05 - Clinical Applications: Infections

pulpal inflammation

pulp is unusual because it is trapped inside rigid dentin

• no room to expand, one narrow route for neurovascular entry/exit through apical foramen, no collateral circulation

• mechanism —

  1. bacterial irritation / injury

  2. vasodilation + increased vascular permeability

  3. exudate accumulates, causing tissue pressure in rigid dentin

  4. thin-walled venules compressed first, decreasing venous outflow

  5. blood accumulates, causing pressure to rise faster

  6. arterial perfusion falls, leading to ischemia

  7. ATP depletion and cell injury

  8. necrosis

reversible pulpitis

mild inflammation of the pulp that can return to normal if causative stimulus is removed

• stimulus-dependent

• symptoms — often asymptomatic

  • stimuli to cold, heat, or air can produce a sharp, transient pain

  • pain stops as soon as stimulus is removed

• pathology — an adaptation

  • remove caries, and it can reverse

irreversible pulpitis

pulpal inflammation that will not return to normal even if the original stimulus is removed

• irreversible injury threshold has been crossed

• symptoms — spontaneous pain, lingering pain after stimulus removed, pain that wakes patient at night

• progression — to pulp necrosis as pressure chain completes

• pathology — injury threshold crossed

  • if no pain, tissue may be necrotic

vital vs non-vital pulp

vital pulp — pulpal tissues are alive; non-vital pulp — pulpal tissues are dead

• sequence —

  1. pulp with irreversible pulpitis will become non-vital

  2. necrotic pulp becomes reservoir of bacteria

  3. breakdown products go out through apex

• when pulp dies, the pain from pulp often stops

  • if patient reports that toothache went away, the pulp likely died

endo diagnoses into pathology

• symptomatic apical periodontitis → pain on biting or percussion; peripapical tissues are inflamed

  • acute inflammation of PDL at apex, sometimes with widening of PDL

• asymptomatic apical periodontitis → periapical radiolucency with no symptoms

  • usually periapical granuloma, sometimes a cyst

  • sometimes not painful due to equilibrium of pain vs fighting infection

• acugte apical abscess → rapid onset, pain, tenderness, swelling

  • periapical abscess containing neutrophils and pus

• chronic apical abscess → graudual onset, little discomfort, intermittent drainage through sinus tract

  • abscess that has found a way out and settled into equiibrium

  • relief of neutrophils and debris, bringing in oxygen to kill anaerobes

• condensing osteitis → diffuse radiopacity around apex

  • bone laid down in response to low-grade, long-standing stimulus

lesions at the apex

1. periapical abscess — acute inflammatory focus at the apex of non-vital tooth

   • may sit laterally if drains through accessory canal

   • origin → infected necrotic pulp

   • clinical features → negative to pulp and thermal testing, tender to percussion, may produce swelling and draining into sinus tract

     • Parulis — localized sessile swelling on alveolar mucosa

     • cutaneous sinus — draining into skin

     • cellulitus — process spreading diffusely through overlying soft tissues

   • radiograph → normal early because bone destruction has not yet progressed enough to become radiographically visible

   • histology → mainly neutrophils with liquefactive necrosis (pus)

2. periapical granuloma — chronic inflammatory tissue at apex of non-vital tooth

   • also called asymptomatic apical periodontitis

   • origin → infectious pulp that host has contained but not cleared

   • clinical features → asymptomatic, with a few exceptions

     • negative to thermal and electric pulp testing

     • equilibrium between destruction and repair

   • radiograph → well-defined periapical radiolucency

   • histology → granulation tissue containing macrophages, lymphocytes, plasma cells

3. periapical cyst — inflammatory odontogenic cyst associated with non-vital tooth and epithelial lining derived from rests of Malassez

   • called radicular cyst when along the side of root

   • origin → epithelial rests of Malassez from root development

     • stimulated to proliferate by surrounding inflammation

   • clinical features → usually asymptomatic, with non-vital tooth

     • clinical swelling usually absent

   • radiograph → well-defined radiolucency larger than granuloma

     • cannot reliably distinguish granuloma from cyst on radiograph; must have histologic diagnosis

• in most cases with odontogenic diseases, acute implies painful and chronic implies asymptomatic

severity of odontogenic infection

three major factors:

1. virulence — how aggressive microorganisms are

   • often polymicrobial and mostly anaerobic

   • anaerobes produce enzymes that break down tissue planes

2. quantity — how many organisms, and whether source is seeding more

   • necrotic pulp is a reservoir that keeps delivering bacteria until it is removed

3. host defense — whether patient can contain it

   • diabetes, immunosuppression, chemotherapy, biologics, malnutrition, and alcoholism are risk modifiers

• virulence cannot be changed, but the source can be removed to fix quantity and host defense can be assessed through medical history

odontogenic infection spread

infection follows the path of least resistance, and is determined by thickness of cortical bone and relationship of tooth apex to muscle attachments

• cortical plate thickness:

  • in maxilla → buccal cortical plate is thinner

  • in mandible → anterior labial plate is thinner; posterior lingual plate is thinner

• muscle attachments:

  • above buccinator attachment → vestibular abscess

  • below buccinator attachment → buccal space infection

• the mylohyoid line is the most important relationship in the mandible

  • apices above → drains into sublingual space

  • apices below → drains into submandibular space

    • can potentially spread into the neck

management of dental infection

• managing infection:

  • always remove source of infection → root canal therapy, extraction

  • incision and drainage → introduce oxygen to prevent proliferation of anaerobic organisms

  • selectively prescribe antibiotics

    • if clinical/laboratory signs of infections are identified

    • if elevated risk for developing systemic infection → immunocompromised

    • if clinical signs indicate inflammation is spreading to adjacent soft tissues

• managing inflammation:

  • pain only → NSAIDS

    • contraindicated in patients with renal failure or peptic ulcers

    • refrain from aspirin use in children

  • pain and impingement on airway → corticosteroids

cellulitis vs abscess

cellulitis and abscesses are treated differently

• cellulitis — diffuse spreading soft-tissue infection without localized pus

  • firm, diffuse, poorly-defined palpation

  • treated earlier, within 1-5 days

  • severe and generalized pain without pus

  • aerobic streptococci predominate early

  • manage using source control, often antibiotics

• abscess — localized collection of pus

  • localized, fluctuant, well-defined palpation

  • treated later, often 4-10 days

  • localized pain, with presence of pus

  • anaerobes predominate

  • manage through drainage

osteomyelitis

infection spreading through medullary bone and marrow spaces, rather than escaping through cortex

• mandible infection more common → denser cortex and less abundant blood supply that makes it more difficult to clear

• patients at high risk if they have diabetes, previous radiation, antiresorptive therapy, alcoholism, malnutrition

• clinical features — deep pain, swelling, paresthesia of lower lip from pressure on inferior alveolar nerve

• radiograph — moth-eaten radiolucency and eventually sequestra

  • dead bone is avascular, so neither host nor antibiotic can reach it

  • must be surgically removed to control source

Ludwig angina

bilateral cellulitis of the submandibular, sublingual, and submental spaces; airway emergency

• source — mandibular second and third molars, whose apices sit below the mylohyoid line

• clinical findings — board-like brawny induration of floor of mouth and upper neck without fluctuance

  • tongue is pushed up and back towards palate and pharynx

  • drooling, difficulty swallowing, muffled “hot potato” voice, eventual difficulty breathing

• dangerous because swelling is confined by fascia and can only expand towards the airway

• management — send patient to emergency department immediately

  • airway assessment/protection, imaging, surgical drainage, IV antibiotics, removing odontoenic source

when to refer to hopsital

any one sign can change the plan from “treat here” to “send now”

• airway → difficulty breathing, stridor, drooling, inability to swallow saliva, muffled voice, raised flor of the mouth/tongue

• mouth opening → severe trismus that airway cannot be managed

  • infection may have reached masticatory spaces

• spread → rapid progression over hours, bilateral involvement, extension into neck, periorbital swelling from maxillary source

• systemic toxicity → high fever, rigors, tachycardia, dehydration

• host → immunocompromised, uncontrolled diabetic, chemotherapy

cavernous sinus thrombosis

maxillary infections can spread upwards, towards orbit and brain

• route — fascial and angular veins connect to ophthalmic veins, which drain into cavernous sinus

  • veins lack effective valves, so infected thrombus can travel in either direction

• consequence — cavernous sinus thrombosis (rare, but life-threatening)

• clinical red flags — periorbital swelling, proptosis, painful or restricted eye movement, visual change, severe headache

  • maxillary canine infection close to the eye is a same-day emergency referral

antibiotic stewardship

most important antibiotic decision is often not to prescribe one

• contributes to antimicrobial resistance, allergy and anaphylaxis risk, GI effects, C. difficile infection risk

• source control first by removing infected pulp, pus, necrotic source; then decide whether antibiotics add anything

  • antibiotics do not replace root canal treatment, pulpectomy, extraction, incision and drainage

  • antibiotic without source control may temporarily suppress disease

• antibiotic indicated for pulp necrosis with acute apical abscess and systemic involvement, or progressive/spreading infection

when prescribing antibiotics

• first-line regimen — amoxicillin 500mg 3x a day, 3-7 days

  • or penicillin v potassium 500mg 4x a day, 3-7 days

  • amoxicillin preferred for better activity against gram-negative anaerobes and fewer GI effects

  • always with definitive dental treatment

• duration and follow-up — re-evaluate within 3 days

  • stop 24 hr after symptoms resolve, irrespective of 3-day review

  • if there’s no response, add metronidazole 500mg 3x a day for 7 days or switch to amoxicillin-clavulanate

penicillin allergy

nausea, diarrhea, childhood rash, family history are not IgE-mediated allergy; true allergy includes hives, angioedema, swelling, anaphylaxis

• no history of angioedema/hives/anaphylaxis — cephalexin 500mg QID, 3-7 days

  • cross-reactivity low when history is not true IgE reaction

• history of angioedema/hives/anaphylaxis — azithromycin 500mg on day 1, then 250mg for 4 days

  • higher bacterial resistance

  • may cause QT prolongation, so consider CV history

• same, alternative — clindamycin 300mg QID, 3-7 days

  • C. difficile warning, even after single dose

• no response to any of the above — add metronidazole 500mg TID, 7 days

  • re-evaluate in 3 days

delayed prescribing

delayed prescription strategy if patient is in pain but cannot perform definitive treatment immediately

• for patient in pain only, give prescription to be filled only if things worsen

  • fill prescription if swelling or pus develops, or if symptoms clearly worsen

  • arrange definitive treatment within one to two days, telling patient to call if that cannot happen

• pain alone is not an indication for an antibiotic because it is not an analgesic

antibiotic treatment vs prophylaxis

• antibiotic treatment — given to patients with systemic involvement or spreading infection

  • treatment course over days

• antibiotic prophylaxis — given to endocarditis patients only

  • single dose before procedure

  • highest-risk cardiac conditions like prosthetic valves or previous endocarditis, and for procedures that manipulate gingiva or periapical region