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Oral surgery > infections > Flashcards

infections Flashcards

1
Q

What is the definition of an acute dentoalveolar abscess?

A

A circumscribed suppurative inflammation involving the tooth, alveolar bone, and sometimes surrounding soft tissue.

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2
Q

What are the types of ADAA?

A

Early stage and late stage (cellulitis).

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3
Q

What is characteristic of ADAA in the early stage?

A

Inflammation is confined to the investing bone without overlying soft tissue involvement.

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4
Q

How does late-stage ADAA develop?

A

Exudate and bacteria perforate the bone, spreading through fascial planes to distant parts of the face.

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5
Q

What is the radiographic appearance of early-stage ADAA?

A

Negative unless due to acute exacerbation of chronic abscess.

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6
Q

What causes extrusion of the tooth in early-stage ADAA?

A

Inflammatory pressure on periodontal ligament fibers.

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7
Q

What are the systemic manifestations of early-stage ADAA?

A

Fever, malaise, and other signs of acute inflammation.

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8
Q

What occurs during late-stage ADAA?

A

Bone perforation leads to sub-periosteal abscess formation and infection spread through fascial spaces.

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9
Q

What role does muscle attachment play in late-stage ADAA?

A

Limits intraoral swelling and may cause “gum boil” formation.

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10
Q

What predisposes to the progression to late-stage ADAA?

A

Improper management, immunocompromise, or highly virulent microorganisms.

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11
Q

What is the radiographic appearance of late-stage ADAA?

A

Widening of the periodontal membrane as a uniform radiolucent line around the apex.

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12
Q

What are the key symptoms of ADAA?

A

Severe throbbing pain, tenderness on percussion, and systemic signs like fever.

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13
Q

What clinical feature distinguishes late-stage ADAA?

A

Diffuse swelling and trismus with involvement of the masticator space.

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14
Q

What systemic symptoms accompany late-stage ADAA?

A

Malaise, fever, and lymphadenitis.

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15
Q

How can late-stage ADAA be differentiated radiographically?

A

Presence of periapical radiolucency with diffuse margins.

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16
Q

What is the management of early-stage ADAA?

A

Antibiotics, analgesics, bed rest, a high-protein diet, and removal of the cause (e.g., RCT or extraction).

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17
Q

What additional treatment is needed for late-stage ADAA?

A

Proper drainage of pus and close monitoring to prevent systemic spread.

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18
Q

How is gum boil in late-stage ADAA treated?

A

Incision and drainage with antibiotics.

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19
Q

Why is early intervention crucial in ADAA?

A

To prevent progression to cellulitis and systemic complications.

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20
Q

What is chronic dentoalveolar abscess?

A

A condition caused by untreated acute abscess or highly virulent bacteria in the presence of strong host immunity.

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21
Q

What are the symptoms of a chronic dentoalveolar abscess?

A

Usually asymptomatic with the presence of a fistula draining pus.

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22
Q

What are the radiographic findings?

A

Rounded or irregular periapical radiolucent area.

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23
Q

How is chronic dentoalveolar abscess treated?

A

Similar to ADAA treatment, with excision of the fistula after drainage ceases.

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24
Q

What is pericoronitis?

A

Infection of pericoronal tissues around a partially erupted tooth, often the mandibular third molar.

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25
Q

What are the predisposing factors for pericoronitis?

A

Humidity, warmth, food debris accumulation, and trauma from opposing teeth.

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26
Q

Which tooth is most commonly affected by pericoronitis?

A

The mandibular third molar.

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27
Q

Why is the pericoronal flap susceptible to infection?

A

It provides an incubator-like environment: humidity, warmth, food debris, and protection from saliva.

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28
Q

What are the common symptoms of pericoronitis?

A

Severe pain, trismus, difficulty swallowing, and foul odor.

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29
Q

What are the extreme complications of pericoronitis?

A

Systemic inflammation, cellulitis, and spread to adjacent fascial spaces.

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30
Q

How does the pericoronal tissue appear clinically?

A

Shiny, erythematous, and edematous with possible pus extrusion.

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31
Q

How is mild pericoronitis managed?

A

Debridement of the pocket, irrigation with warm saline, and local antiseptics.

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32
Q

What additional treatment is needed for severe pericoronitis?

A

Antibiotics and incision and drainage of the abscess if fluctuant.

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33
Q

What is operculectomy?

A

Removal of the pericoronal flap, preferably with laser therapy, when proper eruption is anticipated.

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34
Q

When is tooth extraction indicated in pericoronitis?

A

When the tooth is malposed or cannot erupt properly to occlude with the opposing tooth.

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35
Q

What is osteomyelitis?

A

An inflammatory condition of bone that begins as medullary infection and rapidly involves surrounding structures.

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36
Q

What are the common causes of osteomyelitis?

A

Odontogenic infections, trauma (e.g., compound fractures), excessive heat from rotary burs, and hematogenous spread.

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37
Q

Why is the mandible more affected than the maxilla?

A

Denser cortical bone and poorer blood supply compared to the maxilla.

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38
Q

What is the pathogenesis of osteomyelitis?

A

Infection compromises blood supply, causing ischemia and necrosis; pus travels through haversian systems to periosteum.

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39
Q

What is sequestrum?

A

A localized section of necrotic bone separated from surrounding healthy bone by granulation tissue.

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40
Q

What are the types of non-specific osteomyelitis?

A

Suppurative (acute and chronic forms) and non-suppurative (e.g., sclerosing osteomyelitis).

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41
Q

What are the examples of specific osteomyelitis?

A

Syphilitic, tuberculous, and actinomycotic osteomyelitis.

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42
Q

How does chronic sclerosing osteomyelitis present?

A

With diffuse or localized sclerosis and bone thickening.

43
Q

What are the key symptoms of acute osteomyelitis?

A

Rapid onset fever, severe diffuse pain, trismus, and dysphagia.

44
Q

What is a common radiographic finding in acute osteomyelitis?

A

Ill-defined lucency due to trabecular destruction.

45
Q

What distinguishes chronic osteomyelitis radiographically?

A

“Moth-eaten” bone destruction with radiopaque islands (sequestra).

46
Q

What are the medical measures for osteomyelitis management?

A

Antibiotics, hyperbaric oxygen therapy, and supportive measures to enhance immunity.

47
Q

What surgical procedures are used for osteomyelitis?

A

Sequestrectomy, saucerization, decortication, and resection in severe cases.

48
Q

Why is hyperbaric oxygen therapy used in osteomyelitis?

A

It enhances tissue oxygenation, angiogenesis, and sequestra formation.

49
Q

How long is antibiotic therapy required for chronic osteomyelitis?

A

A minimum of 4 weeks of IV antibiotics, followed by oral antibiotics if necessary.

50
Q

What is osteoradionecrosis?

A

Exposed bone in a previously irradiated site lasting more than three months, unrelated to tumor recurrence.

51
Q

What is the pathophysiology of ORN?

A

Radiation arteritis leads to hypoxic, hypovascular, and hypocellular tissue, causing bone necrosis.

52
Q

What are the main risk factors for ORN?

A

High radiation dose, poor oral hygiene, alcohol/tobacco use, and dental extractions.

53
Q

Why is the mandible more affected by ORN?

A

Poor blood supply, higher bone density, and proximity to radiation fields.

54
Q

What are pre-radiation preventive measures for ORN?

A

Dental extractions 14–21 days before radiation, periodontal therapy, and oral hygiene instructions.

55
Q

Why are dentures avoided post-radiation?

A

To prevent trauma to irradiated bone during the first year after therapy.

56
Q

What is the role of hyperbaric oxygen therapy in preventing ORN?

A

It improves tissue vascularity and reduces ORN risk during and after dental extractions.

57
Q

How is ORN managed in early stages?

A

Hyperbaric oxygen therapy followed by debridement.

58
Q

What surgical options are available for ORN?

A

Resection of necrotic bone and reconstruction with vascularized flaps.

59
Q

What medications are used in ORN management?

A

PENTOCLO (pentoxifylline, tocopherol, clodronate).

60
Q

What is MRONJ?

A

Necrosis of jaw bone associated with antiresorptive or antiangiogenic medications like bisphosphonates and denosumab.

61
Q

What are bisphosphonates commonly used to treat?

A

Osteoporosis, metastatic bone disease, multiple myeloma, and Paget’s disease.

62
Q

How do bisphosphonates cause MRONJ?

A

They inhibit osteoclast function, preventing bone remodeling and renewal.

63
Q

What are the clinical criteria for diagnosing MRONJ?

A

Exposed bone for >8 weeks, history of antiresorptive therapy, and no radiation history.

64
Q

What are the clinical features of stage 0 MRONJ?

A

Non-exposed bone variant with signs like loosening of teeth and swelling.

65
Q

What defines stage 1 MRONJ?

A

Exposed necrotic bone without infection or inflammation.

66
Q

What distinguishes stage 2 MRONJ from stage 1?

A

Presence of infection or inflammation with exposed necrotic bone.

67
Q

What are the complications in stage 3 MRONJ?

A

Pathologic fracture, extraoral fistula, or osteolysis extending to sinus floor or mandible.

68
Q

How is MRONJ prevented in nonmalignant disease?

A

Dental optimization and patient education about regimented oral care.

69
Q

What is the treatment approach for stage 1 MRONJ?

A

Antimicrobial rinses and monitoring.

70
Q

What surgical interventions are needed for advanced MRONJ?

A

Debridement, resection, and reconstruction if necessary.

71
Q

Why are dental implants contraindicated in MRONJ patients?

A

Impaired bone healing increases the risk of complications and implant failure.

72
Q

What are the four stages of odontogenic infection?

A

Inoculation, cellulitis, abscess formation, and resolution.

73
Q

What factors influence the severity of infection?

A

Host immunity, organism virulence, and environmental factors like compromised blood supply.

74
Q

What are the differences between cellulitis and abscess?

A

Cellulitis: diffuse, painful, and firm; Abscess: localized, fluctuant, and painful.

75
Q

How does muscle attachment affect the spread of infection?

A

Determines whether infection spreads intraorally or extraorally.

76
Q

What anatomical factors govern the spread of odontogenic infections?

A

Bone thickness, root apex relation to muscle attachments, and fascial space organization.

77
Q

What is the primary space of infection for maxillary anterior teeth?

A

Buccal space for central incisor and canine; palatal space for lateral incisor.

78
Q

What are the common fascial spaces involved in mandibular infections?

A

Submental, sublingual, and submandibular spaces.

79
Q

How does infection spread from maxillary molars?

A

Buccally from buccal roots; palatally from palatal roots.

80
Q

What is Ludwig’s angina?

A

Bilateral cellulitis involving submental, submandibular, and sublingual spaces.

81
Q

What are the complications of Ludwig’s angina?

A

Airway obstruction, mediastinitis, and death if untreated.

82
Q

What are the principles of managing odontogenic infections?

A

Determine severity, evaluate host defenses, surgical treatment, medical support, and antibiotic selection.

83
Q

Why is surgical intervention essential in odontogenic infections?

A

To secure the airway, remove the cause, and provide drainage.

84
Q

What is the role of incision and drainage (I&D)?

A

Drains pus, reduces tension, and promotes healing.

85
Q

What are the key factors in prescribing antibiotics for odontogenic infections?

A

Severity of infection, surgical adequacy, and host defense state.

86
Q

What is Ludwig’s angina?

A

Rapidly spreading cellulitis involving the submental, submandibular, and sublingual spaces bilaterally.

87
Q

What are the clinical features of Ludwig’s angina?

A

Hard, painful swelling in the floor of the mouth; protruded and swollen tongue; trismus; dysphagia.

88
Q

What are the life-threatening complications of Ludwig’s angina?

A

Airway obstruction, mediastinitis, and death.

89
Q

How is airway management achieved in Ludwig’s angina?

A

Emergency cricothyroidotomy or tracheostomy, and intravenous dexamethasone for edema reduction.

90
Q

How can odontogenic infections cause orbital abscess?

A

Direct spread from anterior teeth or via infratemporal space and maxillary osteomyelitis.

91
Q

What are the clinical features of orbital abscess?

A

Proptosis, ophthalmoplegia, decreased visual acuity, and periorbital edema.

92
Q

What are the complications of orbital abscess?

A

Cavernous sinus thrombosis, meningitis, and vision loss.

93
Q

How is orbital abscess managed?

A

Hospitalization, IV antibiotics, and surgical drainage (e.g., lateral canthotomy).

94
Q

What are the causes of brain abscess in odontogenic infections?

A

Spread from sinuses, orbit, or directly via osteomyelitis.

95
Q

What are the symptoms of brain abscess?

A

Headache, fever, vomiting, altered mental status, and neurological deficits.

96
Q

What is the treatment for brain abscess?

A

Empirical IV antibiotics, corticosteroids for edema, and surgical intervention.

97
Q

What is cavernous sinus thrombosis?

A

Infection-induced thrombosis in the cavernous sinus, often caused by spread from the danger triangle of the face.

98
Q

What are the signs of cavernous sinus thrombosis?

A

Ptosis, proptosis, ophthalmoplegia, and vision loss.

99
Q

How is cavernous sinus thrombosis diagnosed?

A

Based on clinical features and imaging (CT/MRI).

100
Q

What is the management of cavernous sinus thrombosis?

A

Broad-spectrum IV antibiotics, heparin, and drainage of the primary infection source.

101
Q

What are the key signs of severe odontogenic infections?

A

Trismus, dysphagia, respiratory distress, and systemic involvement (fever, tachycardia).

102
Q

Why is early intervention critical in odontogenic infections?

A

To prevent life-threatening complications like airway obstruction and systemic sepsis.

103
Q

How do fascial spaces guide infection management?

A

Understanding the anatomical spread helps determine appropriate surgical drainage sites.

104
Q

What are the principles of incision and drainage?

A

Use dependent drainage, blunt dissection, and secure drains to promote healing.

Oral surgery (5 decks)

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