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BDS5 oral disease > bone lesions > Flashcards

bone lesions Flashcards

1
Q

define alveolar osteitis (4)

A
  • post-operative pain in and around extraction site
  • increases in severity at any time between the first and third day after extraction
  • with partial/total disintegration of blood clot within socket
  • +/- halitosis
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2
Q

what is the aetiology of alveolar osteitis? (2)

A
  • excessive local fibrinolysis of clot due to plasminogen pathway activation (direct and indirect activator substances)
  • mechanical loss of clot (rinsing, exercise, etc)
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3
Q

risk factors for alveolar osteitis (6)

A
  • mandibular
  • single extraction
  • more difficult or traumatic procedure
  • females, esp on OCP
  • excessive rinsing post-op, other mechanical trauma
  • smoking
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4
Q

briefly describe the clot formation and socket healing following an extraction (4)

A
  • damage to vessel wall and platelet activation
  • formation of loose clot
  • formation of stable clot
  • clot fibrinolysis after a few days and bony infill
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5
Q

management for alveolar osteitis (6)

A
  • educate patient BEFORE extraction (consent)
  • reassurance - self-limiting, not an infection
  • pain control - regular analgesics
  • copious irrigation of debris in socket with saline
  • obtundent dressing (eg Alveogyl)
  • review
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6
Q

what analgesic regime may you advise for alveolar osteitis?

A
  • ibuprofen 400-600mg TDS/QDS (max 2400mg/day)
  • paracetamol 1g QDS
  • take together up to 4x/day or staggered
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7
Q

what does Alveogyl contain? (3)

A
  • butamben (anaesthetic)
  • eugenol (analgesic)
  • iodoform (antimicrobial)
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8
Q

why do we try not to use CHX for irrigating dry socket?

A

rare but serious allergic reactions

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9
Q

define osteomyelitis

A
  • extensive inflammation of a bone, usually due to infection
  • involving the cancellous portion, bone marrow, cortex and periosteum
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10
Q

difference between compact and cancellous bone

A

compact = dense
cancellous = sponge-like, large spaces

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11
Q

what is the pathogenesis of and factors affecting osteomyelitis?

A
  • inflammatory process of entire bone, modulated by local and systemic factors
  • local (decrease vascularity) = trauma, major blood supply disease, local infection, osteoporosis
  • systemic (impaired host defence) = leukaemia, anaemia, AIDS, malnutrition, IV drug abuse, chronic alcoholism, autoimmunity, diabetes
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12
Q

what local factors may contribute to osteomyelitis? (4)

A
  • trauma
  • major blood supply disease
  • local infection
  • osteoporosis
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13
Q

what systemic factors may contribute to osteomyelitis? (up to 8)

A
  • leukaemia, anaemia, AIDS
  • malnutrition, IV drug abuse, chronic alcoholism
  • autoimmunity, diabetes
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14
Q

osteomyelitis classification

A
  • suppurative osteomyelitis = acute or chronic or infantile
  • non-suppurative osteomyelitis
    – chronic focal sclerosing
    – chronic diffuse sclerosing
    – Garres sclerosing
    – actinomycotic
    – radiation
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15
Q

describe acute suppurative osteomyelitis (what, early/late s/s, radiology, histology)

A
  • <4 weeks
  • medullary infection, thromboses in vessels leads to extensive bone necrosis
  • early = severe throbbing pain, inflammatory oedema
  • late = distention of periosteum (pus), firm swelling, paraesthesia, bone sequestrum
    radiology:
  • thin, poor density, blurred trabeculae (early)
  • loss of lamina dura continuity of >1 tooth
    histology:
  • necrotic bone, lacunae filled with pus, sequestrum, peripheral resorption, acute inflammatory infiltrate
  • +/- periosteum and cortex necrosis
  • +/- bacterial colonisation
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16
Q

acute suppurative osteomyelitis s/s (early/late)

A
  • early = severe throbbing pain, inflammatory oedema
  • late = distention of periosteum (pus), firm swelling, paraesthesia, bone sequestrum
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17
Q

acute suppurative osteomyelitis histology (3)

A
  • necrotic bone, lacunae filled with pus, sequestrum, peripheral resorption, acute inflammatory infiltrate
  • +/- periosteum and cortex necrosis
  • +/- bacterial colonisation
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18
Q

acute suppurative osteomyelitis radiograph (2)

A
  • thin, poor density, blurred trabeculae (early)
  • loss of lamina dura continuity of >1 tooth
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19
Q

acute suppurative osteomyelitis management (2)

A
  • conservative = antibiotics (from culture), drainage, analgesia, debridement
  • radical = sequestrectomy or resection and reconstruction if extensive +/- hyperbaric oxygen
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20
Q

describe chronic suppurative osteomyelitis (what, s/s, radiology, histology)

A
  • > 4 weeks, primary or secondary
  • inadequate tx of acute disease = granulation tissue and calcific depositions
  • swelling, pain, sinus formation, purulent discharge, tooth loss, paraesthesia, pathological fracture
    radiology:
  • initially thin/fuzzy trabeculae
  • later calcified/sclerosed
  • pathological fracture
    histology:
  • inflamed connective tissue in marrow space, marrow fibrosis
  • bone resorption and reactive bone formation
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21
Q

chronic suppurative osteomyelitis s/s (5)

A
  • swelling
  • pain +/or paraesthesia
  • sinus formation with purulent discharge
  • tooth loss
  • pathological fracture
22
Q

chronic suppurative osteomyelitis radiolograph (3)

A
  • initially thin/fuzzy trabeculae
  • later calcified/sclerosed
  • pathological fracture
23
Q

chronic suppurative osteomyelitis histology (2)

A
  • inflamed connective tissue in marrow space, marrow fibrosis
  • bone resorption and reactive bone formation
24
Q

chronic suppurative osteomyelitis management (small, large)

A

always invasive
- small = curettage, sequestrectomy then primary wound closure +/- antibiotics
- large = resection +/- vascular reconstruction or bone graft if not resolving

25
Q

describe chronic focal sclerosing osteomyelitis (age, presentation, radiology, histology)

A
  • unusual localised reaction
  • children/young adult
  • mandible, premolar/molar
  • associated with non-vital/pulpitic tooth with no jaw expansion
  • localised uniform increase in radiodensity associated with tooth, widened PDL space
  • histology = dense sclerotic bone with scanty connective tissue and inflammatory cells
26
Q

chronic focal sclerosing osteomyelitis age group

A

children/young adult

27
Q

chronic focal sclerosing osteomyelitis site

A

mandible, non-vital/pulpitic premolar/molar

28
Q

chronic focal sclerosing osteomyelitis radiograph (2)

A
  • localised uniform increase in radiodensity associated with tooth
  • widened PDL space
29
Q

chronic focal sclerosing osteomyelitis histology

A

dense sclerotic bone with scanty connective tissue and inflammatory cells

30
Q

chronic focal sclerosing osteomyelitis management

A

XTN/RCT (remove source of infection/inflammation)

31
Q

describe chronic diffuse sclerosing osteomyelitis

A
  • asymptomatic incidental finding
  • adulthood only
  • mandible, multiple teeth
  • diffuse area of radiodensity
    histology:
  • bone sclerosis and remodelling, reduced marrow spaces
  • bone sequestrum
  • inflammatory cells +/- secondary bacterial colonisation
32
Q

chronic diffuse sclerosing osteomyelitis age group

A

adulthood only

33
Q

chronic diffuse sclerosing osteomyelitis site

A

mandible, multiple teeth

34
Q

chronic diffuse sclerosing osteomyelitis radiograph

A

diffuse area of radiodensity

35
Q

chronic diffuse sclerosing osteomyelitis histology

A
  • bone sclerosis and remodelling, reduced marrow spaces
  • bone sequestrum
  • inflammatory cells +/- secondary bacterial colonisation
36
Q

chronic diffuse sclerosing osteomyelitis management (2)

A
  • XTN/RCT (remove source of infection/inflammation)
  • resection +/- reconstruction if symptomatic
37
Q

criteria for MRONJ (3)

A
  • current or previous treatment with anti-resorptive or anti-angiogenic agents
  • exposed bone/bone for >8 weeks that can be probed through a fistulae in maxillofacial region
  • no history of radiation therapy to jaws or obvious metastatic disease to jaws
38
Q

give examples of types of medications associated with MRONJ (up to 5)

A
  • bisphosphonates (-dronic acid)
  • tyrosine kinase inhibitors (-inib)
  • immunosuppressants (methotrexate, steroids, thalidomide, -umab)
  • mTORs (-limus)
  • monoclonal antibodies (-umab)
39
Q

contributing factors to MRONJ (5)

A
  • disruption to bone turnover (eg bisphosphonates)
  • anti-angiogenic medications (reduced vascularity)
  • microbial biofilm infiltrate
  • reduced mucosal healing
  • genetics
40
Q

how may MRONJ present? (3)

A
  • non-healing/delayed extraction socket with exposed bone
  • pain, paraesthesia, mobile teeth
  • infection in the area, pus, swelling
41
Q

describe the staging of MRONJ

A
  • at risk = no apparent necrotic bone in those who have been treated with oral/IV bisphosphonates
  • stage 0 = no clinical evidence of necrotic bone BUT non-specific clinical findings, radiographic changes and symptoms
  • stage 1 = exposed and necrotic bone or fistulae that probes to bone BUT asymptomatic and no evidence of infection
  • stage 2 = exposed and necrotic bone or fistulae that probes to bone WITH infection in the area (pain, erythema, purulent discharge)
  • stage 3 = exposed and necrotic bone or fistulae that probes to bone WITH pain, infection and ≥1 of:
    – exposed bone beyond alveolar bone with pathological fracture
    – extraoral fistula
    – OAC/ONC
    – osteolysis extending to inferior border of mandible/sinus floor
42
Q

describe “at risk” MRONJ and its management

A
  • at risk = no apparent necrotic bone in those who have been treated with oral/IV bisphosphonates
  • no treatment indicated, education only
43
Q

describe stage 0 MRONJ and its management

A
  • stage 0 = no clinical evidence of necrotic bone BUT non-specific clinical findings, radiographic changes and symptoms
  • systemic management with analgesia and antibiotics
44
Q

describe stage 1 MRONJ and its management

A
  • stage 1 = exposed and necrotic bone or fistulae that probes to bone BUT asymptomatic and no evidence of infection
  • antibacterial mouthrinse
  • 3/12 follow up
  • education, review of indications for continued bisphosphonate therapy
45
Q

describe stage 2 MRONJ and its management

A
  • stage 2 = exposed and necrotic bone or fistulae that probes to bone WITH infection in the area (pain, erythema, purulent discharge)
  • symptomatic treatment with oral antibiotics
  • antibacterial mouthrinse
  • pain control
  • debridement to relieve soft tissue irritation and infection control
46
Q

describe stage 3 MRONJ and its management

A
  • stage 3 = exposed and necrotic bone or fistulae that probes to bone WITH pain, infection and ≥1 of:
    – exposed bone beyond alveolar bone with pathological fracture
    – extraoral fistula
    – OAC/ONC
    – osteolysis extending to inferior border of mandible/sinus floor
  • antimicrobial mouthrinse
  • antibiotics
  • pain control
  • surgical debridement/resection for longer term palliation of infection/pain
47
Q

how large is the risk for MRONJ? (2)

A

for those having bisphosphonates for:
- cancer treatment = 1%
- osteoporosis = 0.1%

48
Q

which categories of patients have high risk of MRONJ? (4)

A
  • previous MRONJ dx
  • current treatment with anti-resorptive or anti-angiogenic drugs for cancer
  • bisphosphonate use >5 years
  • bisphosphonate use <5 years but within the last 9 months WITH concurrent systemic glucocorticoid treatment
49
Q

which category of patients has low risk of MRONJ?

A

bisphosphonate/denosumab use <5 years with NO concurrent systemic glucocorticoid

50
Q

how can the risk of MRONJ be reduced by the patient? (5)

A
  • excellent OH
  • reduce sugary snacks/drinks, healthy diet
  • limit alcohol intake
  • stop smoking
  • regular checkups and reporting symptoms early
51
Q

how are patients at low risk of MRONJ managed? (3)

A
  • carry out ALL routine dental tx and provide personalised preventive plan
  • XTNs = discuss risk/benefit, proceed if clinically indicated with NO antimicrobials, review healing 4-6wks
  • refer to oral surgery/SSCD if suspecting MRONJ
52
Q

how are patients at high risk of MRONJ managed? (3)

A
  • carry out MOST routine dental tx and provide personalised preventive plan
  • XTNs = consider other tx options (RCT, decoronation), discuss risk/benefit, proceed if clinically indicated with NO antimicrobials, review healing 4-6wks
  • refer to oral surgery/SSCD if suspecting MRONJ
    (little evidence for drug holiday)

BDS5 oral disease (26 decks)

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