Pulpal and Apical Diagnosis Flashcards
1
Q
• Is unlikely to often present as PURELY
A
PULPAL
2
Q
Each tooth needs 2 Diagnoses:
A
– Pulpal
– Peri-Radicular
(Maybe Perio & Restorative also)
3
Q
1st Question to ask the patient in pain:
A
What is your CC = Chief Complaint?
4
Q
Can you point to the tooth that hurts?
Can you localize the source of your pain?
If Purely PULPAL –
A
probably NOT (diffuse pain = pulpal)
5
Q
The CC is what brought the patient here:
The Objective of Clinical Testing is to
A
find and confirm the etiology of the patient’s CC.
6
Q
Clinical Testing is performed (based on CC) (5)
A
thermal
EPT
percussion
palpation
periodontal probing and mobility
7
Q
– Thermal:
A
cold, heat (pulp vitality)
8
Q
EPT: (only if pulpal status is in doubt)
A
This test is not done
routinely*
9
Q
– Percussion:
A
tapping with mirror (PDL sensitivity)
10
Q
Palpation:
A
digital touching of gingival (inflammation, redness,
swelling, tenderness)
11
Q
Radiographs of the suspect area(s) are obtained
– Minimum 3 Diagnostic films:
A
• Straight-on PA film
• PA Shift Shot (20° change in horizontal angulation) M or D
• Bite-Wing (to determine Restorability & Bone level)
12
Q
Answering the question of “WHY?” usually leads to
A
an accurate diagnosis and a more successful treatment
outcome*
13
Q
It may be helpful to think of the pulp existing
in only 3 basic conditions:
A
normal
inflammed
infected
14
Q
- Normal
A
(should remain normal & healthy)
15
Q
Inflamed (could recover or deteriorate)
A
A. Reversible (No Tx or symptomatic TX > recovery)
B. Irreversible (Pain Lingering & often Spontaneous)
a) Symptomatic
b) Asymptomatic (rare)
16
Q
Infected
A
(infected pulp will proceed to necrosis)
17
Q
Normal Pulp=Within Normal Limits (WNL )
(5)
A
• CC: None (Asymptomatic Currently & Historically)
• Clinical Testing:
- Thermal testing (Hot-Cold WNL)
- EPT responsive (similar to other WNL teeth)
- Percussion Negative (WNL)
• No Radiographic Changes
• Another Clue: Minimal or No Apparent Damage
• No Axial cracks. Leave it ALONE
18
Q
Always test 2-3 adjacent teeth prior to the tooth in
question-WHY?
A
(Establish a STANDARD BASE-LINE: 1
st)
19
Q
Reversible Pulpitis
A
• CC: Cold Sensitive
• Clinical Testing:
– Cold sensitivity #6 and #8 - pain relieved almost immediately once
stimulus is removed-(does NOT linger)*
– Patient was referred for retreatment of #7,
BUT only #6 & #8 symptomatic (with cold
stimulus, not lingering No spontaneous pain)
– Percussion Negative (all 3 teeth)
–Radiographic Changes?*
What did the referring DDS miss?
• Failure to LISTEN to patient’s CC
• Improper DX due to failure to do Clinical Testing
• No need to do Hot (CC was COLD)
20
Q
RP may follow 1 of 3 outcomes:
A
- If properly treated – may revert to normal
- May remain RP symptomatic for extended period
- May deteriorate to SIP or AIP (even if properly treated)
21
Q
Irreversible Pulpitis
(Symptomatic)
A
• CC: Cold Sensitive
• Clinical Testing:
– Cold Sensitivity #6 only – LINGERS*** 15-20 sec.
after stimulus is removed.
– Percussion Negative
– Radiographic Changes: None at apex
– Look for etiology
22
Q
- Early SIP
A
cold hurts, >10 and lingers
23
Q
- Late SIP
A
hot hurts – cold helps
24
Q
hot sensitivity?
A
Normal Teeth are NOT sensitive to HOT. Gingiva are more
sensitive to hot than teeth. HOT sensitivity usually indicates a
deteriorating pulp = SIP Normal: HOT coffee hurts soft T. not
tooth !
25
• Rarely, deep caries will not
produce any symptoms, though
clinically or radiographically,
caries may extend well into the
pulp.
• In such cases, RCT is definitely
indicated in order to prevent a
later exacerbation.
26
Necrosis of Pulp
• CC: May be currently asymptomatic – usual history
of symptomatic previously)
• Clinical Testing:
– Cold Sensitivity: No Response to hot, or electric pulp
tester.
27
Irreversible Pulpitis
(asymptomatic)
•CC: May be currently
asymptomatic – usual
history of symptomatic
previously)
•Clinical Testing:
Cold Sensitivity: No
Response to cold hot, or
electric pulp tester.
28
Previously Treated: P
Obturated with final RC filling materials other than
medicaments which is not healing or requires remedial
treatment of some type. This becomes a Non-Surgical
retreatment or a surgical RETX or simply extraction &
replacement.
29
Previously Initiated Treatment:
Tooth has been previously treated by partial endodontic
therapy.
This could be a failed pulp cap or pulpotomy or it could
be a pulpectomy
30
WNL: (Normal Pulp) –
Pulp is symptom free with normal response to pulp tests
31
RP : (Reversible Pulpitis) –
Inflammation of the pulp based on subjective and objective
findings that should revolve and return the pulp to normal
32
SIP (Symptomatic Irreversible Pulpitis) -
Vital inflamed pulp that is incapable of healing. i.e.
lingering pain to cold, sensitivity to heat, spontaneous pain.
33
AAP (Asymptomatic Irreversible Pulpitis) –
Vital inflamed pulp incapable of healing. No
clinical symptoms. Inflamed due to caries (chronic hyperplastic pulpitis) caries excavation (pulp
exposure), trauma (fracture with exposed pulp tissue)
34
Pulpal Necrosis (Necrosis) –
Death of the dental pulp (No Response to pulp tests)
35
PT: (Previously Treated) –
Tooth has been endodontically treated with canals obturated with
final root canal filling materials other than medicaments..
36
PIT (Previously Initiated Treatment) –
Tooth has been previously treated by partial
endodontic therapy, i.e. pulp cap, pulpotomy/pulpectomy. RCT NOT completed
37
Always remember everything in DX is continually
CHANGING
A pain which is diffuse today may be localized tomorrow
A severe cold sensitivity may abate overnight
The same tooth may become newly sensitive to bite next day as pulp vitality
succumbs to challenge.
38
Both seriously Inflamed and Infected Pulpitis
cases will ultimately lead to a
Necrotic pulp if left
untreated long enough.
39
If you cannot arrive at a supportable DX,
you cannot do any
treatment
40
RARELY do we see APICAL RADIOGRAPHIC
CHANGES in cases of pure pulpitis or even
EARLY necrotic pulp *** – WHY?
• Advanced pulpal disease or necrosis of the
pulp is generally required to allow infection
to affect the apical tissues.
41
“There is very little correlation between
clinical symptoms and
histo/pathological reality”.
42
This DX must be
SUPPORTED &
DOCUMENTED by CLINICAL
EXAMINATION & TESTING before
ANY TREATMENT PLANNING
can be done.
43
We must use EVIDENCE gained from CLINICAL EXAMINATION &
CLINICAL TESTING along with our knowledge and experience:
(5)
1. Medical & Dental History
2. CC + Signs & Symptoms
3. Clinical examination
4. Clinical testing
5. Radiological indications
44
Radiographs which are generally of limited use in DX of purely
pulpal disease may become of some value in --- DX as you
will see.
Apical
45
Never attempt to make a Dx from
radiographs alone ***
• Many unrelated non-odontogenic
entities can mimic “Lesions of Endodontic
Origin” (LEO)s radiographically but in fact
be something entirely different*
46
If a radiograph indicates P/A rarefaction
which appears to be associated with a root
apex and:
Pulp Testing is WNL*
Patient is Asymptomatic*
No CC*
No Damage to the tooth is apparent *
No Trauma is reported *
47
The radiolucency that we think we
see near the apex may be (4)
Artifact
(3 X-Rays
minimum)
Nonodontogenic
lesion
Oral
manifestation
of systemic
disease
Normal
anatomical
landmark
48
skipped
Look for the
DAMAGE
(4)
• Do you see any
damage to the tooth?
• Caries, Restoration,
Fracture,
Extreme/Rapid Wear?
• Trauma of any sort?
Ask more than once!
Check 4 Crack
• Discoloration of the
crown?
49
Following Pulpal Necrosis:
(2)
• The disease process rapidly extends peri-apically.
• The tooth often will become percussion + &/or
spontaneous pain may appear BEFORE radiographic
evidence is clear.
50
Following Pulpal
Necrosis:
• Ultimately, radiographic evidence will
develop but TAKES TIME
(2)
– 100% OF THE MEDULLARY BONE CAN BE
DESTROYED & no PARL may show on the
standard radiograph.
– A Visible PARL is ONLY VISABLE when
40% of the Cortical Bone has been
destroyed.
51
Progression of RC System Infections
(7)
1. Carious Lesion or Trauma opens tubules to
bacterial invasion
2. Bacteria inflame pulp locally
3. Inflammation may overcome pulpal defenses and
localized abscesses may form in coronal pulp
4. Infection increases in pulp and necrosis begins
5. Necrosis involves entire RC System
6. Infection uses “portals of exit” (apical foramen
and lateral canals) to invade peri-radicular tissues
(apical periodontitis)
7. Periradicular infection occurs beyond apex ( apical
abscess )
52
ALL ---- IS
SENSITIVE TO
PERCUSSION.
PERI-RADICULAR
INFLAMMATION
53
PURELY --- IS NOT SENSITIVE TO PERCUSSION
PULPAL PAIN
54
Can the Patient
point to the tooth
that hurts?
Probably yes, but
why? (4)
• Mechanoreceptors (Proprioceptors) are present in PDL not in Pulp
• It means that inflammation/infection from the pulp has already
reached the P/Apical tissues and we are dealing with an Apical DX of
some type.
• The offending tooth will now be sensitive to percussion but a
lesion may NOT yet show on XR*
• (Recent or chronic occlusal trauma – possible exception)
55
“Condensing Osteitis”
(2)
Radiopaque appearance on
the XR.
Treatment is determined
by symptoms
56
WNL: (Normal) –
Teeth not sensitive to percussion or
palpation. Lamina dura is intact and the PDL is uniform and
unbroken.
57
SAP:
(Symptomatic Apical Periodontitis) – Inflammation
of the periodontium producing a painful response to
biting/percussion/maybe palpation.
58
AAP (Asymptomatic Apical Periodontitis) –
Inflammation
and destruction of the periodontium that is of pulpal origin
appearing as a radiolucent area with no clinical symptoms
59
AAA (Acute Apical Abscess) –
Inflammatory reaction to
pulpal infection with rapid onset, spontaneous pain, tooth
tender to pressure, pus formation and SWELLING &
FEVER
60
CAA: (Chronic Apical Abscess) –
Inflammatory reaction to
pulpal infection with gradual onset, little or no discomfort and
DRAINING SINUS TRACT
61
CO: (Condensing Osteitis) –
Diffuse radiopaque lesion
representing a localized boney reaction to a low-grade
inflammatory stimulus.
62
Dx: Normal (Within normal limits)
Radiographic findings
PAIN
No Radiolucency NO PAIN
63
Dx: SAP
Radiographic findings
PAIN
YES/NO
Radiolucency
PAIN
64
Dx: AAP
Radiographic findings
PAIN
YES Radiolucency NO PAIN
65
Dx: AAA
Radiographic findings
PAIN
YES/NO
Radiolucency
PAIN
66
Dx: CAA
Radiographic findings
PAIN
YES Radiolucency NO PAIN
67
Dx: CO (Condensing Osteitis)
Radiographic findings
Radiopaque lesion
68
APICAL DX: SAP (Symptomatic
Apical Periodontitis)
(5)
Tooth sensitive to percussion & biting pressure
Palpation variable
No swelling, No DST
Pulp Vitality variable (Vital to NV)
Radiographic appearance variable: Minor or No significant apical
radiographic changes or thickened PDL space to frank PARL (EARLY ON)
69
SAP
Beware: OTHER situations may result in similar symptoms:
(3)
- recent restoration (high)
- occlusal habits (bruxism)
- trauma , etc.
70
APICAL DX: AAA (Acute Apical
Abscess)
(6)
➢ PULP NECROTIC
➢ SEVERE Pain to: biting, percussion or
palpation
➢ Apical radiographic changes, thickened PDL
space or P/A radiolucency.
➢ Often Mobile due to active infection in
apical tissues.
➢ Rapidly developing infection - usually
swelling (intra and extra- oral &
fever)*
➢ No DST *
71
Chronic Apical Abscess: CAA
swelling, pain
Usually no extraoral swelling.
Pain minimal/none
72
DST is pathognomonic
for ---
CAA
73
Always trace out a Draining Sinus Tract (DST) with
Gutta Percha cone & Radiograph
74
What if the ostium of the DST doesn’t point to
a PARL?
ALWAYS TRACE & XR*
75
SAP, AAP, AAA, & CAA:
▪ Discerning Observers will
note: the same XR was used
for 3 of the 4 conditions:
▪ Diagnosis Depends on the SUM of
patient history & symptoms, clinical
exam, signs & testing & +
Radiographic interpretation***
▪ It is often inaccurate and always
unacceptable and unethical to
attempt to diagnose from
Radiographs alone***
76
CO (Condensing Osteitis)
(5)
➢ Radio-opaque formative or reactive
bone
➢ Asymptomatic and no apparent pathology =
NO TREATMENT (Continue to monitor)
➢ Treatment of CO is based upon
symptoms
➢ Develops in response to a mild or “sub clinical”
inflammation or infection where bone is actually
formed instead of being resorbed or destroyed
Differential DX: Sclerotic Bone which is a non-pathology & requires no TX. (no DAMAGE)
77
• Craze Lines (Confined to enamel)
– Common & Generally Unimportant (don’t stop
light)
78
• Fractured Cusp (Oblique shearing FX ) FacialLingual
– Often involves undermined cusp, may be
restorable
79
• Cracked Tooth (Incomplete “Greenstick” FX)
– M-D FX involving 1 or both marginal ridges
– May or may Not involve the pulp
– May be confined to crown or extend to root
80
• Split Tooth (Crack extends to a surface in all
areas)
– Involves Crown, Root & generally Pulp
– Must remove FX segment & determine
restorability
81
• Vertical Root Fracture*** (VRF) Begins
INTERNALLY (at root apex or from crown)
(2)
– Primarily in axial plane may be F-L or M-D*
– Often occur in RCT teeth
82
Horizontal Fractures are
also important but are
generally easily seen and are
usually associated with
known traumatic events.
83
CRAZE LINES
Vertical lines in the enamel of your teeth are called Craze Lines. These are best observed
by trans-illuminating using a fiberoptic light from the palatal aspect. This is common and
generally asymptomatic and not a concern for endodontics but when the craze lines
stain, an esthetic issue may develop and can be treated by several restorative techniques.
84
FRACTURED CUSP
Always look carefully during your examination to identify cracked or fractured cusps
which may be stained or made more obvious via trans-illumination.
If the pulp tested WNL, the normal procedure is to remove the fractured cusp and see if
the remaining tooth structure will support a restoration (intra-coronal or extra-coronal).
1st Step: Always do all necessary DX testing.
Determine condition of pulp. If vital and
restorable, anesthetize and remove the
fractured portion and restore if possible.
Anything from simple intracoronal
restoration to endodontic intervention to
extraction of the tooth may ensue in
this highly variable injury
In some cases, removal of the FX cusp will reveal either a FX too far below the attached
gingiva to maintain periodontally (crown lengthening may help) or so little tooth
structure remains that RCT + post, build-up and crown will be necessary to properly
restore.
85
CRACKED TOOTH aka “Green Stick FX”
A Cracked Tooth is most often discovered following patient complaint of
acute, sharp, momentary pain upon biting or release of biting pressure. An
old crack may often be seen as stained. Generally pulp is vital in early stages
& may remain so for some time. Often, the untreated patient may learn to avoid
biting on the tooth and the pulp may survive for a time in this manner before eventually
succumbing to the bacterial challenge &/or extension of the crack at which point the
pulp becomes necrotic & the previous pain stops because the pulp is now necrotic and
can no longer respond. Later SAP will develop as infection invades the peri-radicular
tissues.
86
CC: “I get a Quick, Sharp pain when I bite on
something hard.” “It’s gone in a second but
I’m afraid to bite on that tooth.” They
probably can’t point to the exact tooth but
avoid using the quadrant for fear of pain!
• When a cracked tooth with a vital pulp is bitten upon in a manner to wedge open
the crack, air & saliva enter the defect. When biting pressure is released, typically
the wedged crack moves rapidly toward closure forcing a change in the fluid
gradient in the dentinal tubules producing the characteristic acute & sharp,
momentary pulpal pain as long as the pulp remains vital.
• At this point, the tooth is generally NOT sensitive to percussion and if the crack is
confined to the crown & the pulp remains healthy, it may be possible to protect &
preserve the pulp and stabilize the crack by extra-coronal restoration to achieve
stability of the crack. RCT may become necessary nevertheless if pain continues or
the pulp succumbs. It is important to note that the crack may extend to the root
even with the stabilization. RCT or Extraction may become necessary depending
upon the extent of extension of the crack ( if the crack extends to the pulpal floor
or a canal, RCT will not be successful).
87
Clinical Testing Devices for Cracked tooth:
(6)
-Transillumination
-Staining (Sable Seek)
-P. Probing (drop-off Pocket)
-B/W XR why? (restorability)
-Angular crestal bone loss
-Bite Stick:
88
-Bite Stick:
(2)
-“Frac Finder”
- “Tooth Slooth”
89
Most common site:
(2)
Mandibular 2ND Molar
Followed by:
Maxillary premolars
90
“Drop-Off” Pockets
A “Drop-Off ” Periodontal Pocket in an otherwise healthy
periodontal mouth may be a tip-off that a longitudinal (axial)
crack may extend into the root and therefore create a guarded
or hopeless prognosis.
A drop-off pocket is when you measure 3-3-3-3-8-3. It is a
NARROW pocket and often indicate the extension of a crown
fracture into the root. May signal a non-restorable tooth. Of
course, the example in the image here is already compromised
with a sizeable furcal perforation which was attempted to be
repaired with MTA.
A VRF on a PT RCT case after success for several years now
shows a “J” Shaped Lesion (as shown on the next slide).
Chances are good that a VRF fracture may have occurred.
91
Vertical Root Fracture
Look for J-Shaped (HALO) apical
boney lesion
Probe for Drop-off Pocket
VRF difficult to confirm
radiographically –UNLESS . . .
separation of segments occurs
92
Classic “J” endo lesion?
This is simply a drainage
path of a CAA along the
PDL as evidenced by the
sealer extrusion from the
lateral accessory canals
along this path. No
angular crestal bone loss,
no drop-off pocket,
unable to transilluminate
due to crown.
Again, XR can fool us . .
CBCT may be helpful
93
The only absolutely certain way to
determine a VRF is to
expose it
surgically and demonstrate the
fracture using stain and a possibly
a microscope* or wait for it to
separate?
94
A THICKENED PDL
can be caused by
(2)
OCCLUSAL Trauma
OR PARL:
So check the occlusion
esp. if NEW(HIGH)
RESTORATION
