineralised extracellular matrix (known as osteoids) which is later mineralised

  • regulate bone resoprtion: rich in APL
    -Synthesis matrix
  • express receptors for PTH, Glucortocioids, vit D, Oestrogen (influence remodelling)
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4
Q

What is an osteoid

A

Unmineralised extracellular matrix

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5
Q

What is an osteocytes function

A

Osteoblast that is entomed in lamella in lacunae- mineralises osteoids

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6
Q

What is the function of osteoclasts

A

Monocyte derivatives, resorb bone via secretion of H+ and lysozyme enzymes

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7
Q

What are the phases of bone formation

A

Woven:
- embryo/ fracture
- full of osteoids (unmineralised ecm)
- collagen randomly arranged

Lamella:
- Compact/ spongy

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8
Q

What is meant by ‘Compact bone’

A

Type of lamella bone
- dense rigid
- found in outerbone

Contains:
Haversian canal- nerve & lymphatic vessels

Volkmans canal- Horizontally connected- transmit blood

Cannalculi = osteocytes between laemalla and connect by interconnecting tunnels

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9
Q

What is meant by spongy bone

A
  • interior of bone
  • Honeycomb texture
  • Light and porous
  • non structural fill
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10
Q

How are osteoblasts activated

A

hormone/ damage

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11
Q

What affects bone formation

A
  • PTH
  • Vitamin D
  • Calcitonin
  • (BMP) Bone morphogenic proteins
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12
Q

What is the effect of PTH

A

Regulated by blood calcuium, vitamin D and phosphate levels

  1. Increases intestinal transport of CA & phosphate
  2. Removal of calcium from bone
  3. Increases absorption of vitamin D in upper small intestine
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13
Q

What is the role of calcitonin

A

Opposes action of PTH
-Lowers blood calcium levels
- deposits calcium in bones

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14
Q

What are the stages of fracture healing

A
  1. Fracture: inital haematoma: formed with granulation tissue- results in inflammation causing immune response
  2. Proliferation stage: macrophages move in and devour debris & dead cells
  • proliferation of fibroblasts
    -differenation of osteoclasts and osteoblasts

3.Bone callus: primary callus, osteoids replace with mature bone & becomes mature callus (6 weeks- 3months+) new bone is liad down along lines of stress,

  1. Remodelling:
    reduces size of bone callus, bone ends rejoin so now a whole bone
    - bone marrow cavity is restored, new bone is laid down along lines of stress
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15
Q

What is osteogenesis imperfecta & signs and symptoms

A

Autosomal dominant
collagen defect (affect 1-5)

signs & symptoms:
- blue sclera, bruising easily, deafness, loose joints/ tendons
- +/- cardiac complications
- short stature
- multiple fractures

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16
Q

How does osteogenesis imperfecta affect dentistry

A
  • Caution with XLA
    -GA risk: chest defomity/ cardiac issues
  • Brown/ blue/ pruple/ soft dentine teeth
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17
Q

What is cleidocranial dysplasia & its presentations

A

Autosomal domiant- defect of skull & clavicle

Presentations:
- clavicles absent/ defective
- brachycephalic: broad short skull
- hypoplastic midface: mandibular protrusion
- +/- clefts

18
Q

How does cleidocranial dysplasia affect dentistry

A
  • Hypodontia
  • supernumeraries
    -Retained decidious dentition
  • abnormaltieis with dentition: root formation, cysts
19
Q

What is osteopetrosis & how does it present

A

Excessive bone density due to defect in osteoclastic activity & remodelling
- risk of fracture for bones but normal healing

clinical presentations:
- incidental radiographically
-bone pain, fractures, osteomyelitis
- +/- anaemia
- susceptible to infections : RISK OF SEPSIS

20
Q

How does ostepetrosis affect dentistry

A
  • fractures of jaw
  • osteomyelitis (surgical complications)
  • if infection confirmed it is difficult to eradicate
    -consider abx
21
Q

What is rickets

A

acquired childhood disease due to lack of vitamin D/ calcium:

  • fish & eggs
22
Q

How does rickets affect dentistry?

23
Q

What is osteoporosis
- How is it diagnosed

A

Demineralised bone mass
Low bone density
Results in fragile bones

affects: 1 in 3 women

diagnosed: FRAX tool, DEXA scan

24
Q

What are the signs and symptoms of osteoporosis

A

asymptomatic until fracture- back pain, reduced height overtime with stooped posture

25
How does osteoporosis affect dentistry
Patients are on bisphosphonates- risk of MRONJ - Pt weaker bones fractures
26
How is osteporosis managed
Exercise Ca, Vit D supplements HRT +/- Bisphosphonates Medications: hormone replacement, bisphosphonates, PTH, fluoride, vitamin D, calcitonin
27
What is the mechanism of bisphosphonates
1. Attach to hydroxyapatite binding sites Particularly on surfaces that are actively resorbing 2. Impairs osteoclastic ability to bind to the bony surface & inhibit resorption - Reduce osteoclast activity by promoting osteoclast apoptosis & inhibit new osteoclast developing
28
What is fiborous dysplasia
benign, chronic fibro-osseous lesions in craniofacial region - monostoic/ polystoic - chronic disorder: scar tissue grows in place of normal bone - fiborous tissue weakens bone overtime Linked with Albrights syndrome: bone, skin, endocrine tissues
29
How does a pt with fibrous dysplasia present & how is it diagnosed
Firm swelling in maxilla Diagnosis: Imaging: appear dense ground glass, poorly defined margins raised APL & urinary hdroxyproline biospy
30
What is pagets disease
Common in 40 years old, unknown aetiology, change in balance of remodelling of bone
31
What are the signs and symptoms of pagets disease & how is it diagnosed
Bone pain, no symptoms in early stages, systemic effects - Enlargement of maxilla -bulging zygomatic area - hypercementosis of teeth Diagnosis: radiographs shows lysis and sclerosis - raised ALP - normal Ca, PO
32
What is the tx for pagets disease
bone bisphosphonates - calcitonin: pain relief
33
What are the systemic effects associated with pagets disease
Musculoskeletal: - bone pain, bone deforbity, fractures, osteoarthritis, spinal stenosis Neurological: Tinnitus, cranial nerve, basilar impressions, hearing loss, cardiovascular: - congestive heart disease, increase CO, aortic stenosis, generalised atheroscleoriss metabolic: hypercalcaemia, immboilsation neoplasia: - sarcoma, giant cell tumour
34
How does PTH work
- acts on kidneys : increases renal reabsorption -reabsorption of phosphate - increases absoprtion of calcium in gut - promote osteoclastic bone resoprtion: rise in calcium plasma levels & ALP
35
What is primary hyperparathyroidism
too much PTH - associated with adenoma
36
What are the signs and symptoms of primary hyperparathyroidism
- Associated with renal tones - Hypercalcemia - Bone pain - Fractures -Pathological fractures -Giant cell tumours -peptic ulcers - pancreatitis - hypertension
37
How does hyperparathyroidism affect the hesd and neck
- Local swelling in mandible - corneal calcification - thinning bone trabeculae - Develop bony lesions - jaw/ skull lesions - pepperpot skull - fibrous replacement of reabsorbed bone- osteitis fibrosa cystica
38
What is the tx for hyperparatyrodisim
Surgical removal of adneoma post-op issue with hypocalcemia
39
What is secondary hyperparathyroidism caused by
Response to persistently low calcium: - chronic renal failure - malabsoprtion
40
How does secondary hyperparathyroidism affect dentistry
- Giant cell lesions - Brown tumourd -GC lesions - Other systemic issues