infections Flashcards
What is the definition of an acute dentoalveolar abscess?
A circumscribed suppurative inflammation involving the tooth, alveolar bone, and sometimes surrounding soft tissue.
What are the types of ADAA?
Early stage and late stage (cellulitis).
What is characteristic of ADAA in the early stage?
Inflammation is confined to the investing bone without overlying soft tissue involvement.
How does late-stage ADAA develop?
Exudate and bacteria perforate the bone, spreading through fascial planes to distant parts of the face.
What is the radiographic appearance of early-stage ADAA?
Negative unless due to acute exacerbation of chronic abscess.
What causes extrusion of the tooth in early-stage ADAA?
Inflammatory pressure on periodontal ligament fibers.
What are the systemic manifestations of early-stage ADAA?
Fever, malaise, and other signs of acute inflammation.
What occurs during late-stage ADAA?
Bone perforation leads to sub-periosteal abscess formation and infection spread through fascial spaces.
What role does muscle attachment play in late-stage ADAA?
Limits intraoral swelling and may cause “gum boil” formation.
What predisposes to the progression to late-stage ADAA?
Improper management, immunocompromise, or highly virulent microorganisms.
What is the radiographic appearance of late-stage ADAA?
Widening of the periodontal membrane as a uniform radiolucent line around the apex.
What are the key symptoms of ADAA?
Severe throbbing pain, tenderness on percussion, and systemic signs like fever.
What clinical feature distinguishes late-stage ADAA?
Diffuse swelling and trismus with involvement of the masticator space.
What systemic symptoms accompany late-stage ADAA?
Malaise, fever, and lymphadenitis.
How can late-stage ADAA be differentiated radiographically?
Presence of periapical radiolucency with diffuse margins.
What is the management of early-stage ADAA?
Antibiotics, analgesics, bed rest, a high-protein diet, and removal of the cause (e.g., RCT or extraction).
What additional treatment is needed for late-stage ADAA?
Proper drainage of pus and close monitoring to prevent systemic spread.
How is gum boil in late-stage ADAA treated?
Incision and drainage with antibiotics.
Why is early intervention crucial in ADAA?
To prevent progression to cellulitis and systemic complications.
What is chronic dentoalveolar abscess?
A condition caused by untreated acute abscess or highly virulent bacteria in the presence of strong host immunity.
What are the symptoms of a chronic dentoalveolar abscess?
Usually asymptomatic with the presence of a fistula draining pus.
What are the radiographic findings?
Rounded or irregular periapical radiolucent area.
How is chronic dentoalveolar abscess treated?
Similar to ADAA treatment, with excision of the fistula after drainage ceases.
What is pericoronitis?
Infection of pericoronal tissues around a partially erupted tooth, often the mandibular third molar.
What are the predisposing factors for pericoronitis?
Humidity, warmth, food debris accumulation, and trauma from opposing teeth.
Which tooth is most commonly affected by pericoronitis?
The mandibular third molar.
Why is the pericoronal flap susceptible to infection?
It provides an incubator-like environment: humidity, warmth, food debris, and protection from saliva.
What are the common symptoms of pericoronitis?
Severe pain, trismus, difficulty swallowing, and foul odor.
What are the extreme complications of pericoronitis?
Systemic inflammation, cellulitis, and spread to adjacent fascial spaces.
How does the pericoronal tissue appear clinically?
Shiny, erythematous, and edematous with possible pus extrusion.
How is mild pericoronitis managed?
Debridement of the pocket, irrigation with warm saline, and local antiseptics.
What additional treatment is needed for severe pericoronitis?
Antibiotics and incision and drainage of the abscess if fluctuant.
What is operculectomy?
Removal of the pericoronal flap, preferably with laser therapy, when proper eruption is anticipated.
When is tooth extraction indicated in pericoronitis?
When the tooth is malposed or cannot erupt properly to occlude with the opposing tooth.
What is osteomyelitis?
An inflammatory condition of bone that begins as medullary infection and rapidly involves surrounding structures.
What are the common causes of osteomyelitis?
Odontogenic infections, trauma (e.g., compound fractures), excessive heat from rotary burs, and hematogenous spread.
Why is the mandible more affected than the maxilla?
Denser cortical bone and poorer blood supply compared to the maxilla.
What is the pathogenesis of osteomyelitis?
Infection compromises blood supply, causing ischemia and necrosis; pus travels through haversian systems to periosteum.
What is sequestrum?
A localized section of necrotic bone separated from surrounding healthy bone by granulation tissue.
What are the types of non-specific osteomyelitis?
Suppurative (acute and chronic forms) and non-suppurative (e.g., sclerosing osteomyelitis).
What are the examples of specific osteomyelitis?
Syphilitic, tuberculous, and actinomycotic osteomyelitis.
How does chronic sclerosing osteomyelitis present?
With diffuse or localized sclerosis and bone thickening.
What are the key symptoms of acute osteomyelitis?
Rapid onset fever, severe diffuse pain, trismus, and dysphagia.
What is a common radiographic finding in acute osteomyelitis?
Ill-defined lucency due to trabecular destruction.
What distinguishes chronic osteomyelitis radiographically?
“Moth-eaten” bone destruction with radiopaque islands (sequestra).
What are the medical measures for osteomyelitis management?
Antibiotics, hyperbaric oxygen therapy, and supportive measures to enhance immunity.
What surgical procedures are used for osteomyelitis?
Sequestrectomy, saucerization, decortication, and resection in severe cases.
Why is hyperbaric oxygen therapy used in osteomyelitis?
It enhances tissue oxygenation, angiogenesis, and sequestra formation.
How long is antibiotic therapy required for chronic osteomyelitis?
A minimum of 4 weeks of IV antibiotics, followed by oral antibiotics if necessary.
What is osteoradionecrosis?
Exposed bone in a previously irradiated site lasting more than three months, unrelated to tumor recurrence.
What is the pathophysiology of ORN?
Radiation arteritis leads to hypoxic, hypovascular, and hypocellular tissue, causing bone necrosis.
What are the main risk factors for ORN?
High radiation dose, poor oral hygiene, alcohol/tobacco use, and dental extractions.
Why is the mandible more affected by ORN?
Poor blood supply, higher bone density, and proximity to radiation fields.
What are pre-radiation preventive measures for ORN?
Dental extractions 14–21 days before radiation, periodontal therapy, and oral hygiene instructions.
Why are dentures avoided post-radiation?
To prevent trauma to irradiated bone during the first year after therapy.
What is the role of hyperbaric oxygen therapy in preventing ORN?
It improves tissue vascularity and reduces ORN risk during and after dental extractions.
How is ORN managed in early stages?
Hyperbaric oxygen therapy followed by debridement.
What surgical options are available for ORN?
Resection of necrotic bone and reconstruction with vascularized flaps.
What medications are used in ORN management?
PENTOCLO (pentoxifylline, tocopherol, clodronate).
What is MRONJ?
Necrosis of jaw bone associated with antiresorptive or antiangiogenic medications like bisphosphonates and denosumab.
What are bisphosphonates commonly used to treat?
Osteoporosis, metastatic bone disease, multiple myeloma, and Paget’s disease.
How do bisphosphonates cause MRONJ?
They inhibit osteoclast function, preventing bone remodeling and renewal.
What are the clinical criteria for diagnosing MRONJ?
Exposed bone for >8 weeks, history of antiresorptive therapy, and no radiation history.
What are the clinical features of stage 0 MRONJ?
Non-exposed bone variant with signs like loosening of teeth and swelling.
What defines stage 1 MRONJ?
Exposed necrotic bone without infection or inflammation.
What distinguishes stage 2 MRONJ from stage 1?
Presence of infection or inflammation with exposed necrotic bone.
What are the complications in stage 3 MRONJ?
Pathologic fracture, extraoral fistula, or osteolysis extending to sinus floor or mandible.
How is MRONJ prevented in nonmalignant disease?
Dental optimization and patient education about regimented oral care.
What is the treatment approach for stage 1 MRONJ?
Antimicrobial rinses and monitoring.
What surgical interventions are needed for advanced MRONJ?
Debridement, resection, and reconstruction if necessary.
Why are dental implants contraindicated in MRONJ patients?
Impaired bone healing increases the risk of complications and implant failure.
What are the four stages of odontogenic infection?
Inoculation, cellulitis, abscess formation, and resolution.
What factors influence the severity of infection?
Host immunity, organism virulence, and environmental factors like compromised blood supply.
What are the differences between cellulitis and abscess?
Cellulitis: diffuse, painful, and firm; Abscess: localized, fluctuant, and painful.
How does muscle attachment affect the spread of infection?
Determines whether infection spreads intraorally or extraorally.
What anatomical factors govern the spread of odontogenic infections?
Bone thickness, root apex relation to muscle attachments, and fascial space organization.
What is the primary space of infection for maxillary anterior teeth?
Buccal space for central incisor and canine; palatal space for lateral incisor.
What are the common fascial spaces involved in mandibular infections?
Submental, sublingual, and submandibular spaces.
How does infection spread from maxillary molars?
Buccally from buccal roots; palatally from palatal roots.
What is Ludwig’s angina?
Bilateral cellulitis involving submental, submandibular, and sublingual spaces.
What are the complications of Ludwig’s angina?
Airway obstruction, mediastinitis, and death if untreated.
What are the principles of managing odontogenic infections?
Determine severity, evaluate host defenses, surgical treatment, medical support, and antibiotic selection.
Why is surgical intervention essential in odontogenic infections?
To secure the airway, remove the cause, and provide drainage.
What is the role of incision and drainage (I&D)?
Drains pus, reduces tension, and promotes healing.
What are the key factors in prescribing antibiotics for odontogenic infections?
Severity of infection, surgical adequacy, and host defense state.
What is Ludwig’s angina?
Rapidly spreading cellulitis involving the submental, submandibular, and sublingual spaces bilaterally.
What are the clinical features of Ludwig’s angina?
Hard, painful swelling in the floor of the mouth; protruded and swollen tongue; trismus; dysphagia.
What are the life-threatening complications of Ludwig’s angina?
Airway obstruction, mediastinitis, and death.
How is airway management achieved in Ludwig’s angina?
Emergency cricothyroidotomy or tracheostomy, and intravenous dexamethasone for edema reduction.
How can odontogenic infections cause orbital abscess?
Direct spread from anterior teeth or via infratemporal space and maxillary osteomyelitis.
What are the clinical features of orbital abscess?
Proptosis, ophthalmoplegia, decreased visual acuity, and periorbital edema.
What are the complications of orbital abscess?
Cavernous sinus thrombosis, meningitis, and vision loss.
How is orbital abscess managed?
Hospitalization, IV antibiotics, and surgical drainage (e.g., lateral canthotomy).
What are the causes of brain abscess in odontogenic infections?
Spread from sinuses, orbit, or directly via osteomyelitis.
What are the symptoms of brain abscess?
Headache, fever, vomiting, altered mental status, and neurological deficits.
What is the treatment for brain abscess?
Empirical IV antibiotics, corticosteroids for edema, and surgical intervention.
What is cavernous sinus thrombosis?
Infection-induced thrombosis in the cavernous sinus, often caused by spread from the danger triangle of the face.
What are the signs of cavernous sinus thrombosis?
Ptosis, proptosis, ophthalmoplegia, and vision loss.
How is cavernous sinus thrombosis diagnosed?
Based on clinical features and imaging (CT/MRI).
What is the management of cavernous sinus thrombosis?
Broad-spectrum IV antibiotics, heparin, and drainage of the primary infection source.
What are the key signs of severe odontogenic infections?
Trismus, dysphagia, respiratory distress, and systemic involvement (fever, tachycardia).
Why is early intervention critical in odontogenic infections?
To prevent life-threatening complications like airway obstruction and systemic sepsis.
How do fascial spaces guide infection management?
Understanding the anatomical spread helps determine appropriate surgical drainage sites.
What are the principles of incision and drainage?
Use dependent drainage, blunt dissection, and secure drains to promote healing.
