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Module 5 - Bone Biology > Bisphosphonates > Flashcards

Bisphosphonates Flashcards

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1
Q

What are the 2 functions of bone remodeling?

A
  • Allows repair of fractures, microfractures, infections and inflammations.
  • Allows replacement of old BRITTLE BONE (less resilient + elastic).
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2
Q

What is bone a reservoir for?

A

Calcium and phosphate

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3
Q

What are the 7 hormones that regulate bone remodelling?

A

Parathyroid hormone, calcitonin, vitamind D (calcitriol), sex hormones, growth hormones, thyroid hormone, cortisol.

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4
Q

What is another name for the vitamin D hormone?

A

calcitriol.

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5
Q

What are osteoblasts derived from?

A

Derived from MESENCHYMAL CELLS in the bone marrow, recruited via BLOOD SUPPLY.

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6
Q

What are osteoclasts derived from?

A

Derived from WBCs (mast cells and macrophages) – join to form multi-nucleated giant cells with rough border, live in lacunae and resorb bone.

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7
Q

Where do osteoclasts live?

A

lacunae

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8
Q

What are the 5 steps of bone remodelling?

A
  1. Activation.
  2. Osteoclast recruitment and resorption.
  3. Reversal.
  4. Osteoblast recruitment and bone formation.
  5. Termination - quiescence.
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9
Q

What are osteocytes? Where do they live?

A

Osteoblasts stuck in the mineralized matrix. Live in Haversian systems.

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10
Q

What are two types of genetic bone abnormalities?

A
  • Osteogenesis imperfecta.
  • Osteopetrosis.
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11
Q

What is osteogenesis imperfecta?

A

Affects the WHOLE skeleton (ex. thin, narrow mandible), defect of COLLAGEN FORMATION.

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12
Q

What is osteopetrosis? What is another term for this?

A

defect of OSTEOCLASTIC BONE RESORPTION, also called MARBLE BONE DISEASE as bone has increased density.

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13
Q

What would be a dental finding in patients with osteogenesis imperfecta?

A

Thin, narrow mandible.

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14
Q

What would be a dental finding in patients with osteopetrosis?

A

Teeth fail to erupt/ impacted teeth.

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15
Q

What is osteoporosis?

A

Loss of BONE VOLUME, makes more brittle and prone to fracture.

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16
Q

What are two examples of metabolic bone diseases?

A

Fibrous dysplasia, paget’s disease.

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17
Q

What are 8 abnormalities of bone?

A
  • Genetic (osteogenesis imperfecta, osteopetrosis).
  • Osteoporosis.
  • Paget’s disease.
  • Fibrous dysplasia.
  • Glucocorticoid- induced osteoporosis.
  • Hypeparathyroidism.
  • Localized (inflammatory, infective).
  • Drug induced.
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18
Q

What are the 2 types of localized bone abnormalities, give examples.

A
  • Infective: periodontal disease.
  • Inflammatory: rheumatoid arthritis.
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19
Q

What is the process of sequestered bone?

A
  • Inflammatory process secondary to infection
  • Piece of bone die
    Body mounts acute inflammatory response to mobilize the piece of dead bone through the mucosa OR it is osteoclastically resorbed.
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20
Q

What happens after extraction?

A

Osteoclastic bone resorption.

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21
Q

Where does the greatest amount of bone loss occur following extraction?

A

HORIZONTAL dimension, mainly on the labial/ buccal/ facial aspect.

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22
Q

What type of bone loss is seen following extraction.

A
  • Mostly HORIZONTAL bone loss on buccal aspect.
  • VERTICAL bone loss on buccal aspect.
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23
Q

How does resorption following extraction affect ridge shape?

A

NARROWER, SHORTER ridge that is more PALATALLY/ LINGUALLY placed.

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24
Q

How long does the remodelling process last?

A

6 MONTHS.

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25
Q

What should be done in terms of denture provision if extractions have just been undertaken?

A
  • Provide TRANSITIONAL replacement until 6 months have elapsed, then give DEFINITIVE after resorption has become STATIC.
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26
Q

Name the 4 main drug types that affect bone remodelling.

A
  1. Bisphosphonates.
  2. Denosumab + antiangiogenic drugs.
  3. Steroids.
  4. NSAIDs.
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27
Q

What are bisphosphonates?

A

Non-metabolized ANALOGUES OF PYROPHOSPHATE.

  • Inhibit osteoclast function (ANTIRESORPTIVE) + antiangiogenic.
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28
Q

Where are high levels of bisphosphonates found?

A
  • Bind to exposed bone mineral around resorbing osteoclasts thus HIGH LEVELS IN RESORPTION LACUNAE.
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29
Q

What is the half life of bisphosphonates?

A

Not metabolized thus very long half life - TEN YEARS.

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30
Q

What are the 2 classes of bisphosphonate drugs? Name an example.

A
  • Non nitrogen containing, clodronate.
  • Nitrogen containing, alendronate.
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31
Q

How do non-nitrogen containing bisphosphonates work? Named example.

A

Resemble pyrophosphate, incorporate themselves into phosphate chain of ATP, makes ATP UNUSABLE for energy production in osteoclasts.

Clodronate

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32
Q

How do nitrogen-containing bisphosphonates work? Named example.

A

Block enzyme FARNESYL DIPHOSPHATE SYNTHASE thus prevention formation of ISOPRENOID LIPIDS in osteoclasts. Thus CANNOT ANCHOR PROTEINS TO CELL MEMBRANE and CELL DEATH.

Alendronate.

33
Q

What enzyme do nitrogen containing bisphosphonates block?

A

Farnesyl diphosphate synthase.

34
Q

How do patients with osteoporosis take bisphosphonates?

A
  • Tablet once a week.
  • UPRIGHT because acidic.
35
Q

Patient says the have a DEXASCAN. What does this measure and what drug could they be on?

A

Determines bone volume, patient may be on BISPHOSPHONATES.

36
Q

What type of malignancy do bisphosphonates treat? How do patients with malignancy take bisphosphonates?

A
  • Metastatic malignancy to bones (ex. breast cancer) or primary bone cancers (ex. multiple myeloma).
  • IV bisphosphonates.
37
Q

Who is considered a LOW RISK bisphosphonate patient?

A
  • Not yet started bisphosphonates.
  • Taking bisphosphonates for the prevention or management of osteoporosis.
38
Q

How is a low risk bisphosphonate patient managed?

A

i. If unavoidable then atraumatic extractions (suggested to avoid LA with high dose of vasoconstrictor), avoid raising flaps, achieve good haemostasis.
ii. Review at 4 weeks.
iii. If not healing at 4-6 weeks then refer to oral/ maxillofacial surgeon.
iv. There is no evidence for antibiotics or topical antiseptics.

39
Q

What is the cutoff for bisphosphonate administration that determines if low/ high risk?

A
  • Less than 5 years = low risk.
  • More than 5 years = high risk.
40
Q

What is the cutoff for denosumab administration that determines if low/ high risk?

A

NO CUTOFF.

41
Q

Name 6 characteristics that would make a patient taking bisphosphonates high risk of MRONJ.

A
  • Previous MRONJ.
  • Treating malignant condition.
  • Non malignant abnormality of bone (ex. Paget’s disease).
  • Rare condition (ex. osteognesis imperfecta).
  • Concurrent use of systemic steroids/ other immunosuppresants.
  • Coagulopathy, chemotherapy, radiotherapy.
42
Q

What is the management of high risk bisphosphonate patients?

A

i. Contact oral/ maxillofacial surgeon for advice whether case should be treated in primary care or whether referral appropriate.
ii. Included full details of medical and dental history by letter (Duration they are on it, dose, reason they are on it (malignant disease, osteoporosis).

43
Q

What are the 3 MRONJ criterias?

A
  • Current or previous treatment with bisphosphonates, antiangiogenic drugs or RANKL inhibitors.
  • Exposed bone in the maxillofacial region or bone that can be probed/ has for MORE THAN 8 WEEKS.
  • No history of RADIATION TO THE JAWS.
44
Q

What duration is considered normal physiological healing following extraction?

A

8 weeks.

45
Q

9 symptoms of MRONJ.

A
  • EXPOSED, NECROTIC BONE: creamy color, does not bleed.
  • Pain (can be painless).
  • Mobile teeth.
  • Dysesthesia
  • Paresthesia
  • Anaesthesia
  • Internal or external discharging fistulas.
  • Bone sequestrate.
  • Mandibular preference.
46
Q

What is a bone sequestrate?

A

piece of necrotic bone.

47
Q

What is paresthesia

A

altered sensation ex. pins and needles.

48
Q

What is dysesthesia?

A

Abnormal intense pain sensation

49
Q

What is anesthesia?

A

complete numbness

50
Q

Does MRONJ occur more in the maxilla or mandible and why.

A

MANDIBLE (60-70%).

Maxilla has better vasculature, mandible is more predisposed to all forms of necrosis of the jaw (MRONJ, RRONJ).

51
Q

What is the best management for established MRONJ?

A

CONSERVATIVE - patience and symptomatic management (analgesia, sequestrectomy).

52
Q

What is a sequestrectomy?

A

removal of small/ loose sequestrate.

53
Q

How long can an MRONJ lesion take to heal?

A

Up to 6 months.

54
Q

Is surgical intervention recommended in established MRONJ lesions? Why?

A

NOT unless the bone is MOBILE - can interfere with blood supply and cause further necrosis.

55
Q

How will a sequestrum appear on radiograph?

A
  • DARK BAND around the sequestrum which is OSTEOCLASTIC RESORBTION.
  • Indicates the sequestrum is free, mobile and able to be lifted out.
56
Q

Is hyperbaric oxygen recommended for MRONJ?

A
  • May have no effect.
  • Not easily accesible.
57
Q

What anelgesia can be given to MRONJ patients?

A

Paracetamol, mouthwash with LA in it.

58
Q

Is a drug holiday recommended for MRONJ?

A

If safe to do so- some benefit but they have a long half life - estimated up to 10 yrs.

59
Q

What type of drug is Denosumab? How does it work?

A
  • Human monoclonal antibody.
  • Inhibits osteoclast function - blocks RANKL which is the first sine for bone removal.
60
Q

What is the function of RANKL?

A

Primary signal for bone removal.

61
Q

What does denosumab mimic?

A

The function of endogenous osteoprotegerin (OPG).

62
Q

How is denosumab administred? How quick does it work and when does it effect stop?

A
  • Subcutaneous injection.
  • Osteoclastic function limited within 6 hours, comes back in 6 months.
63
Q

A drug ends in MAB. What does this mean?

A

Monoclonal antibody.

64
Q

When is the best time to treat a denosumab patient?

A

JUST BEFORE THEY ARE DUE FOR THEIR NEXT SUBCUTANEOUS INJECTION.

65
Q

What is another name for denosumab?

A

Prolia.

66
Q

How do steroids affect bone?

A

High dose systemic steroids DELAY HEALING due to antinflammatory effects, fibroblast inhibition, collagen synthesis and epithelization.

67
Q

2 examples of systemic steroids.

A

Predniselone, hydrocortisone,

68
Q

What is the relevance of steroids to dental practice?

A

High dose steroids (ex. for COPD) can cause osteoporosis and patients are prescribed bisphosphonates to combat this - MRONJ.

69
Q

Why is short term use of NSAIDs following extraction beneficial?

A

Analgesic + anti inflammatory.

70
Q

What is the effect of long term NSAID use on bone?

A
  • Interfere with the activity of COX enzymes and thus the production of PROSTAGLANDINS.
  • impact blood vessels, nerve endings, inflammatory cells –> IMPACT BONE HEALING.
71
Q

Two named examples of NSAIDs.

A

Ibuprofen, diclofenac.

72
Q

What is the relevance of long term NSAIDs to dentistry?

A

long-term NSAIDS can impact on bone healing so may be avoid following bone augmentation surgery for dental implants if possible.

73
Q

Why do anti-epileptic drugs affect bone? (2 named examples).

A

affect absorption of calcium from the stomach

  • Carbamazepine, phenytoin.
74
Q

Why do PPIs affect bone?

A

Affect absorption of calcium from the stomach.

75
Q

Why do diuretics affect bone?

A

Increase renal excretion of calcium

76
Q

Why do SSRIs affect bone? Named example.

A
  • Ssteoblasts and osteoclasts have serotonin receptors although the mechanism of action is not understood.
  • Fluoexetine.
77
Q

Why do drugs for breast and prostate cancer affect bone?

A

Reduce androgen and oestrogen levels.

  • Evorolimus, raloxifene, teriparatide
78
Q

What two pieces of literature are leading MRONJ research/ guidelines?

A

American Association of Oral and Maxillofacial Surgeon Position paper on MRONJ - 2014 update.

SDCEP managment of patients at risk of MRONJ 2017.

Module 5 - Bone Biology (1 decks)

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