lesiones endoperio usadas con lanueva clkasificacion

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REVIEW
Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand1
, Vivek Govila2
, Minkle Gulati3
1. Department of Periodontics, Faculty of Dental Sciences, Chhatrapati Shahuji Maharaj Medical University, Lucknow,
Uttar Pradesh. 2.Dept. of Periodontics, Babu Banarasi Das College of Dental Sciences, Babu Banarasi Das University,
Lucknow, Uttar Pradesh. 3. Department of Periodontics, Babu Banarasi Das College of Dental Sciences, Babu Banarasi
Das Campus, Akhilesh Das Nagar, Faizabad Road, Lucknow, Uttar Pradesh.
The periodontal tissues and the pulp-dentine complex form an intimate continuum
through which pathological changes of either one may lead to infection of the other.
When a periapical lesion communicates with a deep periodontal pocket, the etiology
can be either endodontic or periodontal. The purpose of this review paper is to explain
the nature of that relationship. Successful therapy will only result from the
establishment of an accurate diagnosis and forming such a diagnosis requires a
methodical mutli-staged approach.
Key Words: Endodontology, periodontology, endo-perio lesion.
communication remain patent, however, and these-
in addition to the apical foramen and dentinal tubules
are pathways through which etiologic agents may
pass between the pulp and the periodontium.2
Periodontal disease
Periodontal disease has a progressive nature. It
begins in the sulcus and migrates to the apex as
depositsofplaqueandcalculusproduceinflammation,
which slowly destroys the attachment apparatus.
These lesions may infiltrate lateral canals, accessory
canals or exposed dentinal tubules, but the path of
least resistance is generally sulcular. As long as the
vascular supply is maintained through the apical
foramen, the pulp usually resists attack via these
other pathways, although calcifications or minor
degenerative changes may be seen histologically.4
If
the periodontal lesion ultimately compromises the
vascular supply through the apical foramen, pulpal
necrosis will occur and further exacerbate the
periodontalbreakdown.Theprognosisforsuchatooth
basically depends on the nature of the periodontal
lesion.2
Pulpal Disease
Unlike periodontal disease, pulpal disease
commonly exhibits both chronic and acute phases.
When chronic, pulpal degeneration may occur rather
slowly; the highly polymerized nature of the pulp
makes it quite resistant to enzymatic degradation.
Pulpal inflammation, in a low-compliance system, is
© Archives of Dental Sciences
Vol.3, Issue 1, Jan.-Mar., 2012
http:www.archdent.org
Introduction
In 1964, Simring and Goldberg1
firstly defined
the relationship between periodontal and endodontic
disease, the term endo-perio has become an integral
part of the dental vocabulary. Unfortunately, this
term has been indiscriminately used to categorize
disease of either periodontal or endodontic aetiology,
with or without secondary involvement of the other,
as well as true combined lesions. An in-depth
understanding of the mechanisms by which these
two disease processes interact, together with a
thorough diagnostic examination, usually will help
direct the proper course of treatment.2
The
relationship between pulpal and periodontal disease
can be traced embryological development, since the
pulp and the periodontium are derived from a
common mesodermal source. In the course of root
development, strands of mesodermal tissue may get
trapped and later become lateral and accessory
canals. These offshoots also may result from dentin
formation around existing blood vessels or a loss of
continuity of Hertwig’s root sheath during dentin
formation.3
In time, most of these communications are
sealed by cementum or secondary dentin, leaving the
pulp basically dependent on the apical foramen for
metabolic exchange (and thus forming a low-
compliance system). Some of these portals of
Correspondence: Vishal Anand, Senior Resident, B 103,
Gautum Buddha Hostel, KGMC/ CSMMU Chowk, Lucknow,
Uttar Pradesh, India. Email: drvishalanand@hotmail.com.
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2. 4
is not involved. In any case, these effects are certainly
less dramatic than the effects commonly seen in the
periodontium of endodontic lesions, an interesting
situation, as the pathways involved are reciprocal. A
closer examination of the two disease processes is
necessary to explain this apparent discrepancy.
Endodontic disease and the Peridontium
When the pulp becomes necrotic, there is a
direct inflammatory response by the periodontal
ligament at the apical foramen and/or opening of
accessory canals.16
Inflammatory by-products of
pulpal origin may leach out through the apex, lateral
and accessory canals and dentinal tubules to trigger
an inflammatory vascular response in the
periodontium. Among those are living pathogens
such as bacteria and their toxic by-products, fungi,
viruses as well as nonliving pathogens.17,18,19, 20,21,22
Many of these are similar pathogens encountered in
periodontal infections. In certain cases pulpal disease
will stimulate epithelial growth that will affect the
integrity of the periradicular tissues.23,24
It has been
suggested that periodontal disease has no effect on
the pulp, at least until it involves the apex.10
On
the other hand, several studies suggested that the
effect of periodontal disease on the pulp is
degenerative in nature including an increase in
calcifications, fibrosis and collagen resorption, as
well as a direct inflammatory affect.4,25
It seems that
the pulp is usually not directly affected by periodontal
disease until recession has opened an accessory canal
to the oral environment. At this stage, pathogens
penetrating from the oral cavity through the
accessory canal into the pulp may cause a chronic
inflammatory reaction and pulp necrosis. However,
as long as the accessory canals are protected by
sound cementum, necrosis usually does not occur.
In addition, if the microvasculature of the apical
foramen remains intact, the pulp will maintain its
vitality.4
The effect of periodontal treatment on the
pulp is similar during scaling and root planing or
periodontal surgery if accessory canals are severed
and/or opened to the oral environment. In such cases
microbial invasion and secondary necrosis of the pulp
can occur.
Classification
Traditionally perio-endo lesions have been
classified as: 26
1. Primary periodontal lesions
2. Primary endodontic lesions
accompanied by an increase in intrapulpal pressure.
With this increase in intrapulpal pressure, toxic
agents may be expressed through patent channels,
including the apical foramen, lateral and accessory
canals. Corresponding lesion in the adjacent
periodontium may eventually coalesce.2
While any
endodontic lesion may drain along the periodontal
ligament and form fistula, it is termed a retrograde
periodontitis, this type of lesion progresses in the
opposite direction of a marginal periodontitis and
possibly without permanently damaging the
cementum and its fibers.5
The loss of attachment
producedbytheselesionsmaybecompletelyreversible
with endodontic therapy alone; however, if not treated
early, secondary periodontal involvement may
progressively underline the prognosis.2
The relationship of Pulpal and Periodontal
disease
While the harmful effects of pulpal disease on
theperiodontiumarewelldocumented,5,6,7
theopposite
effect of periodontal disease on the pulp remains
unclear. Some authors have reported a strong
correlation between periodontal disease and
inflammatory and degenerative changes in the
pulp7,8,9
, while others have found no such
correlation10,11
. Langerland and others4
found that
the pulp succumbed only when periodontal lesions
involved the apical foramen; otherwise, only minor
changes occurred in the pulp. The clinical symptoms
of pulpitis commonly seen in periodontal patients are
related more closely to the treatment than to the
disease.Vigorousrootplaningmayremovecementum
and expose numerous dentinal tubules through which
etiological agents may enter and inflame the pulp.6,
12
Furthermore, these exposed tubules are subject to
hydrodynamic stimuli.13
This has been shown to be
mitigated by smear layer formation,14,15
but
unfortunately, this smear layer has been shown to
dissolve as early as one week after surgery, resulting
in a return of dentin hypersensitivity.14
Although this
pulpitis is usually reversible, palliative endodontic
therapy may be necessary is some cases. As previous
stated, the pulp generally will not succumb to
periodontal lesions that do not involve the apical
foramen,4
however, it must be remembered that the
effects of a lifetime of caries, operative procedures,
periodontal disease and treatment are cumulative,
with the pulp losing some of its recuperative power
with each added insult.
Periodontal disease, therefore, can contribute to
pulpal inflammation even when the apical foramen
Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand, Vivek Govila, Minkle Gulati
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3. 5
3. Primary periodontal lesions with secondary
endodontic involvement
4. Primary endodontic lesions with secondary
periodontal involvement
5. True combined lesions
Thisclassificationtriedtocategorizetheprimary
source of infection, which with hindsight now seems
unrelated to the management of the lesion in
question. The significant issue is to determine the
status of the pulpal and periodontal complex at the
time of presentation, because the vitality of the pulp
and/orpresenceorabsenceofaprogressingperiodontal
lesion should dictate the nature of treatment
indicated. If the pulp is necrotic or has irreversible
pulpitis the tooth requires a root filling; if it is viable,
it doesn’t. Similarly, if a tooth has a periodontal lesion
that appears to be progressing, periodontal therapy
is necessary; if the lesion appears stable (as
determined by repeated failure to bleed upon probing
and stable attachment levels) or there is no lesion,
then periodontal therapy is not indicated. If the pulp
is necrotic and there is concomitant periodontal
pathology, then the tooth needs root canal therapy
and periodontal treatment. The former should be
performed first in case that is sufficient to allow the
body to heal the combined lesion without the need for
periodontal therapy.26
Simon, Glick and Frank (1972) further
categorised endodontic lesions into two sub-
categories:5
1. Primary Endodontic lesions - when a sinus tract
has formed to establish drainage.
2. Primary Endodontic lesions with Secondary
Periodontal Involvement - when plaque
formation occurring in the sinus tract with
progression to periodontics and associated
calculus formation.
This classification assists in eliminating a
differential diagnosis and ensuring the correct choice
of treatment for an endodontic lesion.
Simon, Glick and Frank (1972) also further
categorized periodontal lesions into two sub-
categories:5
1. Primary Periodontal lesions - when there is
progression of the periodontal lesion to involve
the apex of the tooth and the pulp is vital (there
may be some pulpal degenerative changes).
2. Primary Periodontal lesions with Secondary
Endodontic Involvement - periodontal disease
causes a resultant pulpal necrosis as it progress
apically. As for endodontic lesions this
classification assists in eliminating a differential
diagnosis and ensuring the correct choice of
treatment for a periodontal lesion.
A more sensible classification system for perio-
endo lesions would thus seem to be: 27
1. Endodontic lesions - an inflammatory process
in the periodontal tissues resulting from noxious
agents present in the root canal system of the
tooth.
2. Periodontal lesions - an inflammatory process
in the pulpal tissues resulting from
accumulation of dental plaque on the external
root surface.
3. True-combined lesions - both an endodontic and
periodontal lesion developing independently and
progressing concurrently which meet and merge
at a point along the root surface.
4. Iatrogenic lesions - usually endodontic lesions
produced as a result of treatment modalities.
PATHOGENESIS
Pathogenesis: Endodontic Lesions
Pulpal inflammation and necrosis are initiated
by dental caries, restorative procedures, trauma,
chemical irritation and severe thermal stimulation.
These inflammatory lesions causes localized edema
and a resulting increase in intra- pulpal pressure
and cell death.28
Increased damage associated with
an inflammatory exudates cause local collapse of the
venous part of the local microvasculature. This causes
local tissue hypoxia and anoxia resulting in localized
necrosis, the chemical mediators of which cause
further localized edema, completing the cycle.29
As
the root canal system is a low compliance system an
increasedintrapulpalpressuremaycausetoxicagents
to be expressed through patent channels, such as the
apical foramen, lateral and accessory canals and
dentinal tubules, which can result in a retrograde
periodontitis.2
Noxious agents from a root canal which
cause a clinically detectable inflammatory lesion in
the surrounding periodontal ligament have been
shown to originate from a non-sterile necrotic pulp,
or remnants of such from unfilled spaces in an
inadequately root filled tooth.30
Carious lesions or any
direct exposure to the oral cavity of dentine or pulp
may allow ingress of bacteria to contaminate an
otherwise sterile lesion. This is predominantly a
Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand, Vivek Govila, Minkle Gulati
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4. 6
added insult.2
Periodontal occlusal trauma may, in
theory, cause pulp ischemia, especially in teeth with
a greatly reduced periodontal support further adding
to cumulative detrimental effects mentioned
previously.32
Lateral, accessory canals and dentinal
tubules are therefore potential sources of pulpitis and
pulpal necrosis.28
The presence of an intact cementum
layer is important for the protection of the pulp from
pathogenic agents produced by the plaque bacteria.30
Therefore the exposure of dentinal tubules by the
removal of cementum due to rigorous scaling and
root-planing for the treatment of periodontal disease
willallowbacterialinvasionofthetubules.Thiswould
increase the likelihood of cumulative damage to the
pulp.2
A retrograde pulpitis follows local pulpal
inflammation and necrosis and can result in a
progression to total necrosis of the pulpal tissues. The
microbiological composition of pathogenic root canals
in advanced periodontal lesions is similar to that in
the periodontal pocket - a mixed anaerobic infection.
Results from microbiological and immunological
studies support the suggestion that the source of
endodontic infection in perio-endo lesions of
periodontal etiology is the periodontal pocket
bacteria.33
Pathogenesis: True-Combined Lesions
The pathogenesis of a true-combined lesion is
identical to the pathogenesis of primary endodontic
and periodontal lesions. These independent lesions -
theperiapicallesionoriginatingfromthenecroticpulp
and the periodontal lesion progressing apically -
eventually merge.31
These lesions are often
indistinguishable from an advanced primary
endodontic lesion with secondary periodontal
involvement and/or a primary periodontal lesion with
secondary endodontic involvement.32
Pathogenesis: Iatrogenic Lesions
The causes of iatrogenic lesions are root
perforations, the overfilling of root canals, intra-canal
medicaments and vertical root fractures.32
Root
perforations occur during instrumentation of root
canals, while preparing root canals for the insertion
of posts, from carious exposure as well as internal
and external resorption. A communication between
the pulp and periodontium is produced through the
lateral walls of the root or the pulpal floor in multi-
rootedteeth.Atthesiteofperforationaninflammatory
reaction in the periodontal ligament produces
degradation of the surrounding tissues and the
formation of a lesion which can progress as a
Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand, Vivek Govila, Minkle Gulati
mixed anaerobic infection.29
Endodontic lesions are
most frequently initiated and sustained by the apical
foramen, followed by accessory and lateral canals,
and most infrequently by dentinal tubules. Abscess
formation follows periodontal inflammation which
spreads through the periodontium. The abscess may
drainthroughafistulaorviatheperiodontalligament,
with ligament and adjacent bone destruction, which
can involve the entire root length.31,32
Drainage may
tract along the periodontal ligament and into the
gingival sulcus or in multirooted teeth into the
furcation. A periapical lesion may perforate the
cortical bone close to the apex, elevate the periosteum
and overlying soft tissues, and drain into the gingival
sulcus.30
These form pseudopockets that simulate
periodontal disease without necessarily permanently
damaging the cementum and its fibers.2
If the acute
periapical drainage becomes chronic and drainage
through the gingival sulcus continues a downgrowth
of epithelium round the tract can result in a
periodontal pocket in which secondary periodontal
disease may complicate the lesion. Plaque and
calculus are detected within the pocket.31
Pathogenesis: Periodontal Lesions
Periodontal lesions are initiated by deposits of
plaque and calculus. Inflammatory mediators cause
destruction of gingival connective tissue, periodontal
ligament and alveolar bone. Alteration of the root
surface occurs by loss of the outer cementoblast layer
and results in shallow resorptive lesions of cementum.
Endotoxins produced by plaque bacteria also have an
irritant effect on overlying soft tissue, preventing
repair.32
Migration of the lesion to the apex continues
withdrainageviathegingivalsulcuspreventingacute
episodes.2
Most authors agree that healthy pulpal
tissue is a highly polymerized, highly vascular tissue
- quite resistant to infection. This prevents the
occurrence of clinically detectable degeneration in the
presence of periodontal disease, as once the dentine/
pulpcomplexhasbeenexposedtoabacterialchallenge
repair and healing will leave the remaining tissue
relatively unaffected.30
Although periodontal disease
has been shown to have a cumulative damaging effect
on the pulp tissue, total disintegration of the pulp is
only a certainty if bacterial plaque involves the main
apical foramina, compromising the vascular
supply.2,28,30
Evidence to the contrary shows
inflammatory lesions, as well as localized necrosis of
pulptissueobservedadjacenttolateralcanalsinteeth
exposed by periodontal disease.30
As the effects of
caries and noxious stimuli are also cumulative, the
pulp loses some of its recuperative power with each
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5. 7Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand, Vivek Govila, Minkle Gulati
conventional primary endodontic lesion.30
The
overfilling of root canals produces a lesion in exactly
the same way, the lesion originating adjacent to the
apical foramen rather than the lateral wall or pulpal
floor.
Vertical root fractures are most often caused
when a tooth - often weakened due to undermining
by caries, previous restorative treatment or a non -
vital pulp becomes traumatized.32
Leaching of the
root canal contents or bacterial contamination of the
fracture line may cause an inflammatory lesion in
the periodontal tissues.30
The continuing lesion
mimics those due to root perforation or over - filling
of root canals. A fracture that has penetrated the
pulp initiating pulpal necrosis may be difficult to
distinguish from a true -combined lesion. Strong
antiseptic drugs used for root canal disinfection and
pulp devitalisation can cause severe damage if they
leak into the periodontal tissues.27
The relationship between the vital pulp and
the periodontal tissues
The pulpal complex is a highly organized tissue,
comprising vascular, neural, cellular (odontoblast,
fibroblast,undifferentiatedcells)andconnectivetissue
components confined within a non-expandable
structure. Thus any build-up of pressure within that
chamber, caused through inflammation, can escape
only through the apical foramen or accessory root
canals into the periodontium and invariable blood
supply and whilst it has this supply the pulp appears
relatively resistant to bacterial influx because the
host’s inflammatory-immune response is delivered
to the root canal system to fight off potential infective
agents.26
However, the root canal system is unique for
each tooth and far more complex and tortuous in its
extension within the dentine than initially thought.
Inflammation within the pulp system can be induce
by various means:34
Restorative procedure (thermal change,
chemical damage or pulp exposure)
Caries
Trauma (acute or chronic)
Dentine exposure (either coronal or radicular
dentine)
The inflammation lesion that develops will not
necessarily devitalize the root canal system and may
be contained by the inflammatory-immune response
to it. With the exception of rapidly advancing caries
such lesions rarely involve the periodontal complex
and remain contained within the pulp. Indeed, it is
possible for a tooth radiographically to have a small
periapical radiolucent zone yet to remain vital.34
The relationship between the non-vital pulp
and the periodontal tissues
A non-vital pulp may be sterile, and may thus
not cause inflammation of the periodontal tissues.35
Pulpal infection may, however, lead to periodontal
involvement in the form of widening of the apical
ligament space caused by the inflammatory lesion
moving through the apical foramen, or widening of
the lateral periodontal ligament by infection moving
through lateral or furcation canals. It is unsurprising
that the infected pulp has a microflora similar to those
putative pathogens associated with progressive
periodontal lesion.36
Such organism include
Fusobacterium sp., Eubacterium sp., Prevotella,
Porphyromonas sp. and some spirochaetes, although
endodontic infections appear to involve fewer species
than periodontal infections.18
Therearetwobroadscenariostopulpalinfection:
acute abscess formation, involving suppuration and
symptoms of pain from physical or thermal stimuli,
or chronic inflammatory lesions, during which the
body’s attempts to repair the damage caused result
in the formation of granulation tissue (the apical
granuloma) and fibrous repair tissue. On occasions,
epithelial proliferation may occur within established
granulomas and lead to inflammatory/radicular cyst
formation.26
A tracking pulpal infection finds the path of
least resistance to spread along and ultimately
discharge. This may involve tracking along the
periodontal ligament itself to discharge. This may
involve tracking along the periodontal ligament itself
to discharge via a narrow sinus at the gingival
margin. The clinical features of this apparent
periodontal lesion would be a non-vital tooth and a
narrow tract-like pocket detectable with a periodontal
probe, but radiographically bone loss may be
inconsistent with the depth of probing. Alternatively,
the infection may exit the root through a lateral or
apical foramen and progress through the overlying
alveolus to form a mucosal swelling and ultimately,
a sinus. The latter usually arise over the apex, and
in the stages of this process the tissues over the apex
may be acutely tender to palpation. However, once
the abscess has discharged the symptoms often
resolve.26
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6. 8
15. Cuenin MF, Scheidt MJ, O’Neal RB et al. An in vivo
study of dentin sensitivity: The relation of dentin
sensitivity and the patency of dentin tubules. J
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16. Seltzer S, Bender IB, Nazimov H et al. Pulpitis-
induced interradicular periodontal changes in
experimental animals. J Periodontol 1967: 38: 124–
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17. Baumgartner JC, Falkler WA Jr. Bacteria in the
apical 5 mm of infected root canals. J Endod 1991:
17: 380–383.
18. Dahle UR, Tronstad L, Olsen I. Characterization of
new periodontal and endodontic isolates of
spirochetes. Eur J Oral Sci 1996: 104: 41–47.
19. Jansson L, Ehnevid H, Blomlof L et al. Endodontic
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20. Jung IY, Choi BK, Kum KY et al. Molecular
epidemiology and association of putative pathogens
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the pulp of a primary tooth. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 2000: 90: 365–368.
22. Nair PNR. Cholesterol as an aetiological agent in
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23. Nair PNR, Pajarola G, Schroeder HE. Types and
incidence of human periapical lesions obtained with
extracted teeth. Oral Surg Oral Med Oral Pathol
1996: 81: 93-101.
24. Simon JHS. Incidence of periapical cysts in relation
to the root canal. J Endod 1980: 6: 845–848.
25. Mandi FA. Histological study of the pulp changes
caused by periodontal disease. J Br Endod Soc 1972:
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26. Iain LC, Chapple and Philip J, Lumley. The
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27. Mhairi R Walker. The pathogenesis and treatment
of endo-perio lesions. Continuing Professional
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Summary
This paper has attempted to describe the
biological and physical relationship between
periodontal and pulpal tissues. We have attempted
to discuss how the two tissue form a continuum and
how disease of one may impact upon the other.
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Archives of Dental Sciences, Vol.3, Issue 1
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Endo-Perio Lesion: Part I (The Pathogenesis) – A Review
Vishal Anand, Vivek Govila, Minkle Gulati