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4th Yr - CMS 1 > Bone and Joints 1 > Flashcards

Bone and Joints 1 Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

What are the three main types of bone tissue?

A

cortical
cancellous
woven

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2
Q

what is cortical bone?

A

Dense and compact bone tissue, forming the outer shell of bones.
- its formed of concentric rings of bone which is adapted to withstand the strain of pressure

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3
Q

what is cancellous bone?

A

Also known as trabecular or spongy bone, it is less dense and more porous than cortical bone.
- has interconnecting network of rods and plates of bones
- allows for the resistance and compression loads
- main site of turnover for mineral homeostasis
- found inside flat bones and at the end of long bones

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4
Q

what is woven bone?

A

Immature bone tissue that is temporary and later replaced by more mature lamellar bone.
- more disorganised
- appears in early stages of bone or at fracture sites
- present in pagets or diseases with high bone turnover

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5
Q

what are the 3 major components of bone tissue?

A

type 1 collagen
non collagen protiens
bone mineral

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6
Q

what is type 1 collagen?

A
  • main protein that forms parallel lamella = offers different densities
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7
Q

what is non collagen protein ?

A

eg. osteocalcin, fibronectin, ostepontin
Various proteins other than collagen that contribute to the structure and function of bone.

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8
Q

what are bone minerals?

A
  • consist of Ca and phosphate which is in the form of HAP
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9
Q

what are osteoblasts ?

A

Bone-forming cells that synthesize and secrete the organic components of the bone matrix. they also regulate mineralisation

derived from local mesenchymal stem cells

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10
Q

what are the 2 pathways after the formation of osteoblasts ?

A
  1. apoptosis
  2. or they will line the bone at osteocytes
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11
Q

what are osteoclasts ?

A

regulate bone resorption
- rich in ARP
- express receptors for PTH, oestrogen and glucocorticoids, vit d, inflammorry cytokines and TGF beta = all these influence bone remodelling

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12
Q

what are osteocytes ?

A
  • derived from osteoblasts
  • they activate bone formation by responding to mechanical strain so have a key role in bone resorption
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13
Q

what 3 things affect bone formation, metabolism and blood calcification ?

A

PTH
vit D
calcitonin

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14
Q

what do bone morphogenic protein (BMP) affect?

A

bone formation

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15
Q

what are BMP available as and used for?

A

-available as recombine proteins
- used for grafting/regenerative procedure, in oral surgery

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16
Q

what is the PTH regulated by?

A

blood calcium, vit D and phosphate levels

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17
Q

what happens when PTH is secreted ?

A

intestinal transport of phosphate promoted
and removal of ca from bones is
accelerated.

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18
Q

how is dietary vit D absorbed ?

A

its fat solvable
-absorbed from upper small intestines which promotes intestinal absorption of Ca and P

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19
Q

how is vit D synthesised ?

A

in the skin due to sunlight and converted via liver and then in kidney to the most active metabolite . Process enhanced by PTH and low Phosphate levels.

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20
Q

what does the most active metabolite of vit d do?

A

controls bone and enhances Ca absorption

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21
Q

what is the role of calcitonin?

A

opposes action of PTH and lowers blood Ca levels by promoting deposition of Ca in bones
- other hormones effect formation and metabolism:growth hormone + oestrogen.

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22
Q

bone growth

A
23
Q

stages of fracture healing

A
24
Q

what are the different types of bone disease ?

A

Genetic =osteogenesis imperfecta, cleiodocranial dysplasia, osteopetrosis

Acquired = osteomalacia, osteoporosis, fibrous dysplasia, pagets, primary and secondary hyperparathyroidism
Joint Disorders
Arthritides
Muscular dystrophies

25
Q

what is osteogenesis imperfect ? signs and symptoms

A
  • Rare
  • Autosomal dominant
  • it is a Collagen defect- Types I-IV = the vary in severity
  • AKA brittle bone disease
  • Blue sclera
  • Deafness
  • Brusing easily
  • Loose joints/tendons
  • +/- cardiac complications
  • Short stature
  • Multiple fractures easily
26
Q

what are some dental considerations of osteogenesis imperfecta?

A

Care with extractions - fracture risk
GA risk - chest deformity / cardiac issues
Teeth - disorder in dentition brown/purple/wear/soft dentine

27
Q

what is cleiodocranial dysplasia ? signs and symptoms?

A

Rare defect - mainly involving skull and clavicle- shoulders pointing forwards
Autosomal dominant

Clinically
Clavicles absent or defective - charateristic look Brachycephalic (broad short skull)
Hypoplastic midface = set back
mandibular protrusion= class 3
+/- clefts
Other skeletal defects

28
Q

what are some dental considerations of cleidocranial dysplasia?

A

Hyperdontia
Supernumeraies
Retained deciduous dentition
Abnormalities with dentition e.g root formation, cysts etc.

29
Q

what is osteopetrosis?

A

Rare disorder
Variabel severity
Excessive bone densitry
Defect in osteoclastic activity and bone remodelling
Although bones are more ‘dense’ - risk of fracture but normal healing
may be anaemic

30
Q

what are some dental considerations of osteopetrosis?

A

Often no symptoms
Incidental finding radiographically
Bone pain, fractures, osteomyelitis
+/- anaemia
susceptibility to infections (defective marophages neutrophils) - risk of sepsis
beware of post op = osteomyelitis, jaw fractures
When infection confirmed difficult to irradicate
‘atraumatic’ surgery
consider antibiotics for surgery

31
Q

what is osteomalacia/ rickets?

A

childhood disease,
inadequate skeletal mineralisation due to lack of vitamin D / calcium
- vitamin D from sunlight, foods (oily fish and eggs)
recent increase in UK - still low numbers
worse in dark skin and premature children
Tx - vitamin supplements and dietary advice

32
Q

what are some dental considerations of osteomalacia ?

A

Rare to see dental effects
If malabosprtion diagnosis - nb radiolucencies and hyperparathyroidism/vit K deficiency

33
Q
A
33
Q

what is osteoporosis?

A

Diminised bone mass
Low bone density
Causes fragile bones
Elderly
menopausal
asymptomatic until they have a fracture

34
Q

what are some risk factors with osteoporosis ?

A

Calcium intake
Reproductive hormones
Parathyroid gland
Physical activity
From 30 years - 1% bone loss per year Post menopausal - 5% loss per year
1 in 3 caucasian women, 50yo - 17.5% risk hip fracture, 16% risk foremar fracture

35
Q

what are some symptoms of osteoporosis?

A

often none in the early stages then maybe back pain, reduced height (over time), stooped posture, fracture unexpected

Rx Hormone replacement, bisphosphonates, PTH, fluoride, Vitamin D, Calcitonin

36
Q

how do we investigate and manage osteoporosis?

A

Investigations / Diagnosis
FRAX tool DEXA scan

Management
Avoidance Exercise - weight bearing
Ca and Vit D supps +/- HRT Bisphosphonates

37
Q

mechanism of bisphosphonates?

A
38
Q

what is fibrous dysplasia?

A
  • Benign chronic fibro-osseous lesiosn
  • Frequent in the craniofacial region
  • Monostotic or Polystotic Single bone or multiple
  • common in afrocarribean

Chronic disorder Scar-like tissue grows in place of normal bone Fibrous tissue weakens the bone over time

Ix Radiology - ground glass appearance, poorly defined margins Raised serum ALP and Urinary hydroxyproline (Serum Ca and Po normal)
If significant can be surgically reduced - can bleed a lot during GA

Associated Syndromes:
- McCune Albright Syndrome: Some cases may be associated with McCune Albright Syndrome, which involves abnormalities in bone, skin, and endocrine tissues.

39
Q

what is pagets disease?

A

Common
3% over 40 years
Causes changes in balance of remodelling of bone Aetiology generally unknown ?
viral / genetic

40
Q

what is the clinical presentation of pagets ?

A

Patients often experience bone pain. Systemic symptoms may include various manifestations (see table).

41
Q

how do we investigate and diagnose pagets ?

A

Radiographs: including osteolysis, mixed areas of lysis, and sclerosis.
- Biochemical Markers:
+ Serum alkaline phosphatase (ALP) is typically elevated, while calcium (Ca) and phosphate (PO) levels remain normal.
+ Raised urinary hydroxyproline and pyridinoline excretion may be observed.

42
Q

what happens if pagets becomes widespread?

A

-causes arterial venous fistula casing high output cardiac failure
- lead to osteosarcomas

43
Q

whats the tx for pagets?

A
  • Bisphosphonates
  • Calcitonin: Calcitonin may be used for pain relief.
44
Q

How does Paget’s Disease manifest in terms of dental aspects?

A

may lead to enlargement of the maxilla, and less commonly, the mandible.
- Zygomatic Bulging: Bulging in the zygomatic area can occur.
- Hypercementosis: Hypercementosis of teeth may sometimes be observed

45
Q

what are the associated risks during surgery?

A

Surgery may pose risks related to vascularity, leading to either high vascularity causing bleeding or poor vascularization, increasing the risk of osteomyelitis.

46
Q

Where are the parathyroid glands located, and what is the primary target organ for the hormones they produce?

A

The parathyroid glands are four small glands situated on the posterior surface of the thyroid gland.

The hormones produced by the parathyroid glands primarily act on the kidneys.

47
Q

What is hyperparathyroidism?

A

excessive production of parathyroid hormone (PTH).

48
Q

what are the characteristics of primary hyperparathyroidism?

A
  • female preponderance and is typically associated with a single parathyroid adenoma.
  • Symptoms: About 50% of cases are asymptomatic, but symptoms may include hypercalcemia, bone pain, pathological fractures, giant cell tumors, peptic ulcers, pancreatitis, and hypertension.
  • Association: frequently associated with renal stones.
49
Q

What are the symptoms and characteristics of primary hyperparathyroidism, particularly in the context of bone lesions and dental aspects?

A

-local swelling, sometimes in the mandible.
- corneal calcification.
- Subperiosteal resorption may occur at the fingertips.
- X-ray findings may show thinning of bone trabeculae.
- Osteitis Fibrosa Cystica: This condition involves fibrous replacement of resorbed bone.
- :Bone lesions occur in 10-20% of cases and may affect the jaw and skull. A “pepperpot skull” appearance may be observed on imaging.

50
Q

tx for primary hyperparathyroidism

A

Surgical removal of the adenoma is a common treatment approach.
- Postoperative issues may include hypocalcemia.
- maybe on Ca supplements

51
Q

What characterizes secondary hyperparathyroidism?

A

Cause: Parathyroid hyperplasia occurs in response to persistently low calcium levels, often due to chronic renal failure or malabsorption.
- Bone lesions are more common in secondary hyperparathyroidism compared to primary hyperparathyroidism.

52
Q

what are some of the dental aspects of secondary hyperparathyroidism?

A
  • Giant cell lesions are uncommon and tend to present late in secondary hyperparathyroidism.
  • Brown Tumours: These are a characteristic feature associated with bone involvement.
  • In middle-aged patients with renal issues, suspicion of parathyroid issues may arise if giant cell lesions are present.
  • Patients with secondary hyperparathyroidism may have other systemic issues like renal disease, requiring careful consideration in dental management.

4th Yr - CMS 1 (27 decks)

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