Jan Lindhe. Clinical Periodontology
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DIFFERENTIAL DIAGNOSES: PERIODONTAL TUMORS AND CYSTS • 313
Fig. 13-23. (a) Radiographic manifestation of lateral periodontal cyst between right mandibular first premolar and
canine. The cyst was surgically removed, and the tissue histologically examined. (b) Characteristic histopathologic
features of a non-keratinized lining epithelium with focal thickenings.
The epithelial remnants most frequently forming the epithelium into the connective tissue, or (4) junctional
background of cysts of the periodontal tissues are of epithelium, which in turn is derived from the reduced
odontogenic origin. enamel epithelium. Shear (1992) has been impressed
by the many similarities between the gingival cyst in
adults and the lateral periodontal cyst. He proposed
that the gingival cyst in adults is derived from junc-
tional epithelium after eruption of the tooth, whereas
the lateral periodontal cyst is formed from the reduced
enamel epithelium by dilation of the follicle before
eruption of the tooth.
Histopathology
The gingival cysts in infants are usually small, with a
diameter of 2-3 mm. They are lined by a stratified
squamous epithelium with a parakeratotic surface and
flat basal cells. The cyst lumen is filled with keratin (
Shear 1992).
The gingival cyst of adults (Fig. 13-22b) is lined
with a thin, non-keratinized squamous epithelium
sometimes exhibiting focal thickenings of the epi-
thelial lining as can also be seen in the lateral peri-
odontal cyst (Nxumalo & Shear 1992).
Treatment
There is no reason to treat gingival cysts in infants.
Gingival cysts of adults are treated by local surgical
excision and usually there is no tendency to recur.
Lateral periodontal cyst
Clinical features
The lateral periodontal cysts are rare developmental
cysts most often occurring in adults, predominantly
localized to the canine and premolar region and most
often affecting the mandible as mentioned also for the
gingival cyst (Shear 1992). Lateral periodontal cysts
occur in the lateral periodontal position and the diag-
nosis implies that an inflammatory background is
excluded, as is a collateral keratocyst. The cyst may
present as a gingival swelling but it is usually symp-
tomless. It is usually observed by routine radiography
and sometimes it has features in common with mar-
Gingival cyst
Clinical features
Gingival cysts are of developmental origin. Whereas
the frequency of gingival cysts is high in newborns,
they are rarely seen after 3 months of age because most
of the gingival cysts in newborns undergo involution
and disappear or rupture through the surface epithe-
lium and exfoliate (Shear 1992). Such cysts are fre-
quently referred to as Epstein's pearls or Bohn's nod-
ules, but there is some confusion about the terminol-
ogy. Studies have revealed gingival cysts of infants in
76% and 85%, the majority occurring in the maxilla.
Gingival cysts in infants arise from remnants of the
dental lamina.
Gingival cysts in adults are uncommon. They are
most often found in patients aged more than 40 (Nxu-
malo & Shear 1992). Some cases are diagnosed clini-
cally, but others are recognized histologically in biop-
sies from the gingiva. They may occur with or without
bone involvement in the form of a superficial erosion
and they may give rise to gingival swelling (Fig. 13-
22a), although they are most often unnoticed. The
gingival cyst in adults has a predilection for occur-
rence in the mandibular canine and premolar region,
which are also predilection sites for the lateral peri-
odontal cyst. This is why there is some confusion
about the relationship between the two types of cysts, a
confusion which is further complicated by the fact
that many cysts in the lateral periodontal position are
in fact keratocysts, while others are of inflammatory
origin, for instance associated with accessory root
canals of necrotic teeth (Shear 1992). Clinically recog-
nizable gingival cysts are most frequent in the mandi-
ble. A gingival cyst may arise from (1) odontogenic
epithelial cell nests, (2) degenerative, cystic changes in
proliferating epithelial ridges from the gingival sur-
face epithelium, (3) traumatic implantation of surface
314 • CHAPTER 13
Fig. 13-24. (a) Radiography of inflammatory paradental cyst associated with partially erupted mandibular third
molar. The cyst is lined by irregular non-keratinized squamous epithelium (b). Severe inflammation is seen in the
connective tissue wall.
ginal periodontitis. The radiograph shows a round or
oval radiolucency often less than 1 cm in diameter and
usually with a margin of radiopacity. It is situated
somewhere between the cervical margin and the apex
of the tooth (Fig. 13-23a). The cyst probably arises
initially as a dentigerous cyst developing by expan-
sion of the tooth follicle along the lateral surface of the
crown (Altini & Shear 1992).
Histopathology
The cyst is lined by a thin, non-keratinized stratified
squamous epithelium, sometimes with focal epithelial
thickenings (Fig. 13-23b) (Shear & Pindborg 1975).
Inflammatory cells are only manifest in the case of
secondary infection.
Treatment
The treatment is surgical enucleation with careful han
dling of the root surfaces and vascular supply of the
associated tooth. Clinicians are advised to follow the
cases for a number of years as some variants of the
cysts may have a tendency to recur.
Inflammatory paradental cyst
Clinical features
The inflammatory paradental cyst has previously
been
described as the collateral inflammatory cyst, the
inflammatory lateral periodontal cyst, the paradental
cyst, and the mandibular infected buccal cyst
(
Vedtofte & Prxtorius 1989). The site of predilection
for
this cyst is the mandibular molar area, most fre-
quently the third molar, and the associated tooth is
vital. Bilateral occurrence has been reported and simi
-
lar cysts have been described in the globulomaxillary
region between lateral incisors and canines (Vedtofte
& Holmstrup 1989). The cyst develops most fre-
quently in children and young adults, equally often in
women and men. The cysts are often infected and
pain, swelling and discharge of pus from the peri-
odontal pocket are common due to communication
with the periodontal pocket. Frequently, the cysts are
diagnosed as periodontitis or pericoronitis (Vedtofte
&
Prtorius 1989). Radiographically, the inflamma
tory
paradental cyst presents a well-defined radiolucency
in a position predominantly distal to the in
volved
tooth (Fig. 13-24a). A buccal superimposition
may
give an impression of a periapical lesion. The cyst
may
cause displacement of the tooth distal to the cyst.
The
cyst is frequently diagnosed shortly after tooth
eruption and it is probably initiated by pericoronitis
at
the time of tooth eruption, the most likely origin of
the cyst epithelium being the epithelial cell rests of
Malassez and the reduced enamel epithelium (Craig
1976, Vedtofte & Prxtorius 1989).
Histopathology
The cyst is lined with a thick non-keratinized stratified
squamous epithelium, and the underlying connective
tissue is infiltrated by inflammatory cells (Fig. 13-24b).
The histology is non-specific.
Treatment
It has been demonstrated that the tooth associated
with the cyst can in almost all cases be preserved.
Cystectomy is the treatment, and usually the surgical
treatment is followed by regeneration of bone and a
periodontal sulcus of 2-3 mm (Vedtofte & Prtorius
1989).
Odontogenic keratocyst
Clinical features
Keratocysts may occur at any age and they are most
frequent in males. The cysts are most often seen in the
mandibular third molar region but may occur any-
where in the jaws including the alveolar bone. Radiog
-
raphically, they may be small, round or ovoid, radio-
lucent areas with a smooth periphery or they may
have scalloped margins or even be multilocular (Fig.
13-25a) (Shear 1992). It has been reported that a kera
-
tocyst-like lesion can be seen in the gingival soft tis-
sues as well (Fardal & Johannesen 1994, Chehade et
al. 1994).
DIFFERENTIAL DIAGNOSES: PERIODONTAL TUMORS AND CYSTS • 315
Fig. 13-25. (a) Keratocyst shows well demarcated ovoid
radiolucency between right mandibular premolars. (b)
The
cyst
is lined by keratinized squamous epithelium
piling up in the cyst lumen (top). Note palisading of
nuclei in the basal cell layer of the epithelium.
Fig. 13-26. (a) The radicular cyst shows a radiolucency
surrounding the apex of a maxillary lateral incisor. (b)
The radicular cyst is lined by an irregular non-kerati-
nized stratified epithelium. Note cholesterol clefts in
cyst lumen and connective tissue wall.
Histopathology
The cyst lining is a thin connective tissue capsule
covered by an ortho- or parakeratinized stratified
squamous epithelium with cuboidal or columnar ba-
sal cells (Fig. 13-25b). Inflammatory cells are not pre-
sent unless the cyst is secondarily infected.
Treatment
Surgical intervention results in cure in most cases, but
in contrast to other jaw cysts, the keratocysts show a
propensity for recurrence (Forssell et al. 1988) even
after what appears to be total removal. This is espe-
cially true for the parakeratinized cysts. Large cysts
may be initially treated with marsupialization, i.e.
opening of the cyst cavity into the mouth. This proce-
dure usually leads to progressive reduction in the size
of cysts in the jaws.
Radicular cyst
Clinical features
The radicular cyst is the most common cyst of the jaws,
accounting for about 60% of jaw cysts (Shear 1992).
The background of these cysts is a non-vital tooth with
periapical granuloma in which rests of Malassez are
stimulated to proliferate and finally form a cyst cavity
which grows, probably due to accumulation of fluid
within the cavity. Radiographically, the cysts show a
well-circumscribed round or oval radiolucency related
to the apical part of the root (Fig. 13-26a). The
diameter varies from a few millimeters to a few centi-
meters.
Histopathology
The cyst cavity is lined by a non-keratinized stratified
squamous epithelium of varying thickness and with
irregular ridges proliferating into the underlying con-
nective tissue (Fig. 13-26b). Sometimes mucous cells
form part of the cyst lining, presumably due to meta-
316 • CHAPTER 13
plasia of the epithelium. There is usually a heavy
inflammatory reaction in the underlying connective
tissue, the inflammatory cells usually penetrating the
epithelium and entering the cyst cavity. Numerous
cholesterol clefts may be seen. As with the inflamma-
tory paradental cyst, the histology is non-specific.
Treatment
Radicular cysts need surgical removal, possibly pre-
ceded by marsupialization if the cyst cavity is very
large. Endodontic treatment or revision of previous
endodontic treatment of the tooth involved is impor-
tant.
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CHAPTER
14
Endodontics and Periodontics
GUNNAR BERGENHOLTZ AND GUNNAR HASSELGREN
Influence of pathologic conditions in the
pulp on the periodontium
Manifestations of acute endodontic lesions in
the marginal periodontium
Impact of endodontic treatment measures on
the periodontium
Influence of external root resorptions
Influence of periodontal disease on the
condition of the pulp
Influence of periodontal treatment measures
on the pulp
Endodontic considerations in root resection
of multirooted teeth in periodontal therapy
Differential diagnostic considerations
Treatment strategies for combined
endodontic and periodontal lesions
The fact that the periodontium is anatomically inter-
related with the dental pulp by virtue of apical foram-
ina and lateral canals creates pathways for exchange
of noxious agents between the two tissue compart-
ments when either or both of the tissues are diseased.
Resorptive processes involving the root surface, and
treatment measures aimed at managing periodontal
disease enhance this potential as the accompanying
exposure of dentinal tubules establishes yet another
passage across the body of the tooth structure. Conse
-
quently, under certain clinical conditions discussed in
this chapter, disease in one of the tissue compartments
may result in pathological conditions in the other.
Not only may interactions occur between the peri-
odontium and the pulp to induce or even aggravate
an
existing lesion, they may also present the clinician
with the challenge of deciding the direct cause of an
inflammatory condition in the periodontium. Hence,
inflammatory symptoms often seen as typical of peri-
odontal disease including deep periodontal pockets
with or without swelling and suppuration of the mar-
ginal gingivae, increased tooth mobility and angular
bony defects may also represent symptoms of a patho
-
logical condition present in the root canal system of
the affected tooth.
The differential diagnosis between an endodontic
lesion (the term endodontic lesion is used to denote
an inflammatory process in the periodontal tissues
resulting from noxious agents present in the root canal
system of the tooth, usually a root canal infection) and
a periodontal lesion (the term periodontal lesion is
used to denote an inflammatory process in the peri-
odontal tissues resulting from accumulation of dental
plaque on the external tooth surfaces) can often be
established without much difficulty, since endodontic
lesions most often induce symptoms in the apical
periodontium, while symptoms of periodontal dis
ease
usually are confined to the marginal periodon
tium.
However, the character of the clinical symptoms
may
occasionally be confusing and cause the misin-
terpretation of their etiology. What appears to be a
periodontal lesion may actually be symptoms of an
endodontic disorder and
vice versa.
The establishment
of a correct diagnosis may also be complicated when
both a periodontal and an endodontic lesion affect the
same tooth simultaneously and may present as a sin-
gle lesion. This condition has been termed "true endo
-
dontic-periodontal lesion" and implies that the lesion
either is the result of, or the cause of, the other, or the
lesion may just represent two separate processes, an
endodontic and a periodontal, which have developed
independently.
Proper diagnosis of the various disorders affecting
the periodontium and the pulp is important to
exclude
unnecessary and even detrimental treatment.
The cli
nician should therefore be well acquainted
with the
pathogenesis as well as with available
diagnostic measures aimed at identifying disease
conditions of
these tissues. For this purpose, possible
interrelation
-
ships between disease processes of the
dental pulp
and the periodontium are described in
this chapter. Emphasis is placed upon diagnosis and
treatment.
ENDODONTICS AND PERIODONTICS •
319
Since, in addition, root fractures and iatrogenic root
perforations may be associated with inflammatory
lesions of a similar nature in the periodontium as those
of pulpal and periodontal disease, the clinical features
of these complications are addressed as well. The
mechanisms and the clinical management of different
forms of external root surface resorptions have also
been included in this chapter.
INFLUENCE OF PATHOLOGIC
CONDITIONS IN THE PULP ON
THE PERIODONTIUM
Impact of disease conditions in the vital pulp
Disease processes of the dental pulp frequently in-
volve inflammatory changes. Caries, restorative pro-
cedures and traumatic injuries are the most common
causes. In fact, any loss of hard tissue integrity, expos
-
ing dentin or the pulp directly, may allow bacteria and
bacterial elements present in the oral environment to
adversely affect the normal condition of the pulp. The
resulting inflammatory lesion will then be directed
towards the source of irritation and be confined for as
long as the inflammatory defense does not collapse
and convert into a destructive breakdown of the pul-
pal tissue. Consequently, inflammatory alterations in
the vital pulp will not sustain distinct lesions in the
adjoining periodontium. Yet, occasionally, disruption
of the apical lamina dura or widening of the periodon
-
tal ligament space may be seen in the periodontium.
Even a minor periapical radiolucency may be present
in spite of the fact that vital pulp functions prevail
(
Langeland 1987). In such instances, typical clinical
signs of pulpitis, including spontaneous pain, thermal
sensitivity or tenderness to percussion, may or may
not be present.
If the pulp survives the acute phase of the inflam-
matory response, repair and scarring of the tissue
frequently develop. Reparative dentin (synonymous
with irregular secondary dentin, irritation dentin, ter-
tiary dentin) within areas of the previous lesion, fibro-
sis and dystrophic mineralizations represent typical
sequelae to pulpal repair (Fig. 14-1). Such tissue
changes do not
per se
warrant further concern except
that they may interfere with the nervous and vascular
supply of the tissue, which in turn may jeopardize its
continued vital function upon an iterated insult.
Conclusion
From a diagnostic point of view it is important to
realize that as long as the pulp maintains vital func-
tions, although inflamed or scarred, it is unlikely to
produce irritants that are sufficient to cause pro-
nounced marginal breakdown of the periodontium.
Consequently no benefit will be gained from pulp
Fig. 14-1. Histologic section showing emerging hard tis
sue repair (reparative dentin) along the root canal wall
of a monkey tooth exposed to scaling and root planing
30 days earlier. Specimen is from an experimental
study by Bergenholtz & Lindhe (1978).
extirpation (pulpectomy) as an adjunct or alternative
to the treatment of teeth for periodontal disease.
Impact of pulpal necrosis
Contrary to disease conditions in the vital pulp, pulp
necrosis is frequently associated with inflammatory
involvement of the periodontal tissue. The location of
these lesions is most often at the apex of the tooth (Fig.
14-2). They may also occur at any site where lateral
canals exit into the periodontium (Fig. 14-3, see also
below).
While sterile necrotic pulps are unable to sustain
overt inflammation in the periodontal tissue (Bergen-
holtz 1974, Sundqvist 1976, Moller et al. 1981), animal
experiments (Kakehashi et al. 1965, Fabricius et al.
1982) and clinical studies (Bergenholtz 1974,
Sundqvist 1976) have convincingly demonstrated the
infectious nature of these processes. In this respect
pulpal disease shares an identical etiology with peri-
odontal disease. In fact, the two disease entities show
many characteristics in common in terms of their mi-
crobiologic (Kerekes & Olsen 1990, Sundqvist 1990,
1994) and immunologic/histopathologic features
(
Bergenholtz et al. 1983, Stashenko et al. 1998, Marton
& Kiss 2000). Similar to periodontal disease, potential
pathogens most often associated with endodontic in-
fections are found in the anaerobic segment of the flora
with
Fusobacterium, Prevotella, Porphyromonas, Pep-
tostreptococcus, Eubacterium, Capnocytophaga,
and
Lac-
tobacillus
belonging to the genera most frequently iso-
lated by culture (Sundqvist 1990, 1994, Baumgartner
& Falkler 1991, Wasfy et al. 1992). Also spirochetes
(
Thilo et al. 1986, Molven et al. 1991, Dahle et al. 1996)
320 • CHAPTER
14
Fig. 14-2. Series of images demonstrating features of apical inflammatory lesions caused by a root canal infection. A
lesion at the tip of an extracted palatal root of an upper molar (a). The longitudinally cut tissue section through the
root tip shows an overview of the lesion (b). The outer collagen rich connective tissue confines the soft tissue lesion
and attaches it to the root surface. High magnification of a bacterial front–host tissue interface inside a root canal,
where bacterial organisms (stained blue) are being battled by polymorphonuclear leukocytes (c). A typical mixed
inflammatory cell response is common at the center of a lesion (d). In the most peripheral portion the connective
tissue of an established lesion is rich in collagen and devoid of inflammatory cells (e). Figs 14-2 (a-c) and (e)
have been kindly provided by Dr Domenico Ricucci. Microphotograph in (d) is from a lesion in a monkey (
unpublished study by Bergenholtz & Wikesjo).
and fungi (Waltimo et al. 1997) may reside in infected
root canals. It should be noted that the composition of
the microbiota in necrotic pulps is not as complex as
the one in deep periodontal pockets associated with
periodontal disease and usually comprises a limited
number of bacterial species of which one or two may
predominate.
The host tissue response to the infection will take
the form of either an acute abscess (Fig. 14-4) or a
chronic inflammatory response (Fig. 14-2). Which of
the forms occurs is largely dependent on the quality
and quantity of the bacteria present in the root canal
and the capacity of the host defense to confine and
neutralize the bacterial elements that are released from
the root canal system into the periodontium. Following
the initial expansion, which involves de
struction of the periodontal ligament and the adjacent
alveolar bone, a balanced host-parasite relationship is
usually established (Yu & Stashenko 1987, Stashenko
& Yu 1989, Nair 1997, Stashenko et al 1998). The in-
flammatory process may then remain unchanged in
size for years, although cyst transformation occasion-
ally occurs that can result in substantial destruction of
the alveolar bone.
Histologically, the established lesion is charac-
terized by a richly vascularized granulation tissue,
which, to a varying degree, is infiltrated by inflamma-
tory cells. Neutrophilic granulocytes play a most im-
portant role in confining the infection to the pulpal
space (Fig. 14-2c) (Stashenko et al. 1995) and constitute
a cellular front line that may establish itself even inside
the apical portion of the canal (Nair 1987). The remain-
ENDODONTICS AND PERIODONTICS • 321
Fig. 14-3. Case of a lower second molar that was extracted due to extensive caries on its distal aspect (a). There is
an apical radiolucency associated with the distal root tip. Histologic sections demonstrate different features (b-e). In
the overview the coronal pulp tissue shows evidence of severe breakdown (b). Vital pulp tissue seems to remain in
the mesial root while it is necrotic in the distal root (not shown). Stainings for bacteria reveal invasion of carious
dentin (c) and deep into the pulp tissue of the mesial root (e). A lateral canal is clearly visible and connects the put-
pal space with the periodontium in the furcal region, where an inflammatory lesion has developed (d). Note the
proliferating epithelium adjacent to the exit of this canal into the periodontium (d). There was no increased pocket
probing depth associated with this tooth. Courtesy of Dr Domenico Ricucci.
Fig, 14-4. Microphotograph showing an experimentally
induced periapical inflammatory lesion in a monkey.
Section is through a maxillary incisor with adjacent al-
veolar bone. The inflammatory response shows evi-
dence of spreading. Note also the resorption of the root
tip. From Syed et at. 1982.
322 • CHAPTER
14
Fig. 14-5. (a) Radiolucent area along the distal root surface of tooth #45 combined with a horizontal marginal bone
destruction. (b) The pulp was non-vital and the tooth was endodontically treated. After prosthetic therapy (c), the 2
-
year follow-up radiograph in (d) shows bone fill in the previous angular bony defect, whereas the marginal bone
remains at the same level. On careful examination one can see that a lateral canal communicating with the lateral
bone defect was filled.
der of the lesion will be composed of a mixed cellular
response (Fig 14-2d) typical of a longstanding infec-
tious process where various immunocompetent cells
(
dendritic cells, macrophages, T and B-cells) are
prevalent (Torabinejad & Kettering 1985, Babal et al.
1987, Okiji et al. 1994, Stashenko et al 1998, Marton &
Kiss 2000). With increasing distances from the root
canal apertures, the established lesion harbors a de-
creasing number of inflammatory cells and an increas
-
ing amount of fibro-vascular elements representing
attempts to repair. More peripherally there is a much
stronger expression of fibroblastic activity and forma-
tion of new vessels and in the most peripheral portions
of the lesion, a collagen-rich connective tissue nor-
mally separates it from the surrounding bone tissue
(
Fig. 14-2a,e).
Some, but far from all, lesions contain proliferating
epithelial cells (Nair 1997). The origin of these epi-
thelial strands is thought to be the epithelial rests of
Malassez. In the lesion, they appear to take a random
course, but sometimes they also attach to the root
surface (Fig 14-3d). Their contribution to periodontal
pocket formations, upon an endodontic lesion, devel-
oping in close proximity to the epithelial sulcus of the
marginal periodontium, remains obscure.
In its established form, the lesion is clearly localized
and constitutes an immunologically active protection
zone of importance to preventing the dissemination
of intracanal pathogens into the surrounding peri-
odontal tissue (Stashenko 1990). While most often
effective in this respect (Bystr6m et al. 1987, Haapasalo
et al. 1987, Nair 1987, Molven et al. 1991), bacteria may
occasionally overcome the host defense and be present
in the periapical tissue environment. This is particu-
larly true on purulent lesions. It is also well known
that
Actinomyces
related species, especially
Actinomy-
ces israch
and
Propionibacterium propionicum
may pro-
duce bacterial masses or nests within the lesion site
(
Happonen 1986).
Conclusion
Inflammatory processes in the periodontium associ-
ated with necrotic dental pulps have, similar to peri-
odontal disease, an infectious etiology. The essential
difference between the two disease entities is their
respective source of infection. While periodontal dis-
ease is maintained by bacterial accumulation in the
dento-gingival region, endodontic lesions are directed
towards infectious elements released from the pulpal
space. Rarely will established endodontic lesions in-