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THE HEALTH of the periodontium is important

to the proper function of a tooth.


The periodontium includes the gingiva,
cementum, periodontal ligament (PDL), and
alveolar bone.
Disease that affects the periodontium usually
is a result of the direct extension of pulpal
disease or due to apical progression of
periodontal disease.

When the pulp becomes infected, the disease


can progress beyond the apical foramen and
inflame the PDL.
The inflammatory process results in
replacement of the periodontal ligament by
inflammatory tissue.
Without proper treatment, the inflammatory
response can cause resorption of the alveolar
bone, cementum, and dentin.

Besides going through the apical foramen,


pulpal disease can progress through lateral
canals.
Lateral canals are seen mostly in the apical
third of the root and in the furcation area of
molars.
Pulp disease may cause an inflammatory
response of the PDL at the opening of lateral
canals, resulting in a lateral radiolucency on
the root.

The inflammatory response at the lateral


canals may extend crestally along the lateral
aspects of the root and ultimately involve the
furcation or crestal area of the attachment
apparatus.
The effect of periodontal disease on the pulp
is not as clear-cut as the effect of pulpal
disease on the periodontium.
Periodontal inflammation may exert a direct
effect on the pulp through the same lateral
canal or apical foramen pathways.

The normal pathways of communication between the


endodontium and the periodontium (1 -the apical
foramen, 2, 3 - lateral and accessory canals)

The endodontium and periodontium are


closely related and diseases of one tissue may
lead to secondary diseases in the other.
The differential diagnosis of endodontic and
periodontal diseases can sometimes be
difficult but it is of vital importance to make a
correct diagnosis so that the appropriate
treatment can be provided.

Pulpal infection can drain through the


periodontal ligament space and give an
appearance of periodontal destruction,
termed retrograde periodontitis.
Both pulpal and periodontal infections can
coexist in the same tooth, termed combined
lesions, where the treatment depends on the
degree of involvement of the tissues.
Both endodontic and periodontal diseases
are caused by a mixed anaerobic infection.

Pre-operatory image of the same


lesion while measuring the initial
pocket depth.

X-ray image of an endodonticperiodontal lesion caused by an


internal root resorbtion.

a) Primary endodontic lesion with drainage through


the periodontal ligament.
b) Primary endodontic lesion with secondary periodontal
involvement.
c) Primary periodontal lesion.
d) Primary periodontal lesion with secondary endodontic
involvement.
e) Combined endodontic-periodontal lesion.

An acute exacerbation of a chronic apical


lesion on a tooth with a necrotic pulp may
drain coronally through the periodontal
ligament into the gingival sulcus.
This condition may mimic, clinically, the
presence of a periodontal abscess.
a deep narrow probing defect is noted on just
one aspect of the tooth root .

For diagnosis purposes, it is imperative for the


clinician to insert a gutta-percha cone into the
sinus tract and to take one or more
radiographs to determine the origin of the
lesion.
When the pocket is probed, it is narrow and
lacks width.
Primary endodontic diseases usually heal
following root canal treatment.

The root canal system primarily becomes


infected as a result of dental caries, traumatic
injuries and coronal microleakage.
Pulp inflammation or necrosis may lead to an
inflammatory response in the periodontal
ligament at the apical foramen or foramina or
at the site of a lateral or accessory canal.

Such a lesion may result in a localized or


diffuse swelling that may occasionally involve
the gingival attachment.
Long-term existence of the defect has resulted
in deposits of plaque and calculus in the
pocket with subsequent advancement of the
periodontal disease.
After adequate root canal treatment, lesions
resulting from pulpal necrosis resolve an
exceptionally high percentage of the time.

The integrity of the periodontium will be


reestablished if root canal treatment is done
well.
If a draining sinus tract through the
periodontal ligament is present before root
canal treatment, resolution of the defect that
can be probed is expected

Endodontic-periodontal lesion
with primary endodontic lesions and
secondary periodontal involvement of 16

These lesions are primarily caused by periodontal


pathogens.
In this process, chronic periodontitis progresses apically
along the root surface.
In most cases, pulp tests indicate a clinically normal pulpal
reaction.
There is frequently an accumulation of plaque and calculus
and the pockets are wider.
The prognosis depends on the stage of periodontal disease
and the efficacy of periodontal treatment.
The pulp may remain vital but may show some
degenerative changes over time.

The apical progression of a periodontal pocket


may continue until the apical tissues are
involved.
In this case, the pulp may become necrotic as
a result of infection entering via lateral canals
or the apical foramen.
In single-rooted teeth, the prognosis is usually
poor.
In molar teeth, the prognosis may be better.

The pulp response to cementum and dentin


removal and exposure of patent dentinal
tubules by periodontal root planning will vary
with the remaining dentin thickness.
Unless dentin removal is excessive, pulp
response will be negligible.
Although the pulp is exposed to a bacterial
challenge through patent dentinal tubules, it
is quite capable of repair and healing.
Production of reparative dentin and reduced
canal diameter may result, but pulp tissue
remains relatively unaffected.

Primary periodontal lesions with


secondary endodontic
involvement lesion

These lesions occur when an endodontically


induced periapical lesion exists at a tooth that is
also affected by marginal periodontitis.
The tooth has a pulpless, infected root canal
system and a co-existing periodontal defect.
This is particularly true in single-rooted teeth. In
molar teeth, root resection can be considered as
a treatment alternative if not all roots are
severely involved

Endodontic and periodontal


diseases are occurring
independently of each other.

Endodontic disease is occurring


secondarily to a periodontal
condition due to bacterial
retrograde from distal root

Periodontal disease at the


furcation is occurring secondarily
to a pinpoint perforation at the
furcation floor.

5 mm interproximal periodontal
pocket on teeth #16 and 17 and
inadequate endodontic treatment
on tooth #17.

Pulpal necrosis subsequent to


periodontal treatment and
significant osseous loss. No other
aetiology could be shown.

The major connections between periodontal


and pulpal tissues are the apical foramina.

In addition to the apical foramina and


accessory canals, there is a third possible
route for bacteria and their products, the
dentinal tubules.

They are serious complications during dental treatment and have a


rather poor prognosis.
Perforations may be produced by powered rotary instruments during the
attempt to gain access to the pulp or during preparation for a post.
Improper manipulation of endodontic instruments can also lead to a
perforation of the root.

The second group of artificial pathways between


periodontal and pulpal tissues are vertical root
fractures.

Vertical root fractures are caused by trauma and


have been reported to occur in both vital and
non-vital teeth.
In vital teeth, vertical fractures can be
continuations of coronal fractures in the
"cracked tooth syndrome," or can occur solely
on root surfaces.

A thorough visual examination of the lips,


cheeks, oral mucosa, tongue, palate and
muscles should be carried out .

The alveolar mucosa and the attached gingiva


are examined for the presence of
inflammation,ulcerations or sinus tracts.
Frequently, the presence of a sinus tract is
associated with a necrotic pulp.

Palpation is performed by applying firm digital


pressure to the mucosa covering the roots and
apices .
With the index finger the mucosa is pressed
against the underlying cortical bone .
This will detect the presence of periradicular
abnormalities or ''hot'' zones that produce painful
response to digital pressure .

Although this test does not disclose the condition


of the pulp, it indicates the presence of a
periradicular inflammation.
An abnormal positive response indicates
inflammation of the periodontal ligament that
may be either from pulpal or periodontal origin .
The sensitivity of the proprioceptive fibers in an
inflamed periodontal ligament will help identify
the location of the pain .
This test should be performed gently, especially
in highly sensitive teeth .

Tooth mobility is directly proportional to the


integrity of the attachment apparatus or to the
extent of inflammation in the periodontal
ligament.
Hypermobility is quite common in cases of
primary endodontic involvement and should
not be confused with true mobility caused by
periodontal destruction.
In cases of primary endodontic pathology, the
mobility resolves within a week of initiating
endodontic therapy.

Interpretation of discrete periapical or lateral lesions and


discrete periodontal lesions is of clinical importance in
suggesting the cause of the lesion and the proper diagnostic
procedures to follow to confirm the cause.
Often, the initial phases of periradicular bone resorption from
endodontic origin are confined only to cancellous bone.
Therefore, it cannot be detected unless the cortical bone is
also affected.
However, when there is radiographic evidence that bone loss
extends from the level of crestal bone to or near the apex of
the tooth, the radiograph is of little value in determining the
cause.

Endodontic or periodontal disease may


sometimes develop a fistulous sinus track.

Inflammatory exudates may often travel through


tissues and structures of minor resistance and
open anywhere on the oral mucosa or facial skin.
Intraorally, the opening is usually visible on the
attached buccal gingiva or in the vestibule.

Fistula tracking is done by inserting a semirigid


radiopaque material into the sinus track until
resistance is met.
Commonly used materials include gutta-percha
cones or pre-softened silver cones.

A radiograph is then taken, which reveals the


course of the sinus tract and the origin of the
inflammatory process .

The most commonly used pulp vitality tests


are cold test, electric test, blood flow tests
and cavity test.
The presence or absence of vital tissue in a
tooth with a single canal can be determined
with confidence with the current pulp-testing
procedures.
The same degree of confidence cannot be
ascribed to positive pulp test responses in a
tooth with multiple canals.

In general, when primary disease of one tissue, i.e.


pulp or periodontium, is present and secondary
disease is just starting, treat the primary disease.
When secondary disease is established and chronic,
both primary and secondary diseases must be
treated.
By and large, endodontic therapy precedes
periodontal therapy.
Periodontal therapy may or may not be required,
depending on disease status.
The complete healing of destroyed periodontal
support can be expected following the treatment of
pulpal pathology.

It is important to realize that it is clinically not


possible to determine the extent to which one or the
other of the two disorders (endodontic or
periodontal) has affected the supporting tissues.
Therefore, the treatment strategy must be first to
focus on the pulpal infection and to perform
debridement and disinfection of the root canal
system.

The second phase includes a period of


observation, whereby the extent of periodontal
healing resulting from the endodontic treatment
is followed.
Reduced probing depth can usually be expected
within a couple of weeks while bone regeneration
may require several months before it can be
radiographically detected.
Thus, periodontal therapy, including deep scaling
with and without periodontal surgery, should be
postponed until the result of the endodontic
treatment can be properly evaluated.

It is a known fact that root canal infection


significantly affects periodontal healing.
Pocket depth reduction is significantly lesser in
the presence of canal infection.
Removal of cementum will expose dentinal
tubules, which means that if there are bacteria
in the canal, it could promote inflammatory
resorption.

It may also expose periodontal tissues to


toxic medicaments if used in canal.
This is not so critical in areas with recession.

Early initiation of endodontic treatment


ensures that the cementum layer is kept
intact until root canal infection is eliminated.
Because there would be no exposed dentine
on the root surface, there is reduced chance
of root resorption and improved periodontal
healing.
On the other hand, if the root canal filling
does not have a good seal then the filled
canals may be reinfected from periodontal
bacteria.

The risk of infection is heightened if


periodontal treatment is delayed, especially
when a "combined lesion with
communication" exists between the two
sites.
Sterility is more likely while there is a
medicated dressing like calcium hydroxide in
the canal.
Hence, in some cases, it might be prudent to
delay the root filling until the periodontal
infection has been eliminated.

This would be required when:


both endodontic and periodontal infection are present simultaneously.

The true combined endodontic and periodontic lesion


requires an accurate diagnosis.
This is often a difficult diagnosis and therefore requires
reevaluation after either the periodontal or endodontic
problems are treated.
In such cases, if there is no communication, then complete
the endodontic therapy first and initiate periodontal
treatment soon after.
When lesions communicate, it makes sense to commence
endodontic treatment first and medicate canals until
prognosis is known.

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