bone lesions Flashcards
define alveolar osteitis (4)
- 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
what is the aetiology of alveolar osteitis? (2)
- excessive local fibrinolysis of clot due to plasminogen pathway activation (direct and indirect activator substances)
- mechanical loss of clot (rinsing, exercise, etc)
risk factors for alveolar osteitis (6)
- mandibular
- single extraction
- more difficult or traumatic procedure
- females, esp on OCP
- excessive rinsing post-op, other mechanical trauma
- smoking
briefly describe the clot formation and socket healing following an extraction (4)
- damage to vessel wall and platelet activation
- formation of loose clot
- formation of stable clot
- clot fibrinolysis after a few days and bony infill
management for alveolar osteitis (6)
- 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
what analgesic regime may you advise for alveolar osteitis?
- ibuprofen 400-600mg TDS/QDS (max 2400mg/day)
- paracetamol 1g QDS
- take together up to 4x/day or staggered
what does Alveogyl contain? (3)
- butamben (anaesthetic)
- eugenol (analgesic)
- iodoform (antimicrobial)
why do we try not to use CHX for irrigating dry socket?
rare but serious allergic reactions
define osteomyelitis
- extensive inflammation of a bone, usually due to infection
- involving the cancellous portion, bone marrow, cortex and periosteum
difference between compact and cancellous bone
compact = dense
cancellous = sponge-like, large spaces
what is the pathogenesis of and factors affecting osteomyelitis?
- 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
what local factors may contribute to osteomyelitis? (4)
- trauma
- major blood supply disease
- local infection
- osteoporosis
what systemic factors may contribute to osteomyelitis? (up to 8)
- leukaemia, anaemia, AIDS
- malnutrition, IV drug abuse, chronic alcoholism
- autoimmunity, diabetes
osteomyelitis classification
- suppurative osteomyelitis = acute or chronic or infantile
- non-suppurative osteomyelitis
– chronic focal sclerosing
– chronic diffuse sclerosing
– Garres sclerosing
– actinomycotic
– radiation
describe acute suppurative osteomyelitis (what, early/late s/s, radiology, histology)
- <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
acute suppurative osteomyelitis s/s (early/late)
- early = severe throbbing pain, inflammatory oedema
- late = distention of periosteum (pus), firm swelling, paraesthesia, bone sequestrum
acute suppurative osteomyelitis histology (3)
- necrotic bone, lacunae filled with pus, sequestrum, peripheral resorption, acute inflammatory infiltrate
- +/- periosteum and cortex necrosis
- +/- bacterial colonisation
acute suppurative osteomyelitis radiograph (2)
- thin, poor density, blurred trabeculae (early)
- loss of lamina dura continuity of >1 tooth
acute suppurative osteomyelitis management (2)
- conservative = antibiotics (from culture), drainage, analgesia, debridement
- radical = sequestrectomy or resection and reconstruction if extensive +/- hyperbaric oxygen
describe chronic suppurative osteomyelitis (what, s/s, radiology, histology)
- > 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
chronic suppurative osteomyelitis s/s (5)
- swelling
- pain +/or paraesthesia
- sinus formation with purulent discharge
- tooth loss
- pathological fracture
chronic suppurative osteomyelitis radiolograph (3)
- initially thin/fuzzy trabeculae
- later calcified/sclerosed
- pathological fracture
chronic suppurative osteomyelitis histology (2)
- inflamed connective tissue in marrow space, marrow fibrosis
- bone resorption and reactive bone formation
chronic suppurative osteomyelitis management (small, large)
always invasive
- small = curettage, sequestrectomy then primary wound closure +/- antibiotics
- large = resection +/- vascular reconstruction or bone graft if not resolving
describe chronic focal sclerosing osteomyelitis (age, presentation, radiology, histology)
- 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
chronic focal sclerosing osteomyelitis age group
children/young adult
chronic focal sclerosing osteomyelitis site
mandible, non-vital/pulpitic premolar/molar
chronic focal sclerosing osteomyelitis radiograph (2)
- localised uniform increase in radiodensity associated with tooth
- widened PDL space
chronic focal sclerosing osteomyelitis histology
dense sclerotic bone with scanty connective tissue and inflammatory cells
chronic focal sclerosing osteomyelitis management
XTN/RCT (remove source of infection/inflammation)
describe chronic diffuse sclerosing osteomyelitis
- 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
chronic diffuse sclerosing osteomyelitis age group
adulthood only
chronic diffuse sclerosing osteomyelitis site
mandible, multiple teeth
chronic diffuse sclerosing osteomyelitis radiograph
diffuse area of radiodensity
chronic diffuse sclerosing osteomyelitis histology
- bone sclerosis and remodelling, reduced marrow spaces
- bone sequestrum
- inflammatory cells +/- secondary bacterial colonisation
chronic diffuse sclerosing osteomyelitis management (2)
- XTN/RCT (remove source of infection/inflammation)
- resection +/- reconstruction if symptomatic
criteria for MRONJ (3)
- 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
give examples of types of medications associated with MRONJ (up to 5)
- bisphosphonates (-dronic acid)
- tyrosine kinase inhibitors (-inib)
- immunosuppressants (methotrexate, steroids, thalidomide, -umab)
- mTORs (-limus)
- monoclonal antibodies (-umab)
contributing factors to MRONJ (5)
- disruption to bone turnover (eg bisphosphonates)
- anti-angiogenic medications (reduced vascularity)
- microbial biofilm infiltrate
- reduced mucosal healing
- genetics
how may MRONJ present? (3)
- non-healing/delayed extraction socket with exposed bone
- pain, paraesthesia, mobile teeth
- infection in the area, pus, swelling
describe the staging of MRONJ
- 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
describe “at risk” MRONJ and its management
- at risk = no apparent necrotic bone in those who have been treated with oral/IV bisphosphonates
- no treatment indicated, education only
describe stage 0 MRONJ and its management
- stage 0 = no clinical evidence of necrotic bone BUT non-specific clinical findings, radiographic changes and symptoms
- systemic management with analgesia and antibiotics
describe stage 1 MRONJ and its management
- 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
describe stage 2 MRONJ and its management
- 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
describe stage 3 MRONJ and its management
- 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
how large is the risk for MRONJ? (2)
for those having bisphosphonates for:
- cancer treatment = 1%
- osteoporosis = 0.1%
which categories of patients have high risk of MRONJ? (4)
- 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
which category of patients has low risk of MRONJ?
bisphosphonate/denosumab use <5 years with NO concurrent systemic glucocorticoid
how can the risk of MRONJ be reduced by the patient? (5)
- excellent OH
- reduce sugary snacks/drinks, healthy diet
- limit alcohol intake
- stop smoking
- regular checkups and reporting symptoms early
how are patients at low risk of MRONJ managed? (3)
- 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
how are patients at high risk of MRONJ managed? (3)
- 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)
