Oral Surgery & Oral Pathology Flashcards
(155 cards)
What are the 2 main forms of Anti-resorptive medications?
How do they differ in:
- Method of Action?
- Method of Administration?
- Half life?
- Bisphosphonates
- RANKL Inhibitors (Denosumab)
Both indicated for: Osteoporosis, Cancer or bone disorders (e.g. Pagets)
Method of Action:
Both inhibit bone resorption by inhibiting osteoclast activity
B = via osteoclast apoptosis
R = via inhibition of RANKL (normally stimulates osteoclast function)
Method of Administration:
- *B** = Oral (often once a week) or IV (6 monthly or yearly)
- *R** = Subcutaneous (6 monthly)
Half-life:
- *B** = Longer half-life (~10 years) & binds to bone
- *R** = Shorter half-life () & does NOT bind to bone
What are 5 functions of the maxillary antrum?
- Lighten the skull
- Moistens inhaled air
- Warms inhaled air
- Voice resonance
- Immunological function for upper respiratory tract
What is the definition of an abscess?
Its aetiology is bacterium, what are the 3 main routes of entry?
A pathological cavity filled with pus and lined by a pyogenic membrane.
Bacterial entry via:
- Apical foramen
- PDL
- Bloodstream (“Anchoresis”)
What are the following flap names?

- Envelope (One-sided)
- Triangular (Two-sided)
- Trapezium (Three-sided)
- Semi-lunar
- Y-Incision
- Pedicle
Aspirin:
- What is the MOA?
- How does its affect differ to other NSAIDs?
- What is our OS management for patients taking Aspirin?
- Anti-platelet, inhibits thromboxane A2 via COX-1 pathway inhibition
- Causes IRREVERSIBLE platelet changes (lasting platelet 7-10day lifespan)
- Nothing - Don’t interupt/alter medication. Can treat with cautionary measures (e.g. limiting area/earlier in week) & local haemostatic measures
How many times a day are each NOAC usually taken?
According to SDCEP Guidelines, what instructions should be given to the patient (pre/post-op)?
Rivaroxaban - ONCE
Apixaban - TWICE
Dabigatran - TWICE
Edoxaban - ONCE
Once a day?
Morning = Delay morning dose & take 4hr after haemostasis
Evening = Take evening dose as normal (as long as 4hr after haemostasis)
Twice a day? MISS morning dose & take evening dose as normal (as long as 4hr after haemostasis)
What is the management for a patient with Acute Osteomyelitis? (6)
- URGENT OM/OS referal
- Empirical antibiotics (broad-spec antibiotics, e.g. Benzylpenicillin, Clindamycin and Metronidazole)
* N.B. Clindamycin has good bony penetration but risk of C. difficle → severe diarrhoae* - Pus sample taken
- Specific target antibiotics
- Debridement
- Long-term antibiotics 2+ weeks (Out Patient Antimicrobial Therapy, OPAT)
SDCEP says INR within 72hr is acceptable if patient has stable INR history - specifically, what does this mean?
A patient who does not require weekly INR checks & hasnt had any INR readings above 4 in the last 2 months
The first stage of infection spread is Cellulitis, what is this and what would be observed?
(Think appearance & bacterium present)
Cellulitis = Infection spread to connective tissue → Soft tissue oedema
- Redness
- Shiny
- Fluctuant (but this depends on amount of fluid present)
- Non-suppurative
- Usually streptococcus
What are the 5 aims of surgical extraction?
(THINK: Why raise flap? Why remove bone? Why suture?)
- Remove tooth (duh)
- Improve vision
- Create application point for elevation
- Minimise trauma
- Promote healing (via debridement and sutures)
In taking a good post-XLA pain history what should you ask?
What probing questions may you ask about symptoms?
SOCRATES (duh)
- When did the pain start (how many days after XLA)?
- Is it getting worse?
- Is there any foul smell/taste? - Dry socket or pus
- Is there limited mouth opening
- Is there any swelling
- Systemic features - Fever, temporature or malaise?
What are the 6 main stages involved in surgical tooth extraction?
- Plan access (flap design)
- Raise mucoperiosteal flap
- +/- Bone removal
- +/- Sectioning of tooth - Start at furcation and go to burs depth (avoid drilling through whole tooth, may cause lingual nerve damage - use space created for elevation_
- Debridement/Irrigation - Saline +/- haemostatic agent
- Wound closure with sutures
What are 5 signs of Mandibular fracture?
“Mandibles Open Now Tallulah Says”
- Mobility
- Occlusion change
- Numbness of lower lip (IAN)
- Trismus
- Sublingual haematoma (blood seen under tongue)
What is the definition of MRONJ?
Following this, what are the 4 diagnostic features that must be met?
MRONJ (Medication-Related Osteoonecrosis of the Jaw)
Severe adverse reaction to anti-resorptive or anti-angiogenic drugs → Exposed bone or bone that can be probed through an intra or extra-oral fistula in the maxillo-facial region which has persisted over 8 weeks in a patient with history of taking the above drugs and NO history of radiotherapy or obvious metastatic jaw disease.
Diagnostic Criteria:
- Currently or previously taking anti-resorptive or anti-angiogenic medication
- Exposed bone or bone that can be probed through intra or extra-oral fistula - persisting over 8 weeks
- No history of radiotherapy
- No obvious metastatic jaw disease
What are the gross characteristics of a benign oral lesion?
(e.g. size/shape) - 6
- Encapsulated
- Rounded
- Small (smaller than malignancies)
- Slowed growth
- Rare ulceration or bleeding
- Can produce hormones (e.g. in endocrine tissues)
What are 7 indications for removal of cysts or benign soft tissue lesions?
- Pain
- Infection
- Altered function
- Pressure on adjacent structures
- Weakening of adjacent structures
- Continuous growth
- Poor aesthetics
What are 4 radiographic signs that show close proximity of 3rd molar to ID nerve (/linked with ID nerve damage)?
- Interruption or Loss of white tramline (most common)
- Darkening of the root (“Banding”)
- Diversion of ID canal
- Narrowing of canal
What is the difference between primary & secondary haemostasis?
How can both be adversely affected?
PRIMARY = Platelet aggregation
- Failure in Platelet production (“Thrombocytopenia)
* Bone marrow failure, Congenital disorders or Megakaryocyte depression (e.g. via chemotherapy, infections or drugs - alcohol/heparin/thiazide diuretics)* - Failure in Platelet function
* Von Willebrand’s Disease (reduced/defective vWF) or drugs - NSAIDs (via COX-1)/ Clopidogrel (via ADP)* - Failure in Platelet survival
* Autoimmune, HIV-associated, Malaria, Lymphocytic leukaemia or Drugs - Aspirin/Cytotoxics/Valproate*
SECONDARY = Coagulation pathway into fibrin clot
- CONGENITAL (Haemophilia A/B or vWD)
- ACQUIRED (Anti-coagulant medications, Vit K deficiency, Liver disease or Large volume blood transfusions)
What are the different drugs that are implicated in MRONJ (4)?
How can they be placed into 2 main catagories?
- *1) Anti-resorptive**
- Inhibit bone resorption (impaired osteoclast function)*
-
Bisphosphonates
E.g. Zoledronate (IV) or Alendronate (Oral) -
RANK-L inhibitor
E.g. Denosumab (subcutaneous) - *2) Anti-angiogenic**
- Inhibit blood vessel formation (angiogenesis)*
-
VEGF Inhibitor
E.g. Bevacizumab (IV) -
Tyrosine Kinase Inhibitor
E.g. Sunitinib (Oral)
What is Osteomyelitis?
What are the 5 risk factors?
Osteomyelitis = Inflammation of the medullary bone due to mixed bacterial Infection
- Radiotherapy
- Trauma
- Bisphosphonates
- Bone diseases (e.g. Pagets or Osteoporosis)
- Immunodeficiency (including malnutrition, systemic corticostroids , DM & age extremeties)
What is a “Guardsman’s Fracture”?
Fracture of the right and left mandibular condyle
Also presents with chin laceration from impact
What are some signs & symptoms of MRONJ?
May be ASYMPTOMATIC (MRONJ Stage 1) - AAOMS (2014)
Signs:
- Exposed, necrotic bone
- Gingival swelling
- Secondary Infection (+/- suppuration)
- Pain (persistent)
- Absent or delayed healing
- Pathological #
Symptoms:
- Gingival tenderness
- Halitosis
- Parasethesia
- Pathological #
How might clinical features of an abscess differ if the origin was periapical vs. periodontal?
- Periapical associated with non-vital tooth
- Periapical = history of trauma and/or caries
- Periapical = not well localised pain but TIQ painful to touch
- Periodontal = MOBILE tooth which is TTP
- Periodontal = Vital (or non)
What is the difference between acute and chronic periodontitis?
(Consider symptoms, clinical findings and radiographs)

