Oral Surgery Flashcards

1
Q

What are 7 indications for removal of cysts or benign soft tissue lesions?

A
  1. Pain
  2. Infection
  3. Altered function
  4. Pressure on adjacent structures
  5. Weakening of adjacent structures
  6. Continuous growth
  7. Poor aesthetics
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2
Q

What are the gross characteristics of a benign oral lesion?

(e.g. size/shape) - 6

A
  • Encapsulated
  • Rounded
  • Small (smaller than malignancies)
  • Slowed growth
  • Rare ulceration or bleeding
  • Can produce hormones (e.g. in endocrine tissues)
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3
Q

What are the 4 main methods of surgical cyst removal?

A
  1. Excision (Ellipse-shaped incision and excisional biopsy)
  2. Curettage (raising flap and Mitchell trimmer curettage)
  3. Enucleation
  4. Marsupialisation
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4
Q

What is the difference between Enucleation and Marsupialisation?

A

Enucleation = Complete removal of lesion with in-tact lining (e.g. smaller cysts)

Marsupialisation = 2 stage process

  1. Marsupialisation - Incision (create largest possible window) and suture cyst lining to mucosal wall
  2. Cyst decompression - Return once regressed in size and remove

(e.g. larger cyst or close to vital structures )

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5
Q

What are the advantages (3) and disadvantages (6) of Enucleation?

A

ADVANTAGES:

  1. Complete cyst lining obtained for histology
  2. Cavity closed - Reduced infection risk
  3. Little aftercare needed

DISADVANTAGES:

  1. Cavity clot may become infected
  2. Haemorrhage risk
  3. Large cyst removal → Weakened jaw
  4. Potential damage to adjacent structures or apicies of vital teeth
  5. Primary closure prevents visual inspection of cyst cavity
  6. Incomplete removal → Recurrence
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6
Q

What are the advantages (3) and disadvantages (5) of Marsupialisation?

A

ADVANTAGES:

  1. Open/accessible cavity for visual inspection
  2. Less bone removal, less risk of pathological fracture
  3. Less risk of damage to adjacent structures and can be used to save associated tooth (e.g. dentigerous cyst)

DISADVANTAGES:

  1. Mulitple visits needed (repack cavity as shrinks)
  2. Cooperative patient needed (keep area clean and attend multiple visits)
  3. May close up if not large enough/not packed → Cyst reformation
  4. Whole lining not available for histology
  5. Boney infill may not occur
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7
Q

How would you remove:

  1. Flabby/Fibrous Ridge?
  2. Midline Palatal Tori?
  3. Salivary Gland Stone Obstruction? (5)
A
  1. Incision to bone, remove “mucosal wedge” and stitch mucosa back together
  2. Y-shaped incision over lesion, bone removal and stitch together
  • Surgical removal
  • Basket retrieval with Dormier basked
  • Endoscopy-guided removal
  • Lithotripsy (UV waves shatter stone)
  • Gland removal
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8
Q

What are 3 alternative techniques for cyst/benign lesion removal?

A
  1. Laser
  2. Diathermy (current)
  3. Cryotherapy (cold liquid nitrogen at -196ºC)
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9
Q

How can lasers be used in cyst removal? (How do they work?)

What 3 uses can it have?

A
  • Increase cell temperature (above 100°C causing boiling, rupture and tissue vaporisation), protein denaturing and thrombosis

Uses:

  1. Cutting (tissue vapourisation)
  2. Coagulation (protein denaturing → cell death and haemostasis)
  3. Hard tissue surgery
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10
Q

What are the advantages (4) and disadvantages (3) of Laser surgery of lesions?

A

ADVANTAGES:

  1. Dry surgical field
  2. Reduced bleeding
  3. Reduced post-op oedema, pain and fibrosis
  4. Fibre-optic delivery

DISADVANTAGES:

  1. Expensive
  2. Complex equiptment
  3. No pathology specimen obtained for histology
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11
Q

What is diathermy and what are its 4 main uses?

What are the 2 main forms?

A

Diathermy = Use of current in: Cutting, Coagulation, Fulguration or Blending of Coagulation

  1. MONOPOLAR - Current passes from instrument tip through patient and is then “earthed” via common electrode plate (often used to cut)
  2. BIPOLAR - Current passed from one instrument to another via small volume of tissue (often used in coagulation)
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12
Q

What are 5 considerations/contraindications for use of diathermy on a patient?

A
  1. Pacemaker
  2. Skin preparations (e.g. chemical)
  3. Risk of burns
  4. Risk of electrocution
  5. Risk of explosions
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13
Q

What is Cryotherapy?

What type of lesions is it best for (and why)?

A

Cryotherapy = Tissue denaturing via use of cold medium (e.g. Liquid Nitrogen at -196°C) applied directly or via probes.

  • Series of freeze-thaw cycles = Intra-cellular ice formation → Increased electrolyte concentration, cell expansion (rise in osmotic pressure) and protein/lipid denaturing
  • Complete destruction at -50°C
  • Repeated cycles = Reduced cell mass lesion

Best for fluid-filled lesions as no cutting involved

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14
Q

In cryotherapy, what happens at:

  1. -20°C?
  2. -50°C?
A
  1. Partial destruction
  2. COMPLETE destruction
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15
Q

In Cryotherapy, what 4 factors is the tissue response dependent on?

When do you get best results?

A
  1. Temperature change
  2. Rate of temperature change
  3. Number of freeze-thaw cycles
  4. Time in freeze cycle (time temperature reduced)

Best results = Rapid freeze and thawing

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16
Q

What are the advantages (4) and disadvantages (4) of Cryotherapy?

A

ADVANTAGES:

  1. Non cutting (good for fluid-filled lesions, e.g. with high blood flow)
  2. No bleeding
  3. Can do without LA (best/kinder with)
  4. Great for fluid-filled lesions

DISADVANTAGES:

  1. Expensive
  2. No pathology specimen for histology
  3. Major post-op swelling
  4. Post-op ulceration and depigmentation
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17
Q

What are 8 indications of removal of 3rd molars?

A
  1. Unrestorable caries
  2. Untreatable pulpal/periapical pathology
  3. Pericoronitis (1 severe or multiple episodes)
  4. Abscess / Cellulitis / Osteomyelitis
  5. Cyst / Tumour (disease of tooth follicle)
  6. Internal or External resorption (of TIQ or adj. tooth)
  7. Tooth in line of jaw surgery
  8. Fracture of tooth
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18
Q

What are 3 considerations for removal of 3rd molars which are NOT covered in NICE guidelines?

A
  1. Distal caries in 7’s (mesially impacted 8’s)
  2. GA - If pt undergoing GA and 8’s likely to later become symptomatic
  3. Non-functional 8’s → Over-eruption and trauma
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19
Q

What is pericoronitis?

What type(s) can be considered for 3rd molar extraction?

A

Soft tissue inflammation related to crown of partially erupted tooth, where presence of an overlying operculum makes difficult to clean.

(Build up of plaque, streptococci and anaerobic bacterium)

Considered for XLA if: 1 severe episode or multiple reoccuring episodes

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20
Q

What is the difference between acute and chronic periodontitis?

(Consider symptoms, clinical findings and radiographs)

A
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21
Q

What are the different management options for pericoronitis?

(Can catagorise in 3 main groups)

A
  1. Symptoms: Analgesia, 0.2% CHX Mouthwash and Debridement under Operculum (with LA)
  2. Adjacent tooth: Extract or Smooth cusps if causing trauma
  3. TIQ: Extract
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22
Q

What is Ludwig’s Angina?

How does the patient present?

How is it treated?

A

Bilateral infection of the Sublingual, Submental AND Submandibular space

Presentation:

  • Fever (38.5°C)
  • Raised floor of mouth +/- deviated uvula
  • Difficulty swallowing, speaking or breathing
    (Dysphagia, Dysarthria or Dyspnoea)
  • May have had recent 3rd molar removal

Treatment:

MEDICAL EMERGENCY - URGENT referral to A&E

  • Drainage
  • IV antibiotics
  • +/- Tracheostomy (airway management)
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23
Q

What are 4 radiographic signs that show close proximity of 3rd molar to ID nerve (/linked with ID nerve damage)?

A
  1. Interruption or Loss of white tramline (most common)
  2. Darkening of the root (“Banding”)
  3. Diversion of ID canal
  4. Narrowing of canal
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24
Q

How can “Winter’s Lines” be used to assess angulation of impacted third molars?

A
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25
What is meant by a "POLO" 3rd molar? What might be a good treatment option for its removal?
Mandibular 3rd molar that perforates ID nerve Ideally leave (asymptomatic) but coronectomy if must be removed
26
What are 4 indications of CBCT in dentistry? Why is it not routinely used?
1. Trauma 2. TMJD 3. Large bony lesions (e.g. cysts) where soft tissue doesnt need to be visualised (would use US/MRI) 4. 3rd molar surgery - Where conventional OPG radiograph not sufficient to show relationship to ID nerve Not routinely used as x10 more radiation vs. OPG
27
What is a coronectomy? What happens? When may it be indicated or contra-indicated?
"Intentional Partial Odontectomy" * Crown sectioned at CEJ * Decorination of crown * Drill 2-4mm below crestal bone (root surface lies here and we want no enamel left in situ) Indication: 3rd molar removal where close ID canal proximity Contra-indication: Caries or Mobile roots
28
How can you get valid conset from the patient before extraction? What should you warn them of (general risks)? What is meant by 2-stage consent?
Valid consent = Voluntary, Competent patient & Informed (of benefits vs. risks and all tx options in easy to understand terminology) _Risks:_ * Post-op bleeding, bruising, swelling and pain * Infection * Damage to adjacent teeth * Trismus * Surgical +/- sutures * Upper = OAC and Fractured maxillary tuberosity * Lower = Dry socket and Paraesthesia of lip/chin/tongue _2-Stage Consent:_ 1st = Information given, discussed and consent signed 2nd = Consent reconfirmed before treatment (copy of consent form to be given to patient)
29
What are the 6 main stages involved in surgical tooth extraction?
1. Plan access (flap design) 2. Raise mucoperiosteal flap 3. +/- Bone removal 4. +/- 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\_* 5. Debridement/Irrigation - *Saline +/- haemostatic agent* 6. Wound closure with sutures
30
What is meant by a "complication"?
Any unplanned, adverse event that tends to increase comorbidity above what would usually be expected from a particular operative procedure under normal circumstances
31
What are the 5 aims of surgical extraction? (THINK: Why raise flap? Why remove bone? Why suture?)
1. Remove tooth (duh) 2. Improve vision 3. Create application point for elevation 4. Minimise trauma 5. Promote healing (via debridement and sutures)
32
What are the 6 main principles of flap design in surgical extraction?
1. Maintain blood supply (BROADER at BASE) 2. Avoid vital structures 3. Suture over bone 4. Preserve papillae 5. Maintain ability to extend 6. Maintain ability to close site
33
What is the main flap design for removal of third molars? (2)
Envelope (1-sided) or Triangular (2-sided)
34
What are the following flap names?
1. Envelope (One-sided) 2. Triangular (Two-sided) 3. Trapezium (Three-sided) 4. Semi-lunar 5. Y-Incision 6. Pedicle
35
What are the post-operative instructions for a patient after extraction? (7)
* LA wears off in few hours - Will get pain, take prophylactic pain relief * Soft diet (avoid hot foods esp with LA) * Avoid spitting/rinsing for first 24 hours * After, salt water rinses * Bite on gauze if bleeding/oozing * If serious bleeding & pain (lasting more than few days) - A&E or contact emergency number given * NO SMOKING
36
What are 10 intra/peri-operative complications during extraction?
1. Needle stick injury 2. Damage to adjacent teeth or soft tissues 3. OAC 4. Fractured tooth/apex 5. Swallowing/Inhalation of tooth fragment 6. Fractured mandible 7. Fractured tuberosity 8. Fractured alveolar bone 9. Haemorrhage 10. Lip burn (from drill)
37
What are 8 post-operative complications following tooth extraction?
1. Pain / Bruising / Swelling 2. Bleeding - Reactionary (loss of clot in first 48 hours) or Secondary (infection or bleeding disorder) 3. Infection (+ spread) 4. Dry socket 5. Osteomyelitis 6. Nerve damage 7. Haematoma 8. TMJ injury
38
What is the definition of "pain"?
An unpleasent sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage"
39
What are 5 signs of Mandibular fracture?
"Mandibles Open Now Tallulah Says" 1. Mobility 2. Occlusion change 3. Numbness of lower lip (IAN) 4. Trismus 5. Sublingual haematoma (blood seen under tongue)
40
What 4 signs might you see in a patient with a Zygomatic fracture?
1. Flattening + numbness of cheekbone 2. "Step deformity" on A-P palpation behind pt 3. Eyes - Diplopia, Restricted eye movement + Subconjunctival haemorrhage 4. Limited mandible opening (temporalis often affected)
41
What are 3 signs in a patient with an orbital fracture?
1. **Enophthalmos** (sinking of eye into sockey 2. Diplopia 3. Restricted eye movement 4. Subconjunctival haemorrhage ("Hanging drop" sign seen radiographically)
42
What is a "Guardsman's Fracture"?
Fracture of the right and left mandibular condyle Also presents with chin laceration from impact
43
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:_ 1. Apical foramen 2. PDL 3. Bloodstream ("Anchoresis")
44
Is the bacterium within an abscess: Mono-microbial or Polymicrobial? Endogenous or Exogenous? What bacteria are most often present?
Poly-microbial - Work syngeristiclly (together) Endogenous Bacteria present: * Obligate/Strict Anaerobes (most common) - *Fusobacterium, Prevotella, Porphymonas (esp. P. gingivalis)* * ​Facultative Anaerobes - *Streptococci*
45
What are the local (6) and systemic (3) signs of an Acute Periapical Abscess? Will you see radiographical changes?
_LOCAL_ 1. Pain (often poorly localised but TIQ may be painful and _mobile_ if follows pericapical periodontitis) 2. Swelling 3. Redness 4. Heat 5. Trismus (loss of function) 6. Lymphadenopathy _SYSTEMIC:_ * Fever * Elevated pulse * Elevated WBC, Serum Proteins (e.g. CRP) and ESR Radiographical signs vary - May be too soon to see changes (acute inflammation would take a few days to resorb bone)
46
What are 7 causes of a dental abscess ? (Think about routes of entry)
1. Caries 2. Non-vital tooth 3. Trauma 4. Deep periodontal pockets (via lateral canals) 5. Blood stream ("Anchoresis") 6. Extension of periapical infection from adjacent teeth
47
If a dento-alveolar abscess is left untreated, what will happen? What are the 3 general routes of biological pus drainage?
Untreated → Abscess enlargement and spontaneous pus drainage (through pathway of least resistance) 1. Through sinus tract, into oral cavity or facial skin 2. Through root canal or PDL 3. Through cancellous bone and cortex perforation Spontaneous drainage incomplete and does not address cause → Chronic/Reoccuring Abscess
48
What are 5 special tests you might want to take on a patient with a suspected dental abscess?
1. Radiographs (incl. CT and US) 2. Temperature 3. FBC - CRP 4. Pulse and BP 5. Blood glucose (poorly controlled diabetic = increased infection risk)
49
What are the 3 main treatment principles/stage for dental abscesses? How does each differ for GDP & OMFS?
**1) Drain Pus (Aspiration, Intra/Extra Oral Drainage)** * **GDP =** Intra-oral drainage (LA) * **OMFS** = Intra OR Extra-oral drainage (LA or GA) **2) Remove Cause/Source of Infection** * **GDP** = Extirpation or Extraction * **OMFS** = Extraction * *3) Consider Antibiotics** * (If incomplete drainage, severe infection (spread/fever) or MH concern, e.g. diabetic)* * **GDP =** Oral empirical Antibiotics (e.g. Penicillin or Metronidazole) * **OMFS** = IV antibiotics (empirical initially, thenm can give more specific after lab results from sample)
50
What is meant by "empirical" antibiotics in treatment of dental abscesses? Give examples.
Antibiotics prescribed first "Empirical" = Observation alone E.g. * Penicillins (Penicillin V or Amoxycillin) * Nitroimidazoles (Metronidazole) * Pt with penicillin allergies = Erythromycin, Clindamycin or Tetracyclin Pus sample obtained and sent to labs. More specific antibiotic can then be prescribed to target bacterium present.
51
What are the 3 main classes of a "Periodontium Abscess"? What is the main cause?
_Classes:_ 1. Gingival 2. Periodontal 3. Pericoronal _Main cause:_ Acute/Chronic Periodontium destruction → Localised pus collection Trauma (e.g. occlusion) to periodontal pocket orifice → Infection spread from pocket to supporting tissues
52
How *may* the microbiology of a Periodontal abscess differ from a Dento-alveolar abscess?
Contains spirochetes Otherwise same Polymicrobial, endogenous microbiology: * Obligate anaerobes (Fusobacterium, Prevotella, Porphymonas) * Facultative anaerobes (Streptococci)
53
What are 5 virulence factors for bacterium (e.g. in abscess formation)?
1. Number of bacterium 2. Invasion mechanisms 3. Evasion of host defence (e.g. capsules and proteases) 4. Toxins and Enzymes (e.g. endotoxin, collagenase, hyaluronidase and fibrinolysin) 5. Time & Hose response (acute/chronic)
54
What is meant by an "Odontogenic infection"? Give 5 examples
Any dental infection associated with teeth and surrounding tissues, often pus-producing * Abscesses * Acute Ulcerative Gingivitis * Osteomyelitis * MRORJ/ ORN * Infected cycts
55
What are the 3 stages of abscess infection spread?
STAGE 1: **CELLULITIS** *Oedema as infection spreads to connective tissue* * *Red & shiny* * *Fluctuant (but varied firmness dependent on amount of fluid present* * *Often non-suppurative (except at source)* * *Often Streptococci seen* STAGE 2: **SUPPURATIVE ("PUS-PRODUCING")** *Pus produced from _centre_ of lesion Dependent on: Gravity, Muscle activity and Pressure* STAGE 3: **GANGRENE**
56
What should you consider/do: 1. BEFORE 2. DURING 3. AFTER draining pus from an abscess?
1. BEFORE = Consider anatomical sites to avoid (e.g. Greater Palatine Artery in Palate and Facial artery/vein/nerve + Hypoglossal nerve in Submandibular space) 2. Breakdown/disturb locules in cavity with finger or sinus forceps 3. Keep drainage site open to allow further drainage
57
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*
58
What are the 3 main methods of infection spread? Which is the most common?
1. Direct (most common) 2. Lymophatics 3. Blood Infection spread follows pathway of LEAST resistance (E.g. Periodontal abscess = Through periodontal pocket Periapical abscess = Through thinnest cortical plate)
59
What are the bacterial/immunological (3) and anatomical (3) factors that affect the spread of infection?
_Bacterial/Immunological:_ * Number + virulence of bacterium * Host defence (e.g. immunocompromised) * Failure to drain pus (increased infection) _Anatomical:_ * Source of infection * Point of pus drainage through bone * Natural barriers to spread (e.g. mucous membranes)
60
What are the 4 potential pathways of MAXILLARY infection spread?
1. Canine 2. Buccal 3. Palatal 4. Lateral Pharyngeal (N.B. Buccal + Lateral Pharyngeal also in Mandibular spread)
61
What are the EIGHT (?!) potential pathways of Mandibular infection spread?
1. Submental 2. Sublingual 3. Submandibular 4. Submasseteric 5. Buccal 6. Lateral Pharngeal 7. Peritonsillar 8. Pterygomandibular
62
What anatomical **muscle(s)** affect the spread of infection for: 1. Mandibular incisors? 2. Mandibular pre-molars? 3. Mandibular molars? 4. Maxillary canines? 5. Maxillary molars?
1. Mentalis 2. Mylohyoid 3. Mylohyoid (lingual) AND Buccinator (buccal) 4. Strap muscles 5. Buccinator (and Antrum/Maxillary sinus)
63
Describe how the position of a MANDIBULAR ANTERIOR infection in relation to the MENTALIS MUSCLE would affect direction of spread?
ABOVE Mentalis → Labial sulcus BELOW Mentalis → Submental (Causes swellings in these areas)
64
Describe how the position of a MANDIBULAR POSTERIOR infection in relation to: 1. MYLOHYOID 2. BUCCINATOR would affect direction of spread?
**1) MYLOHYOID** ABOVE → Sublingual BELOW → Submandibular *Mylohyoid runs low anteriorly + higher posteriorly; so posterior infections more likely to have submandibular spread* **2) BUCCINATOR** ABOVE → Buccal sulcus BELOW → Buccal space *This is VICE VERSA for Maxillary posterior teeth!*
65
Describe how the position of a MAXILLARY POSTERIOR infection in relation to the BUCCINATOR muscle would affect the direction of spread?
ABOVE → Buccal Space BELOW → Buccal Sulcus
66
A patient comes in with an abscess/spreading infection, in what cases would you refer them to hospital? (5)
* Obstructed airway (e.g. Ludwig's Angina) * Rapidly spreading infection * Systemic signs: Pyrexic, raised BP, raised WBCs, malaise and toxic appearance * Immunocompromised/Diabetic pt * Severe trismus
67
Rarely, dental infections can spread to fascial planes - what are 5 potential areas of spread? (PIMP C)
1. Prevertebral fascia 2. Investing layer of deep cervical fascia 3. Mediastinum → Pericarditis 4. Pretracheal fascia 5. Carotid sheath
68
When draining an abscess in the submandibular space, what are 4 structures you should watch out for? How can these be avoided (where should you put your incision)?
1. Facial artery 2. Facial vein 3. Facial nerve 4. Hypoglossal Horizontal incision (parellel to lower border of mandible) made 2 fingers width below lower border of mandible
69
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)
70
What are 3 clinical causes of Acute Alveolar Abscess? (THINK 3 P's)
1. Periapical Periodontitis 2. Periodontal disease 3. Pericoronitis
71
What are the 1. Local (5) 2. Systemic (6) risk factors for impaired socket healing post-XLA?
**1) LOCAL** * Inflammation * Foreign body presence (including dressings!) * Bony fragment * Remaining tooth tissue * Radiation exposure **2) SYSTEMIC** * Medications (Bisphosphonates, Corticosteroids, OCP and Immunosuppressants) * Smoking * Diabetes * Malignancy * Nutritional deficiencies * Vascular diseases
72
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?
73
What is Dry Socket? * Alternative name * Aetiology
(Also known as "Localised Alveolar Osteitis") _Aetiology:_ INFLAMMATION due to **absence of blood clot** * Failure to form * Dislodged/lost * Excessive fibrinolytic activity Bacterial colonisation → Further clot lysis Regional inflammation prevents infection spread beyond socket
74
IMP EXAM Q ## Footnote What are 10 risk factors for Dry Socket?
1. Traumatic extraction (e.g. surgical) 2. Mandibular extraction (less vascular) 3. Previous dry socket experience 4. Smoker 5. Female 6. Oral Contraceptive Pill 7. Poor OH 8. Periodontal disease 9. Excessive vasoconstricter (e.g. LA → reduced blood supply) 10. Bone disorders (e.g. Pagets)
75
What are the clinical features you would observe/smell in a patient with Dry Socket? (4) What would be the presenting pain history?
1. _Empty_ socket with visible _exposed bone_ 2. Erythematous and tender surrounding gingivae 3. Throbbing pain 4. Foul smelling odour PAIN: Pain starting 2-3 days post-extraction and getting progressively worse
76
What is the management of Dry Socket?
1. Reassure (right tooth taken out, non-serious and will resolve) 2. Irrigate with saline (or CHX) under LA 3. Place Alvogyl or ZOE dressing 4. Pt Advice - Good OH, avoid smoking and adequate analgesia 5. Review appt (after few days and can be done over the phone)
77
What special investigations do you need for Dry Socket?
NONE - Clinical history and observation enough for diagnosis No radiographs needed - if pt presents again in pain take radiograph (LCPA) to investigate alternative diagnoses.
78
Do you prescribe antibiotics for: 1. Dry Socket? 2. Osteomyelitis? 3. Osteoradionecrosis? 4. MRONJ?
1. NO - This is primarily inflammation! 2. Yes (Empirical ABs them targetted ABs based on pus sample and 2 week course, OPAT) 3. Can do (But new tx = Pentoxifylline & Tocopherol) 4. No evidence for use
79
What is Osteomyelitis? What are the 5 different forms? (Auntie Catherine Cuddles Declan Sometimes)
Osteomyelitis = Infection (mixed bacterial - esp. Porphyromonas and Prevotella) and inflammation of the medullary bone cavity 1. Acute Osteomyelitis 2. Chronic Osteomyelitis 3. Diffuse Sclerosing Osteomyelitis 4. Chronic Low Grade Focal Osteomyelitis 5. Sclerosing Osteitis
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What differences exist between Acute and Chronic Osteomyelitis for: 1. prevalence? 2. pain presentation? 3. clinical presentation 4. management?
1. CHRONIC osteomyelitis is more common! 2. Acute = Throbbing pain Chronic = Above but LESS painful and LONGER LASTING 3. Acute = * Swelling (initially soft but more hard as new bone grows) * CN Viii compression → Paraesthesia of lip/chin * "Male patient with multiple dental infections: Chronic = * Localised sclerotic bone * Pus production and discharge via 1+ extra or intra oral sinus' 4. Acute = * Urgent OS/OM referal * Empirical antibiotics, take pus swap and target antibiotics * Debridement * Long term (2+ weeks ) out patient antibiotics (OPAT) Chronic = 1) Debridement 2) Corticotomy 3) +/- Antibacterial bead placement (e.g. Gentamicin)
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What is the definition of "Osteoradionecrosis"?
A _non-healing_ region of _devitalised_ bone in a _previously radiated_ field, which persists for a _minimum of 3 months_ in the absence of a reoccuring malignancy. Increased radiation dose = Increased risk
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Whats the aetiology of Acute Osteomyelitis? What are the 2 main bacterium present? Where?
Mixed bacterial infection in the _medullary cavity_ of bone most common = Porphyromonas + Prevotella Usually result of periapical infection spread...
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What are 6 clinical features in Acute Osteomyelitis? What is the most common site & why?
1. Throbbing pain (less localised than Dry Socket) 2. Swelling (begins soft but becomes more hard as host responds by laying down new bone) 3. Compression of CN Viii → Paraesthesia of lip/chin 4. Lymphadenopathy 5. Systemic signs (e.g. fever) "Male patient with multiple dental infections" Mandible = Most common site (less vascular)
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What are the 3 main special investigations done when suspected Acute Osteomyelitis? (What would you see on the radiograph (4))
**1) Radiograph (PA/Sectional OPG)** * "Moth-eaten" bone appearance * Loss of trabecular pattern * Periosteal reaction (new bone formed) * "Rarefying osteitis" - Poorly defined radiolucency **2) Pus sample** (Then used to target antibiotic therapy) **3) Blood Tests** Raised WBCs and CRP
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What is the management for a patient with Acute Osteomyelitis? (6)
1. URGENT OM/OS referal 2. 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* 3. Pus sample taken 4. Specific target antibiotics 5. Wound debridement 6. Long-term antibiotics 2+ weeks (Out Patient Antimicrobial Therapy, OPAT)
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What are the main empirical antibiotics of choice for Acute Osteomyelitis? (3)
BROAD-SPEC ANTIBIOTICS E.g. * Benzylpenicillin * Clindamycin * Metronidazole *N.B. Clindamycin is good for bony penetration but risk of C.difficle bacterial infection → severe diarrhoea (cease meds)*
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CHRONIC Osteomyelitis: 1. What is a risk/associated factor? (1) 2. What are some clinical features? (3) 3. What is the management? (3)
1. Radiotherapy 2. Low level dull ache, localised sclerotic bone +/- Suppuration - with one or more intra or extra-oral sinus' 3. Debridement, Corticotomy +/- Antibacterial bead placement (e.g. Gentamicin)
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What is the: 1. OLD (3) 2. NEW (2) treatment for Osteoradionecrosis?
1. OLD = Antibiotics, Hyperbaric Oxygen Therapy and Surgery 2. NEW = Pentoxifylline and Tocopherol (Vit. E) MOST IMP = **Prevention!** * Full dental assessment - extraction of poor prognosis teeth (at least 6 weeks before starting tx) * High fluoride + good OHI * Relieve dental trauma area * Regular review * Good communication with hospital team (OMFS etc)
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What staging can be used for ORN (Osteoradionecrosis)? (HINT: 3 stages)
**"Notani" Staging:** STAGE 1 = ORN confined to alveolar bone STAGE 2 = ORN limited to alveolar bone and/or mandible (above level of mandibular canal) STAGE 3 = ORN extends to mandible UNDER level of mandibular canal WITH ORN skin fistula or pathological fracture
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Osteoradionecrosis has similar features to Chronic Osteomyelitis (e.g. localised sclerotic bone, extra/intra oral fistula)... except...? (2)
1. Healing is slower or non-existent 2. NO periosteal reaction (no new bone growth) → Higher pathological fracture risk
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What is the definition of MRONJ? Following this, what are the 4 diagnostic features that must be met?
MRONJ (Medication-Related Ostoeonecrosis of the Jaw) Severe adverse reaction to a**nti-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:_ 1. Currently or previously taking anti-resorptive or anti-angiogenic medication 2. Exposed bone or bone that can be probed through intra or extra-oral fistula - persisting over 8 weeks 3. No history of radiotherapy 4. No obvious metastatic jaw disease
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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)
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What are 3 indications (conditions) for use of Bisphonates?
1. Osteoporosis 2. Paget's Disease 3. Cancers - Multiple myeloma or Metastatic Bone Cancer
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What are the 2 main forms of Anti-resorptive medications? How do they differ in: * Method of Action? * Method of Administration? * Half life?
1. Bisphosphonates 2. RANKL Inhibitors _Method of Action:_ Both inhibit bone resorption... **B** = via osteoclast apoptosis **R** = via inhibition of RANKL (normally stimulates osteoclast function) _Method of Administration:_ * *B** = Oral (e.g. Alondronate) or IV (Zoledronate) * *R** = Subcutaneous (e.g. Denosumab) _Half-life:_ * *B** = Longer half-life (binds to bone and effect lasts till new bone laid) * *R** = Shorter half-life (does NOT bind to bone and effects last 6 months)
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Outline the general drug features of Bisphosphonates? (E.g. Pharmacology, MOA, Administration, Half life)
* Pyrophospahte analogues * Inhibit bone resorption via osteoclast apoptosis (high affinity to areas of high bone turnover) * Administration: Oral (e.g. Alendronate) or IV (e.g. Zoledronate) * Long half life - Binds to bone and effect deminished after new bone formed * Nitrogen-containing bisphosphonates = Increased likelihood of MRONJ
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What are 7 risk factors which increase chance of a patient getting MRONJ? (Think medication (4), procedure (2) and Pt history)
1. Route of administration (IV \> Oral) 2. Duration (IV = 3+ infusions and Oral = 4+ years) 3. Increased dose and indications (Cancer \>\>) 4. Increased potency 5. Trauma severity of procedure (OS \>\>) 6. Site: Mandible & Posterior 7. Additional pt MH concerns - Immunosuppression - Dual therapy (e.g. chemotherapy)
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For MRONJ, what are the vague dates/duration of treatment that puts a pt at higher risk if having: 1. IV bisphosphonates? 2. Oral bisphosphonates?
IV = 3+ infusions or 1 year Oral = 4+ YEARS
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What is the main method of action for Bisphosphonate medications? What are 4 other suggested mechanisms?
Inhibition of bone resorption via: Inhibition of osteocyte differentiation and function →apoptosis _Alternative:_ * Inflammation/Infection * Inhibition of angiogenesis * Soft tissue toxicity (apoptosis of other cell types)
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How and why would you manage a patient who's about to start taking anti-resorptive (Bisphosphonates/RANKL Inhibitors) or anti-angiogenic (VEGF/Tyrosine Kinase Inhibitors)?
WHY? Pt at higher risk of MRONJ _HOW:_ * Pt education on MRONJ risk * Dental assessment: XLA poor prognosis unrestorable teeth * *Ideally leave 10+ days for healing before starting medication** * Assess prosthesis for mucosal injury and relieve site * Good OH * Smoking cessarion * Regular check-ups and general prevention
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A patient at high risk MRONJ has come in for an extraction, what is your management?
* Consider alternatives for XLA (e.g. extirpate) * Refer high risk to secondary care (hospital) and liase with oncologist/orthopeadist _In hospital:_ * XLA one sextant at a time and monitor healing * CHX mouthwash before AND after XLA (2 wks) * Avoid surgical if possible (If surgical, primary closure with split thickness flap) * +/- (no evidence) pre and post-op antibiotics * +/- (weak evidence) drug holiday - consult oncologist
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What are the 4 management goals for a patient with MRONJ?
1. Prioritise oncology treatment (delay tx) 2. Maintain QoL (extirpate \> XLA) 3. Control pain + infection (analgesics and antimicrobials) 4. Prevent extension or formation of new osteonecrotic lesion
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How can MRONJ be staged (0-3)? What clinical features would you observe at each? How would you manage it?
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How might MRONJ present depending on severity?
MRONJ = Exposed bone or bone that can be probed through intra or extra oral fistula May be ASYMPTOMATIC (MRONJ Stage 1) Symptoms: * Pain * Swelling * Halitosis * Infection * Severe = Numbness of ID nerve or pathological #
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