Download Differential diagnosis of the pain in orofacial system.

Differential diagnosis of the
pain in orofacial system.
Pain of dental origin and
nondental origine pain.
Orofacial pain
Orofacial pain is the pain in the area of
face and its adjacent structures.
The pain is expressing itself in various
clinical syndroms which are arising by the
influence of various mechanisms and they
involve multidiscilpinary approach to
diagnostics and the treatment itself.
Dental pain may be classified as follows:
Pulpal pain
Periapical/periradicular pain
Non-dental pain
Dental pain can be very difficult to diagnose.
Pulpal pain
The pulp may be subject to a wide variety of
insult, (bacterial, thermal, chemical, traumatic)
the effects of which are cumulative and can
ultimately lead to inflamation in the pulp (pulpitis)
and pain.
A characteristic of pulpal pain as that the patient
is unable to localize the affected tooth.
The ability of the pulp to recover from injury
depends upon its blood supply, not the nerve
supply, which must be borne in brain when
vitality (sensibility) testing is carried out
Although numerous classifications of pulpal
disease exist, only limited number of clinical
diagnostic situations require identification before
affective treatment can be given.
1. Dental pain
Expressive pain
Non-expressive
pain
Dentine hypersensitivity Chronic Pulpitis
Pulpitis
Periodontitis
Neuritis from inclusion
teeth
Dental rip
Chronic apical
Periodontitis
Dentitio difficilis
Retentio dentis
Synalgia
Sekundárne neuralgie
2. Non-dental pain, located near the
teeth
Expressive pain
Affection near the
tooth and its
neighbours
Affection of a distant
bodies
Non-expressive
pain
Pregnancy
aerodontalgia
Primary neuralgia
Systemic diseases
PULPAL DISEASE
Classified as:
– Reversible pulpitis
– Irreversible pulpitis
– Necrotic pulp
Reversible Pulpitis
Condition should return to normal with
removal of the cause.
Common causes:
– Caries, recent restorative procedures, faulty
restorations, trauma, exposed dentinal
tubules, periodontal scaling.
Pulpal recovery will occur if reparative
cells in the pulp are adequate.
Symptoms of Reversible Pulpitis
Thermal:
– Hypersensitive with mild pain less than <30 seconds,
but similar to control tooth
Sweets:
– Sensitive (if caries, crack, or exposed dentin) with
mild pain less than<30 seconds (similar to control
tooth)
Biting Pressure:
– None (unless tooth is cracked)
Diagnosis
Reversible Pulpitis
If there is a discrepancy between the
patient’s main complaint, symptoms, and
clinical examination – obtain more
information or data interpretation.
Remember: both a preoperative pulpal
and periapical diagnosis are made before
treatment is initiated (if reversible pulpitis is only
condition, the periapical area should be normal).
If the tooth is percussion sensitive –
consider bruxism or hyperocclusion.
Treatment of Reversible Pulpitis
Remove irritant if present (caries; fracture;
exposed dentinal tubules).
– If no pulp exposure: CaOH, restore, monitor
– If pulp exposure:
Carious: initiate RCT
Mechanical: >1 mm: initiate RCT
<1 mm crown planned: initiate RCT
<1 mm: direct cap or RCT
If recent operative or trauma – postpone
additional treatment and monitor.
Irreversible Pulpitis
Pulpal inflamation and degeneration not
expected to improve.
A physiologically older pulp has less ability to
recover due to decrease in vascularity and
reparative cells.
As inflammation spreads apically, cellular
organization begins to break down.
Localized pressure slows venous return,
resulting in buildup of toxins and lower pH that
causes widespread cellular destruction.
Symptoms of Irreversible Pulpitis
Thermal:
– Hypersensitive with moderate to severe
prolonged pain (>30 seconds) as compared
to the control
Sweets:
– Moderately to severely sensitive (if caries,
crack, or exposed dentin)
Biting Pressure:
– Usually sensitive in later stages (periapical
symptom)
Moderate to severe spontaneous pain
Diagnosis
Irreversible Pulpitis
Hypersensitive to hot or cold that is
prolonged.
A history of spontaneous pain.
Vital or partially vital pulp.
Treatment of Irreversible Pulpitis
Minimum immediate treatment (if not extraction)
Pulpotomy:
– Remove all decay (essential)
– Large canals: passively broach 75% of tooth length
– Small canals: spoon excavate orifice while removing
pulpal tissue from chamber.
– Copious irrigation with sodium hypochlorite (1%).
– Dry chamber with cotton pledget
– Place Ca(OH)² into large and over small canals
– Place dry cotton pellet in chamber, cover with cavit,
temporarily restore with Ketac-fill; completely relieve
occlusion if have acute apical peridontitis
Treatment of Irreversible Pulpitis
Ideal immediate treatment
Pulpectomy (complete removal of pulpal tissue)
– Determine the ideal working length (WL)
– Fully instrument canals with master apical file
At least # 25 file for small canals (and anterior teeth)
# 35 - 40 file for larger canals
Alternate working files with #8 or 10 patency file
– Copious irrigation with sodium hypochlorite (1%)
– Dry chamber with cotton pledget
– Place dry cotton pellet over canals, cover with cavit,
temporarily restore with Ketac-fill; completely relieve
occlusion if have acute periapical peridontitis.
Irreversible Pulpitis
(more treatment considerations)
Any residual decay can result in an inadequate
seal, contamination of canal space, and interappointment flare-ups.
Inflammation can be judged by the amount of
hemorrhage from the remaining pulp stump. If
bleeding continues, re-broach or file for residual
pulpal tags with copious irrigation.
To decrease risk of instrument separation within
the canal space, do not engage the canal walls
with broach.
Irreversible Pulpitis
(additional considerations)
Do not leave teeth open between appointments –
causes contamination of the canals and difficulty
closing them later.
Incomplete tooth fractures involving the pulp will
show symptoms of irreversible pulpitis.
Periodontal probing of associated pocket will
indicate depth of fracture. If depth of pocket
(fracture) extends below the attachment level, the
prognosis is guarded to poor.
Necrotic Pulp
Results from continued degeneration of an
acutely inflamed pulp.
Involves a progressed breakdown of cellular
organization and no reparative potential.
Commonly have apical radiolucent lesion.
(always conduct proper pulp testing to rule out a
non-pulpal origin).
With multi-rooted teeth, one root may contain
partially vital pulp, whereas other roots may be
nonvital (necrotic).
Maxillary first molar with large amalgam restoration and
periapical radiolucencies around all three roots. The tooth
was unresponsive to electrical and thermal testing.
Symptoms of Necrotic Pulp
Thermal:
– No response
Sweets:
– No response
Biting Pressure:
– Usually moderate to severe pain (not symptom of
necrotic pulp, but rather periapical inflammation)
Moderate to severe spontaneous pain
(usually dull and throbbing; associated with periapical area)
Diagnosis of Necrotic Pulp
Distinguishing features:
– No response to cold.
– No response to pulpal test.
Caveats
– Decreased sensitivity to cold/ept may be from
of insulating effects of additional dentin.
– Fluid in canal space conducting electrical
current can give false-positive.
– Periapical radiolucency is strong but not
conclusive evidence that pulp is necrotic.
Treatment of Necrotic Pulp
Minimum immediate treatment (if not extraction)
Partial instrumentation of canals:
–
–
–
–
–
–
–
–
–
Remove all decay, evaluate restorability
Determine working length of all canals
Large canals: up to #40 file, 4mm short of WL
Small canals: up to #25 file, 4mm short of WL
Alternate working file with #8 or 10 patency file
Copious irrigation with sodium hypochlorite (1%)
Dry chamber with cotton pledget
Place Ca(OH)² into all canals
Place dry cotton pellet in chamber, cover with cavit,
temporarily restore with Ketac-fill; completely relieve
occlusion if have acute apical periodontitis.
Treatment of Necrotic Pulp
Ideal immediate treatment
Complete instrumentation of canals:
– Determine the ideal working length
– Fully instrument canals with master apical file
At least # 25 file for small canals (and anterior teeth)
# 35 - 40 file for larger canals
Alternate with #8 or 10 patency file
– Copious irrigation with sodium hypochlorite (1%)
– Place dry cotton pellet over canals, cover with cavit,
temporarily restore with Ketac-fill; completely relieve
occlusion if have acute apical periodontitis.
Necrotic Pulp
(additional considerations)
Antibiotic coverage
– Usually not required unless patient has progressive
swelling or fever.
Pain Management
– Always determine allergy, contraindication, and
interaction with present medications
– Clock regulate NSAID (ibuprofen) for 3 days
– Narcotic for approximately 3 days, if needed
Occlusal Reduction
– Reduction in all cases with acute apical periodontitis
(remember that length measurements may change)
PERIAPICAL DISEASE
Classified as:
– Acute Apical Periodonitis
– Acute Apical Abscess
– Chronic Apical Periodontitis
(Suppurative Apical Periodontitis with sinus tract)
– Condensing Osteitis
Treatment of Periapical Disease
Pulpal status
always dictates treatment
of periapical disease
Acute Apical Periodontitis
Mild to severe inflammation that surrounds
or is closely associated with the apex of a
tooth.
Results from:
– Irreversible inflammation or necrotic pulp.
– Trauma or bruxism of normal or reversibly
inflamed pulpitic conditions.
Consider vertical fractures, periodontal
abscess, and non-odontogenic pain.
Clinical Findings in
Acute Apical Periodontitis
Visual
– Check for decay, fracture lines, swelling, sinus tracts, orientation
of tooth, and hyperocclusion
Palpation
– Sensitive (usually on buccal surface)
Percussion
– Moderate to severe (initially use index finger to reduce patient
discomfort)
Mobility
– Slight to no mobility (if moderate mobility exists, check for
possible periodontal condition before continuing)
Acute Apical Periodontitis, con’t.
Perio Probing
– WNL (unless concomitant periodontal disease or vertical fracture
exists)
Thermal (pulpal symptom)
– Response (not prolonged) – consider traumatic occlussion
– If response prolonged – consider irreversible pulpitis
– No response – consider necrotic pulp
EPT (pulpal test)
– Response – pulp is vital (reversible or irreversible)
– No response – pulp is necrotic
Acute Apical Periodontitis, con’t.
Translumination
– Not used unless fractured is suspected
Selective Anesthesia
– Not necessary, offending tooth easily located
Test cavity
– Not necessary
Radiographic
– Periapical image does not show a radiolucent lesion; some
thickening of the periodontal ligament is common
Immediate Treatment of
Acute Periapical Periodontitis
If from irreversible pulpitis:
Pulpotomy or extraction.
If from necrotic pulp:
Root canal therapy initiated or extraction.
If from hyperocclusion:
When the pulp is normal or reversibly inflamed, adjusting the
occlusion provides immediate relief. Always consider cracked tooth,
irreversible pulpitis, or necrotic pulp if discomfort persists.
If from bruxism:
A biteguard may be indicated.
Acute Apical Abscess
Acute inflammation of the periapical tissue
characterized by localized accumulation of
pus at the apex of a tooth.
A painful condition that results from an
advanced necrotic pulp.
Patients usually relate previous painful
episode from irreversible or necrotic pulp.
Swelling, tooth mobility, and fever are
seen in advanced cases.
Symptoms of Acute Apical Abscess
Spontaneous dull, throbbing, persistent
pain; exacerbated by lying down.
Percussion:
– Extremely sensitive
Mobility:
– Horizontal / vertical; often in hyperocclusion
Palpation:
– Sensitive; vestibular or facial swelling likely
Thermal:
– No response
Clinical Findings of
Acute Apical Abscess
Visual:
– Check for decay, fracture lines, swelling, sinus tracts, orientation
of tooth, hyperocclusion
Palpation:
– sensitive; intraoral or extraoral swelling present
Percussion:
– Moderate to severe (initially use index finger)
Mobility:
– Slight to none; may be compressible
Perio probing:
– WNL (unless have perio disease or vertical fracture)
Acute Apical Abscess, con’t.
Thermal:
– No response (pulp is necrotic)
EPT:
– No response (false-positive from fluid in canal)
Translumination:
– Not used unless fractured is suspected
Selective Anesthesia:
– Not necessary, offending tooth easily located
Test cavity:
– Not necessary unless vitality is suspected
Acute Apical Abscess, con’t.
Radiographic:
Thickening of the periodontal ligament is common; may not show a
frank lesion
If tests indicate pulp vitality: (red flag!)
Review diagnostic information (repeat diagnostic tests)
Rule out lateral periodontal abscess
Review medical history for previous malignant lesions or
other conditions (hyperparathyroidism) that may explain
contradictory information
Do not begin treatment until this discrepancy has been
resolved
Treatment of Acute Apical Abscess
(necrotic pulp)
Minimum immediate treatment (if not extraction)
Partial instrumentation of canals:
– Remove all decay, evaluate restorability
– Determine working length of all canals
– Achieve apical patency all canals with #10 file, look for
drainage and allow to continue until it stops
– Large canals: up to #40 file, 4mm short of WL
– Smaller canals: up to #25 file, 4mm short of WL
– Alternate with #8 or 10 patency file
– Copious irrigation with sodium hypochlorite (1%)
– Dry chamber with cotton pledget
continued on next slide
Treatment of Acute Apical
Abscess, con’t.
– Place Ca(OH)² into all canals
– Place dry cotton pellet in chamber, cover with cavit,
temporarily restore with Ketac-fill, and completely
relieve tooth from occlusion.
– Incision and drainage may be required
– Prescribe antibiotics and analgesics
Continued pain and swelling are common
postoperative problems – so prepare the
patient for several days of discomfort.
Chronic Apical Periodontitis
Results from prolonged inflammation that has
eroded the cortical plate making a periapical
lesion visible on the radiograph.
Caused by a necrotic pulp, the lesion contains
granulation tissue consisting of fibroblasts and
collagen (with macrophages and lymphocytes).
Must rule out central giant cell granuloma,
traumatic bone cyst, and cemental dysplasia.
Usually asymptomatic, but in acute phase may
cause a dull, throbbing pain.
Chronic apical periodontitis. Extensive tissue destruction in
the periapical region of a mandibular first molar occurred as
a result of pulpal necrosis. Lack of symptoms together with
presence of a radiographic lesion is diagnostic.
Chronic Apical Periodontitis, con’t.
Most common pitfall is assuming that the
presence of a periapical lesion automatically
indicates a necrotic pulp.
If tests indicate pulp vitality: (red flag!)
Review diagnostic information (repeat diagnostic tests)
Rule out lateral periodontal abscess, central giant cell
granuloma, traumatic bone cyst, and cemental dysplasia.
Review medical history for previous malignant lesions or
other conditions (hyperparathyroidism) that may explain
contradictory information
Do not begin treatment until this discrepancy has been
resolved
Treatment of Chronic Apical
Periodontitis (necrotic pulp)
If asymptomatic, no immediate treatment needed;
schedule for root canal therapy
If in acute suppurative phase, immediate
treatment same as with acute apical abscess, i.e.,
Partial instrumentation of canals:
– Remove all decay, evaluate restorability
– Determine working lengths of all canals
– Achieve apical patency all canals with #10 file, look for
drainage and allow to continue until it stops
– Large canals: up to #35 file, 4mm short of WL
– Smaller canals: up to #25 file, 4mm short of WL
– Alternate with #8 or 10 patency file
Treatment of Chronic Apical
Periodontitis, con’t.
–
–
–
–
Copious irrigation with sodium hypochlorite (1%)
Dry chamber with cotton pledget
Place Ca(OH)² into all canals
Place dry cotton pellet in chamber, cover with cavit,
temporarily restore with Ketac-fill, and completely
relieve tooth from occlusion.
– Incision and drainage may be required
– Prescribe antibiotics and analgesics
Continued pain and swelling are common
postoperative problems – so prepare the
patient for several days of discomfort.
Condensing Osteitis
Increased trabecular bone in response to
persistent irritant diffusing from the root
canal into the periradicular tissue.
May be either asymptomatic (pulpal necrosis)
or associated with pain (pulpitis).
Therefore, may or may not respond to
diagnostic tests, i.e., thermal, electric,
palpation, percussion.
Root canal treatment, when indicated, may
result in complete resolution.
Inflammation followed by necrosis in the pulp of the first
molar has resulted in the diffuse radiopacity of the
periradicular tissue.
Reversible pulpitis
Symptoms: Fleeting sensitivity/pain to hot, cold or
sweet with inmmediate onset.Pain is usually
sharp and may be difficult to locate. Quickly
subsides after removal of the stimulus.
Signs:
Exaggerated response to pulp testing.
Carious cavity/leaking restoration
Ireversible pulpitis
Symptoms: Spontaneous pain which may last several
hours, be worse at night, and is often
pulsatile in nature. Pain is elicited by hot
and cold at first, but in later stages heat is
more significant and cold may actually
ease symptoms.
A characteristic feature is that the pain remains after the
removal of the stimulus. Localization of pain may be
difficult intially, but as the inflammation spreads to the
periapical tissues the tooth will become more sensitive
to pressure.
Signs: Application of heat elicits pain.
Dentine hypersensitivity
This is pain arising from exposed dentine in response to
a thermal, tactile, or osmotic stimulus. It is thought to
be due to dentinal fluid movement stimulating pulpal
pain receptors.
Cracked tooth syndrome
Symptoms: Sharp pain on biting-short duration.
Signs:
Tooth often has a large restoration. Crack
may not be apparent at first but
transillumination and possibly removal of the
restoration may aid visualization. Positive response to
vitality (sensibility) testing and pain can normally be
alicited by getting the patient to bite with the affected
tooth on a cotton-wol roll or tooth sleuth. May be
associated with bruxing habit.
Periapical/periradicular pain
Progression of irreversible pulpitis ultimately leads to
death of the pulp (pulpal necrosis). At this stage the
patient may experience relief from pain and thus may not
seek attention.
Characteristically the patient can precisely identify the
affected tooth, as the periodontal ligament, which is well
supplied with proprioreceptive nerve endings, is inflamed.
Pulpal necrosis with periapical periodontitis
Symptoms:Variable, but patients generally describe a dull
ache exacerbated by biting on the tooth.
Signs: usually no response to vitality testing, unless one
canal of a multirooted tooth is still vital.
Rtg: Periapical lession- granuloma, cyst
Acute periapical abscess
Symptoms: Severe pain which will disturb sleep. Tooth is
exquisitely tender to touch.
Sings: Affected tooth is usually extruded, mobile. May be
associated with a localized or diffuse swelling. Vitality
testing may be misleading as pus may conduct stimulus to
apical tissues.
Chronic periapical abscess
Often symptomless. Possibly associated with persistent
sinus. Presentation may be: coincidental or acute
exacerbation.
Lateral periodontal abscess
Symptoms: similar to periapical abscess with acute pain
and tenderness, and often an associated bad taste.
Sings: Tooth is usually mobile, with associated localized
or diffuse swelling of the adjacent periodontium.
A deep periodontal pocket is usually associated,
which will exude pus on probing.
RTG: vertical or horizontal bone loss,(vitality testing ) is
usually positive, unless there is an associated perioendo lesion.
Non-dental pain
When no signs of dental or periradicular pathology can
be detected then non-dental causes must be considered.
Other causes of pain that can present as toothache
include:
temporomandibular pain-dysfunction/facial
arthromyalgia
sinusitis
psychological disorders (atypicalodontalgia)
tumours
Temporomandibular pain –
dysfunction/facial arthromyalgia
The prblem being addressed is pain in the
preauricular area and muscles of mastication with
trismus, with or without evidence of internal
derangement of the meniscus.
Clinical features: pain, clicking, locking, crepitus
and trismus are the clasical signs and symptoms.
Some patients may be clinically depressed but most
are not. Pain is elicited by palpation over the muscles
of mastication or the preauricular region.
Sinusitis
Antral pathology: often mimics symptoms attributable
to maxillary teeth. Diagnosis is by exclusion of
dental pathology, nasal discharge or stiffiness,
tenderness over the cheeks, and pain worse on
moving the head.
X-rays may reveal antral opacity, fluid level or
fractures. Other X-rays: DPT (dental panoramic
tomogram) for cysts, and roots and CT scans for
tumours, pansinusitis, and blowout fractures.
Facial pain – pain not directly related to the
teeth and jaws.
Trigeminal neuralgia-it is present as a shooking
electric shock type of pain of rapid onset and short
duration, which is often stimulated by touching a
trigger point in the distribution of the trigeminal
nerve. In the early stages of the disease there may be
a period of prodromal pain not conforming to the
classical description and it may be difficult to arrive
at a diagnosis. Patients often have multiple
extractions in a attempt to relieve the symptoms.
Atypical facial pain
This constitutes a large proportion of patients
presenting with facial pain.
Classicaly, their symptoms are unrelated to anatomical
distribution of nerves or any known pathological
process, and these patients have often been through
a number of specialist disciplines in an attempt to
establish a diagnosis and gain relief. This diagnosis
tends to be used as a catch-all for a large group of
patients, with the connecting underlying supposition
that the pain is of psychogenic origin.
Pointers to a psychogenic etiology include imprecise
localization, often bilateral pain or all over the place.
Pain is described as being continuous for long periods
with no change, and none of the usual relieving or
exacerbating factors apply.
Most analgesics are said to be unhelpful.
Oral dysaesthesia or burning mouth syndrome is an
unpleasant abnormal sensation affecting the oral
mucosa in the absence of clinically evident disease.
Five times more common in women aged 40-50 years
than other groups. Related to atypical facial pain.