Osteonecrosis Flashcards

1
Q

what is the pathological definition of Osteomyelitis

A

Inflammation of bone marrow

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2
Q

in reality, how would you define osteomyelitis? (not the pathological definition)

A

Spectrum of inflammatory and reactive changes in the bone and periosteum

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3
Q

Osteomyelitis is an inflammation and reactive change affecting ….. and …….

A

Bone and Periosteum

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4
Q

How can Osteomyelitis present

A

1) Acute
2) Chronic
3) Subperiosteal
4) Sclerosing
3 and 4 are rare

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5
Q

True/False Osteomyelitis is always suppurative

A

False- it can be Suppurative or Non-suppurative

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6
Q

Syphilitic and Tuberculosis are a rare cause for ….. disease

A

Osteomyelitis

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7
Q

How will the acute form of osteomyelitis present

A

Clinical picture of acute infection and systemic effects

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8
Q

How will the chronic form of osteomyelitis present

A

it can be Primary or Secondary;
- Primary: no acute episode involved
- Secondary: prolonged inflammatory process
(this form is very difficult to manage)

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9
Q

Name 6 risk factors/aetiology for Osteomyelitis

A

1) Odontogenic infection
2) Peri-implantitis
3) Infected cyst
4) Infected tumour
5) Surgical wound that’s not healed
6) Underlying disorders (DM / EtOH / Immunosuppression)

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10
Q

Name some underlying disorders that can be risk factor/aetiology for osteomyelitis

A

1) Fibrous dysplasia
2) Previous radiation bone exposure (cf ORN)
3) Osteoporosis
4) Osteopetrosis
5) Paget’s Disease
6) Bone tumours
7) Immunocompromised (poorly managed diabetes, HIV or other)

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11
Q

what is sequestration (involucrum)?

A

when we get bone resorption, we also have new bone being laid down. This is called involucrum. e.g. little pieces of bones that we get after XLA. In osteomyelitis, bone gets expelled slowly out of surgical wound

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12
Q

Explain the mechanism of Osteomyelitis (OM)

A
  • its main cause are bacteria such as Anaerobic Staphylococcus aureus. (Anaerobic strep Staph in PowerPoint)
  • This bacteria would enter the body system through wound and other way
  • OM forms through one of these mechanisms;
    1) No host defence
    or
    2) Bacteria will proliferate in the bone marrow space.
    increase intramadullary pressure and/or compromise blood supply

Both of these mechanism will lead into
A) Increased vascular collapse
B) Venous stasis (thrombosis)
C) Ischaemia

As a result, necrosis of bone occur

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13
Q

Is Maxilla or Mandible the most commonest site for osteomyelitis?

A

Mandible

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14
Q

State and Explain which arch is more susceptible for osteomyelitis and Why? (give 3 reasons)

A
  • Mandible
    1. Mandible is made of thick Cancellous bone, more likely to become ischaemic so more sensitive to infection compared with Maxilla
  1. Blood supply to mandible less oxygenated than maxilla
  2. Dense overlying cortical bone of mandible prevents penetration of periosteal blood vessels of maxilla
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15
Q

What microbes are responsible to osteomyelitis?

A
  • It’s similar to odontogenic infection which more than one type is responsible. However there are some which are common.

1) Viridans streptococcus
2) Strict anaerobes (e.g. prevotella, fusobacterium, peptostreptococcus)
3) Staph aureus

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16
Q

patient is presenting symptoms of osteomyelitis (OM). how would you treat them initially?

A

Step 1: take a swab test and send to lab for culture test to find which microorganisms are responsible

Step 2: as you are waiting for results, based on previous knowledge of which microorganisms are responsible for OM, provide some antibiotics against those for a short term

Step 3: once the result is back, the definitive Antibiotics should be given specifically to target the microorganisms present.

(Definitive therapy should be empirical until culture & sensitivity )

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17
Q

What are the symptoms of OM and at which stage they appear?

A

1) Initial event:
- Intense pain and high intermittent fever (38 – 40)
- Identifiable causative tooth
- +/- malaise, headache, reduced appetite
- minimal swelling
- no fistulae
(infection usually well localised if treated, this stage lasts 1-2 weeks. if not treated, it will spread)
2) Spreading: Development of systemic toxic symptoms:
- heat (calor),
- pain (dolor),
- redness (rubor),
- swelling (tumor)
- loss of function
3) signs following spreading:
- Purulent discharge erodes bone
- Puss
- Extensive firm swelling, warm erythematous
- +/- trismus
- Throbbing jaw pain
- Severe tenderness
- ‘extrusion’ of teeth
- Nerve involvement

Also

  • increased Leukocytosis
  • Elevated CRP (C. reactive proteins?)
  • Local lymphadenopathy
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18
Q

What are sign/symptoms of Chronic Osteomyelitis?

A

Normothermic
Symptoms resolve / disappear
Teeth locally are tender
Sequestra maybe expelled through mucosa

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19
Q

what special tests can we use to diagnose chroic osteomyelitis and what would be the classic features?

A

Imaging.
1) moth eaten appearance (maybe most imprortant so know for Exam) / sequestrum of bone
2) Involucrum ‘new bone’ appearance
3) Osteosclerosis (hypersensitivity reaction)

20
Q

Why do we have to take chronic osteomyelitis seriously and treat it?

A

There is a risk of pathological fracture if left untreated (especially in edentulous mandible)

21
Q

Compare how to diagnose Acute vs Chronic osteomyelitis

A

Acute: clinical findings – deep intense pain / paraesthesia / bloods

Chronic: Clinical signs/symptoms + Imaging

22
Q

Why do we not use imaging (palin film) to diagnose acute osteomyelitis?

A

signs only visible in the image 1-2 weeks after onset. little value in imaging at this stage
(generally bony imaging detects bone loss 30-50% of calcified constituent
)

23
Q

What are the characteristic features visible in OM after its establishment?

A

1) increased radiolucency / “moth-eaten”
2) islands of bone / sequestra
3) some areas of increased radiodensity surrounding area of radiolucency due to increased bony production
inflammatory reaction

24
Q

Which type of imaging is more useful than plain films, MRI or CT scan?

A
  • CT more useful earlier on than plain films
  • There are some evidence that MRI is helpful early on but lacks specificity
25
Q

What is Radionucleotide Scanning used for and why

A
  • It’s used for scanning for Osteomyelitis.
  • Superior to conventional imaging
  • Gallium accumulates at inflammation/infective sites
26
Q

What are the treatment options for Osteomyelitis?

A

1) Antibiotics
2) Surgery
3) Hyperbaric Oxygen

27
Q

what types of Antibiotics would you prescribe to treat osteomyelitis?

A
  • Starting with high dose penicillin or Clindamycin (broad spectrum)
    +/- Metronidazol (narrow spectrum)
    +/- I.V. (sometimes when the patient’s are really unwell, Antibiotic are delivered through IV)
28
Q

What are the advantages of Surgery for osteomyelitis?

A
  • Remove cause / eliminate source
  • Sequestrectomy (removes sequestrum)
  • Important for micro sample
  • Improve blood supply
  • Allow adequate penetration of Abx
  • Maximise host defences mechanism
  • Allowing self-healing ability
29
Q

How does Hyperbaric Oxygen work to treat Osteomyelitis?

A
  • increase in oxygen results in augmentation of angiogenesis
  • improvement in osteogenesis
  • increase leukocyte activity
  • stimulating growth factors
30
Q

Why may Clindamycin be more advantages to use rather than penicillin when treating osteomyelitis?

A

Clindamycin can penetrate avascular tissues. which is especially useful in this case as patient would have poor blood supply in the area.

31
Q

What are the complications that can happen following Clindamycin intake?

A

Clostridium Difficle- fatal

32
Q

Define Osteoradionecrosis

A
  • Bone necrosis in previously irradiated tissue in the absence of tumour persistence or recurrence.
    or
  • Bone exposed in the irradiated area with a diameter greater than 1cm lasting for at least 6 months without any tendency to heal.
33
Q

What are the clinical features of ORN?

A

1) Follows radiotherapy
2) Exposed bone – often small asymptomatic areas
3) Severe pain
4) Oro-facial fistulas
5) Foul smelling necrotic of the jaw
6) Suppuration
7) Pathological fracture

34
Q

outline the mechanism of ORN formation

A

1) Irradiation of Bone
Causing
2)
A- Endarteritis obliterans: leading to blood vessel obliteration, reducing blood supply so hypovascular and hypoxic bone
and
B- osteocyte and fibroblast damage: this leads to hypocellular bone
3) these factors together cause reduced vitality and inability to repair.
4) at this point, any trauma or infection will lead to necrotic bone.

35
Q

What are the signs and symptoms to diagnose ORN? (not the clinical features)

A
  • Severe pain
  • Non-healing exposed bone (within the area of radiation)
  • Incidents of recurrent infections
36
Q

What radiographs used to diagnose ORN?

A

CBCT or OPT

Plain radiology shows reduced bone density and sometimes # (fracture?)

37
Q

how to manage ORN?

A

1) Prevention best
- Pre-radiotherapy ‘dental fitness’
- Consider prophylactic extractions

2- Irrigation with saline
3- Analgesia
4- Antibiotics if indicated
5- Debridement

38
Q

If XLA is needed, what is the post-radiotherapy management?

A
  • XLA usually done by MDT
  • some suggest usage of CXD/PRF
  • in case of any complications, always refer them to their original surgeon
  • Review them to ensure healing. if in doubt, refer
39
Q

What is the mechanism of Bisphosphnate?

A

1- Attach to hydroxyapatite binding sites
Particularly on surfaces that are actively resorbing

2- Impairs osteoclastic ability to bind to the bony surface and inhibit resorption

3- Reduces osteoclast activity by promoting osteoclast apoptosis and inhibiting the development of new osteoclasts

40
Q

Who / What is Bisphosphnates used for?

A

Metastasising solid cancers

Multiple myeloma

Hypercalcaemia of malignancy

Post menopausal osteoporosis

Steroid induced osteoporosis

Paget’s Disease

41
Q

What’s the definition for MRONJ

A
  • Exposed bone, or bone that can be probed through an intra-oral or extra-oral fistula in the maxillofacial/mandibular region
  • which has persisted for more then 8 weeks
  • in patients with a history of treatment on the above drugs(bisphosphonates) and where there has been NO history of radiation therapy or obvious metastasis to the jaws.
42
Q

What is the pathology of Mronj

A

Inhibition of osteoclastic bone resorption and re-modelling

Inflammation of infection

Inhibition of angiogenesis

‘other’ hypothesis – including toxicity to soft tissues

(Slide 35)
Extractions or mucosal trauma precedes ostoelytic lesion

Patients develop exposed bone in the jaw (non-healing socket)

May worsen or heal slowly (months - years)

Radiographs – may be normal initially

More common in mandible

43
Q

what is the time to onset of Mronj

A

Time to onset ranges from 3 – 10 years

44
Q

when is Intra-venous bisphosphonates used?

A

Incidence variable

Mostly in myeloma and breast cancer

Up to 16% risk in some studies

Risk in prostate / myeloma higher

Higher risk in combination therapy

45
Q

what increass the risk og Mronj?

A

1) Immunosupression
Steroids / Azathioprine /Methotrexate

2) Immunocompromised – D.M. / HIV

3) Other meds
Chemotherapy / Anti-angioenics

46
Q

How to manage Mronj?

A

Prior to treatment – dentally fit where possible (usual OH etc)

Reduce risk – lifestyle factors (smoking

Avoid extractions where possible

Extractions - ensure follow up healing at 8 weeks

NO evidence for Abx or CXD mouth-rinses

?Supporting evidence for use of PRF