John A. Vaughn, MD, Immediate Health Associates, Westerville, OH
Acute orofacial pain—
pain arising from the
teeth or soft tissues of
the mouth—is extremely
common, affecting
22% of people in the United
States.1 Since it is more likely
to affect younger adults
and those without adequate
access to primary care, it is a
frequent presenting complaint
in emergency departments
and urgent care centers.
While there are few
true emergencies, the differential
diagnosis of acute
orofacial pain is wide ranging,
and prompt recognition
of these syndromes is
vital for ensuring the best
possible outcome.
This article will provide an introduction to some of
the more likely origins of acute orofacial pain, and suggest
appropriate management and “next steps” in
the urgent care setting.
Dental Pain
Dental pain is responsible for over 700,000 ED visits a
year.2 While non-odontogenic sources such as maxillary
sinusitis, migraine headaches, temporomandibular
joint (TMJ) syndrome,
and neuralgias can
cause referred teeth pain,
dental sources are the most
common. A basic illustration
of dental anatomy is
presented in Figure 1.
Pathology of Carious
Origin
Dietary carbohydrates on
the crown surface are
metabolized by oral bacteria,
most predominantly Streptococcus
mutans. Prolonged
exposure to these acidic
metabolic byproducts leads
to an erosion of the enamel
layer referred to as dental
caries (cavities). Dental caries
is treated by removal of the
carious tissue and replacement with a filling by a dentist.
Dental caries is asymptomatic until the erosion
breaches the pulp chamber, when it causes an inflammatory
process called reversible pulpitis. Reversible
pulpitis is characterized by pain triggered by thermal,
sweet, or sour stimuli that typically lasts for only
a few seconds. If left untreated, it will progress to
irreversible pulpitis, in which the pain is more severe,
lasts longer, and is more diffuse.
Continued inflammation will lead to pulp necrosis
and apical periodontitis, in which the pain becomes
even more severe, will re-localize to the affected tooth,
and can be associated with regional lymphadenopathy.
Apical periodontitis can become purulent and lead to
the formation of an apical abscess, which is often
associated with buccal or palatal fluctuance.
Definitive treatment of apical periodontitis and apical
abscess is root canal therapy or tooth extraction. Management
in the urgent care setting should include providing
adequate pain control and arranging follow-up with a
dentist within one to two days. If there is evidence of cellulitis,
an antistreptococcal antibiotic should be prescribed:
penicillin VK 500 mg TID-QID (50
mg/kg divided into three or four doses
in children), clindamycin 300 mg QID,
or erythromycin 500 mg QID.3
Ludwig’s Angina
A patient whose clinical presentation
is consistent with an abscess
involving the mandibular teeth
should be carefully evaluated for Ludwig’s
angina, a potentially life-threatening,
rapidly expanding cellulitis
of the submandibular and sublingual
spaces.
As the floor of the mouth becomes
inflamed and indurated, the tongue
is elevated and pushed posteriorly
leading to airway obstruction. Ludwig’s
angina is typically bilateral and
patients present with fever, neck
swelling, drooling, trismus, pain, dysphagia,
and dyspnea.4
The cornerstone of Ludwig’s angina
management in the urgent care setting
is airway protection until the
patient can be transported by EMS to
an ED for surgical consultation. Treatment
involves IV antibiotics, IV
steroids, and, if necessary, incision
and drainage and surgical decompression
with tracheotomy. High-dose
penicillin G is the antibiotic of choice,
typically administered with an antistaphylococcal
drug and metronidazole
for anaerobe coverage.5
Acute Alveolar Osteitis
Acute alveolar osteitis, or dry socket, results from the loss
of the protective blood clot that forms in the alveolar
socket after a tooth extraction. Patients typically present
two to three days postextraction with complaints of
acute pain and foul odor. Exam will reveal a dry appearance
of the exposed bone in the alveolar socket.
Management is supportive until the patient can
follow up with the dentist. The socket can be gently
rinsed with warmed saline or chlorhexidine (Peridex)
to remove any debris and packed with moistened
iodoform gauze or gauze soaked with eugenol. Packing
should be changed daily, and appropriate analgesia
should be prescribed.
Gingivitis
Chronic accumulation of plaque along the gingival
margins in patients with inadequate oral hygiene will
lead to inflammation and bleeding. As gingivitis progresses,
the inflammation can destroy the periodontal
ligament and surrounding alveolar bone. This chronic
periodontitis leads to tooth loss and an increased
risk of developing acute periodontal abscesses from
debris becoming lodged in the periodontal pocket.
Patients with an acute periodontal abscess will typically
present with pain, erythema, and edema over
the affected segment. The tooth is typically tender to
percussion and hyper-mobile. Treatment includes warm
saline rinses and referral to a dentist within 24 hours for
incision and drainage. If there is any evidence of cellulitis,
patients should be started on
oral penicillin or erythromycin.
Acute necrotizing ulcerative gingivitis
(ANUG, or “trench mouth”)
is a rapidly spreading gingival
infection caused by an overgrowth
of normal oral bacteria including
alpha-hemolytic streptococci, Prevotella
intermedia, and Actinomyces
species. When ANUG spreads
beyond the gingiva, it is referred to
as noma, or cancrum oris. As an
opportunistic infection, ANUG
typically affects immunosuppressed
patients with poor diet and poor oral hygiene.
Patients usually complain of pain, spontaneous
gingival bleeding, foul breath, or alterations in taste.
The classic physical findings are gingival edema and
ulceration in the interdental papillae (often associated
with a gray pseudomembrane), halitosis, and fever.
Treatment includes saline or diluted hydrogen peroxide
rinses, topical lidocaine, oral analgesics for pain
relief, and oral antibiotics. Penicillin VK is the drug of
choice (or erythromycin if the patient is allergic to
penicillin). Patients should follow up with a dentist in
one to two days.6
Dental Trauma
Dental trauma is extremely common; it is estimated
that 50% of all children experience some form of
dental trauma.7 Assessment of dental injuries should
always include establishing the mechanism and timing
of the injury, evaluation for the presence of associated
soft tissue injuries or bite malocclusion, and
dental radiography to rule out a fracture if available.
Dental Fractures
Dental fractures may involve the crown, root, or alveolar
bone. Adequate analgesia should be prescribed
and dental follow-up arranged within one to two days.
Fractures that expose the pulp may be more painful,
but do not necessarily require emergent consultation.
Displacement Injuries
While displacement injuries of primary teeth have minimal
long-term sequelae, displacement injuries of permanent
teeth are dental emergencies whose prognosis
directly correlates with timeliness of treatment.
Intrusive luxation is the displacement of the tooth
into the alveolar socket. Since the tooth should be
allowed to spontaneously re-erupt prior to any
attempts at realignment, tetanus
prophylaxis and pain control is
all that is required in the urgent
care setting. The patient should
be non-emergently referred to a
dentist for monitoring and potential
root canal treatment.
Lateral or extrusive luxation is
the loosening and displacement
of the tooth within the alveolar
socket. In the primary dentition, if
the tooth is loose enough that it
could be aspirated or cause malocclusion
the patient should be
referred to a dentist for immediate extraction.8 In
the permanent dentition, the patient should be emergently
referred to a dentist or oral surgeon for repositioning
and splinting. Patients should be placed on
appropriate analgesics and antibiotic prophylaxis,
and tetanus status addressed.
Avulsion is the complete displacement of the tooth
out of the alveolar socket and is a time-sensitive dental
emergency; successful reimplantation is less likely
if the tooth has been out of the socket for more than
20 minutes.
Primary teeth should never be re-implanted. Permanent
teeth should be re-implanted as soon as possible.
The tooth should be gently rinsed in sterile saline
prior to re-implantation and should only be handled
by the crown; any manipulation of the root could
disrupt the periodontal ligament fibers that are vital for
re-attachment. Antibiotic prophylaxis should be prescribed,
tetanus status addressed, and emergent dental
consultation for splinting and follow-up management
should be made.
If the tooth cannot be re-implanted in the urgent care
center, it should be transported with the patient to the
consultant in a specialized tooth transport apparatus. If
this is unavailable, milk can be used as a transport medium;
it is relatively sterile and has pH and osmolality levels
compatible enough with periodontal ligament cells to
keep them viable for up to three hours.9 Using sterile
saline or having the patient carry the tooth in the buccal
sulcus is also a reasonable alternative for transport.
Stomatitis
Over a third of acute orofacial pain syndromes are
caused by mouth sores.10 While the differential diagnosis
is extensive, the following are among the most common
causes seen in the urgent care setting.
effect on healing time.11
Oral Candidiasis
Oral candidiasis (“thrush”) is
caused by an overgrowth of the
ubiquitous fungus Candida albicans.
Predisposing factors include:
the extremes of age, the use of
intra-oral prosthetic devices, recent
antibiotic use, and immunosuppression.
Patients typically present
with white plaques overlying
an erythematous base on the buccal
mucosa and tongue that can
be easily scraped away with a
tongue depressor. Treatment includes topical or oral
antifungal agents, as follows:
Nystatin (Mycostatin) 100,000 Units/mL. Adults: 4-
6 mL swish and swallow QID. (Infants: 2 mL QID).
Mycostatin Pastilles 200,000 Units. 1-2 Pastilles
dissolved slowly in mouth QID.
Fluconazole (Diflucan) 200 mg po QD on day 1,
then 100 mg po QD for at least 14 days. (Peds: 6
mg/kg po QD on day one, then 3 mg/kg po QD.)
Aphthous Stomatitis
Aphthae are associated with nutritional deficiencies
(iron, folate, B-12), Celiac disease, Crohn’s disease and
Bechet syndrome, but the etiology of recurrent aphthous
stomatitis (RAS, or canker sores) is still unknown. They
are extremely painful, well-circumscribed round/oval
ulcerations with erythematous borders and yellow or
gray bases typically measuring 2-4 mm in diameter.
RAS will resolve spontaneously in seven to 10 days.
Topical steroids or viscous lidocaine may be used for
supportive care, as follows:
Dexamethasone (Decadron) elixir 0.5 mg/5 mL.
5 mL swish and spit QAC and QHS.
Triamcinolone (Aristocort) gel 0.1%; apply two to
four times daily.
Fluocinonide (Lidex) gel 0.5%; apply two to four
times daily.
Lidocaine Viscous 2% gel; apply Q 4 hours prn.
Herpes Simplex
Herpes labialis (“fever blisters” or “cold sores”) is
caused by the Herpes simplex virus (HSV). The type 1
virus is responsible for the majority
of cases, but type 2 may also
cause oral lesions. Most people
have been infected with the virus
by adulthood.
HSV stomatitis presents as
painful, grouped vesicles on the
gingiva, buccal mucosa, lips, or
tongue that may extend onto the
peri-oral skin. The vesicles quickly
rupture to form small ulcerations
that will develop a yellow- to
honey-colored crust and heal
spontaneously over two to three
weeks. The pathognomonic feature is a tingling, burning
or itching pain that develops in the affected area
one to two days before the lesions erupt.
Treatment is supportive. If started during the prodromal
phase, antiviral medications have been shown to
shorten the course and lessen the severity of the outbreak.
Topical antivirals are much less effective. Typical
administration is as follows:
Acyclovir (Zovirax) 400 mg PO TID (or 800 mg
PO BID) for five days.
Valacyclovir (Valtrex) 2 g PO Q12 hours for one
day (total of 4 g).
Herpangina
Herpangina is an acute febrile illness caused by coxsackievirus
group A that most commonly affects children
in the summer months. Patients develop fever,
sore throat, headache, cervical lymphadenopathy,
and malaise which is followed by the eruption of
multiple vesicles on the soft tissues of the posterior
pharynx. These vesicles rupture, leaving multiple
ulcerations which may last for a week. Unlike herpes
labialis and RAS, herpangina lesions do not appear on
the gingiva, tongue, or anterior buccal mucosa.
Hand, Foot, and Mouth Disease
Hand, foot, and mouth disease (HFM) is the most
common cause of mouth sores in children.12 It is a
highly contagious acute febrile illness caused by
enteroviruses - typically coxsackievirus A16 - that usually
affects children under the age of 5 with a peak
incidence in summer and fall.
After a prodrome of fever, malaise, and sore mouth,
painful vesicular lesions that rupture to form shallow
ulcers with an erythematous halo will develop on
the buccal mucosa, tongue, gingiva, and soft palate.
The distinguishing feature of HFM is the presence of a
rash on the hands and feet (and often the buttocks).
This rash begins as erythematous macules - classically
on the palmar and plantar surfaces - that progress to
gray vesicles on an erythematous base which may be
asymptomatic or pruritic.
HFM is self-limited, usually lasting a week, and
treatment is supportive.
Angular Cheilitis
Angular cheilitis is a painful inflammation of the corners
of the mouth that involves the formation of
deep fissures. Angular cheilitis can be the result of
an infectious process (usually fungal) or vitamin B
deficiency, but is often due to mechanical irritation:
thumb sucking in children, lip licking/biting in adults,
or excessive pressure in edentulous patients.
Treatment is aimed at correcting the underlying
cause, but patients should be encouraged to keep the
areas dry and well-lubricated with an emollient.
Leukoplakia
Although leukoplakia rarely causes pain, as a precancerous
lesion it should always be included in the differential
diagnosis of a patient with oral lesions. It is a
thick, rough, hardened, and slightly raised white patch
or plaque that develops on the sides of the tongue or
buccal mucosa in response to chronic irritation. If the
lesion is red, it is referred to as erythroplakia.
Leukoplakia develops over weeks to months and is
often asymptomatic. It may become sensitive to touch,
heat, or spicy foods. The cause is unknown, but tobacco
use - especially pipe smoking and the use of chewing
tobacco/snuff - is associated with a high risk of developing
leukoplakia. Unlike oral candidiasis, it is adherent
and cannot be easily scraped off with a tongue depressor.
The patient with leukoplakia must be non-emergently
referred to a dentist or oral surgeon for biopsy
evaluation of the lesion. Removal of the underlying
irritation may result in complete resolution, but surgical
removal of the lesion may be necessary.
Summary
It would behoove the urgent care provider to bear
the following key points in mind when treating a
patient who has presented with a complaint discussed
in this article:
A patient with an abscess involving the mandibular
teeth should be carefully evaluated for Ludwig¡¯s
angina, a potentially life-threatening condition.
Displacement injuries of permanent teeth are
dental emergencies whose prognosis directly correlates
with timeliness of treatment.
Avulsed primary teeth should never be reimplanted.
An avulsed tooth should never be handled by
the root, as this could disrupt the periodontal
ligament fibers that are vital for re-attachment.
Any patient with an oral lesion suspicious for leukoplakia/
erythroplakia must be referred for biopsy
evaluation since this is a pre-cancerous lesion.
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