Jan Lindhe. Clinical Periodontology

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THE PERIODONTAL ABSCESS • 263

Fig. 11-2. Periodontal abscess (arrows) associated with

a lower right first molar. Observe the association be-

tween the abscess formation and the furcation lesion in

this molar.

Fig. 11-4. Periodontal abscess associated with the distal

surface of a lower right first molar. Observe the sponta-

neous suppuration expressed through the gingival

pocket at the distal surface.

Fig. 11-5. Periodontal abscess associated with an upper

right third molar. Observe how this lesion is associated

with tooth extrusion and the tooth exhibits an in-

creased mobility.

and radiological signs found during the oral examina- Abscesses located deep in the periodontium may be tion.

less easy to identify by the swelling of the soft tissue The most prominent symptom of a periodontal and may

present as diffuse swellings or simply as a

abscess is the presence of an ovoid elevation of the red area (Fig. 11-3). Another common finding is sup-

gingiva along the lateral side of the root (Fig. 11-2). puration, either from a fistula or, most commonly,

Fig. 11-3. Periodontal abscess associated with a lower

second molar. Observe the diffuse swelling affecting all

the buccal gingiva of the molar.

264 • CHAPTER 11

Fig. 11-6. (a) Periodontal abscess associated with a lower left canine. Observe the fistulous tract opening demon

strated with a gutta-percha point. (b) Radiological image of the lower canine from (a). The differential

diagnosis with a periapical abscess was done by the positive tooth vitality sign and absence of caries or

restoration in the ca-nine, and the presence of a deep periodontal pocket in the lingual aspect of this tooth.

from the pocket (Fig. 11-4). This suppuration may be

spontaneous or occur after pressure on the outer sur-

face of the gingiva. The clinical symptoms usually

include pain (from light discomfort to severe pain),

tenderness of the gingiva, swelling and sensitivity to

percussion of the affected tooth. Other related symp-

toms are tooth elevation and increased tooth mobility (

Fig. 11-5).

During the periodontal examination, the abscess is

usually found at a site with a deep periodontal pocket.

Signs associated with periodontitis such as bleeding

on probing, suppuration and sometimes increased

tooth mobility are also present (Smith & Davies 1986,

Hafstrom et al. 1994, Herrera et al. 2000b). The radio-

graphic examination may either reveal a normal ap-

pearance of the interdental bone, or some bone loss,

ranging from a widening of the periodontal ligament

space to pronounced bone loss involving most of the

affected tooth (Fig. 11-6a,b).

In some patients the occurrence of a periodontal

abscess may be associated with elevated body tem-

perature, malaise and regional lymphadenopathy (

Smith & Davies 1986, Carranza, 1990, Ibbott et al.

1993, Herrera et al. 2000b). Herrera et al (2000b) pro-

vided laboratory data from blood and urine of pa-

tients immediately after a periodontal abscess had

been identified, and reported that in 30% of the pa-

tients there was an elevated number of blood leuko-

cytes. The absolute number of blood neutrophils and

monocytes was also enhanced in 20-40% of the pa-

tients.

Differential diagnosis

The differential diagnosis of periodontal abscesses

should always be made with other abscesses that can

occur in the oral cavity. Acute infections, such as pe-

riapical abscesses, lateral periapical cysts, vertical root

fractures and endo-periodontal abscesses, may have a

similar appearance and symptomatology as a peri-

odontal abscess, although with a clearly different eti-

ology. Signs such as lack of pulp vitality, the presence

of deep caries lesions, the presence of a sinus tract and

findings made in the radiographic examination, will

aid in the distinction between abscesses of different

etiologies.

Other lesions may appear in the oral cavity with a

similar appearance to a periodontal abscess. Parrish et

al. (1989) described three cases of osteomyelitis in

periodontitis patients, initially diagnosed as peri-

odontal abscess. Also, different tumors may have the

appearance of a periodontal abscess. Such tumors

include gingival squamous cell carcinoma (Torabine-

jad & Rick 1980, Kirkham et al. 1985), a metastatic

carcinoma from pancreatic origin (Selden et al. 1998)

and an eosinophilic granuloma diagnosed by rapid

bone destruction after periodontal therapy (Girdler

1991). A pathologic anatomic diagnosis must be made

if the abscess fails to respond to conventional therapy (

see also Chapter 12).

TREATMENT

The treatment of the periodontal abscess usually in-

cludes two stages: (1) the management of the acute

lesion, and (2) the appropriate treatment of the origi-

nal and/or residual lesion, once the emergency situ-

ation has been controlled. For the treatment of the

acute lesion, alternatives were proposed, such as: (1)

incision and drainage, (2) scaling and root planing, (3)

periodontal surgery, (4) the use of different systemi-

cally administered antibiotics, and (5) tooth extrac-

tion.

Although some authors have recommended a pure

mechanical treatment including surgical drainage

through the pocket, or scaling and planing of the root

surface and compression and debridement of the soft

THE PERIODONTAL ABSCESS • 265

Fig. 11-7. (a) Treatment of a periodontal abscess with systemic antibiotics (azithromycin, 500 mg, 3 days) without

any mechanical therapy. Baseline situation. (b) 5 days after antibiotic therapy. (c) 12 days after antibiotic

therapy, immediately before the final periodontal instrumentation.

tissue wall (Ahl et al. 1986, Ammons 1996), this purely

mechanical treatment may cause irreversible damage

to healthy periodontal tissues adjacent to the lesion.

Such damage may occur in particular when the swel-

ling is diffuse or is associated with marked tissue

tension.

In order to avoid damage to healthy periodontal

tissue it is recommended to use systemically adminis-

tered antibiotics as the only initial treatment in ab-

scesses with marked swelling, tension and pain. In

such instances, once the acute condition has receded,

mechanical debridement, including root planing, is

performed. The effect of treatment of abscesses has

been determined in only a few studies. Smith and

Davies (1986) studied 62 abscesses in 55 patients. Their

proposed treatment included incision, drainage and

systemic metronidazole (200 mg, tid, 5 days) and after

the acute phase, regular periodontal treatment. Haf-

strom et al. (1994) recommended drainage, irrigation

and supragingival debridement, together with sys-

temic tetracycline therapy for 2 weeks. Similar good

treatment outcomes were obtained in a recent control-

led parallel study in which two systemic antibiotic

regimes (amoxicillin/clavulanate, 500+125 mg, tid, 8

days; and azithromycin, 500 mg, once per day, 3 days)

were used as the only measure during the phase of

initial therapy. This was followed by regular peri-

odontal treatment once the acute phase was resolved

(Herrera et al. 2000c). The study showed that the

infectious process in the acute periodontal abscess

was controlled by means of systemic antibiotics with-

out concomitant or prior debridement (Fig. 11-7a,b,c).

The short-term clinical outcome with the use of both

antibiotics regimens was successful. There was a rapid

control of the pain levels, significant reduction in the

edema, redness and swelling, and further the suppu-

ration was almost entirely eradicated. Periodontal pa-

rameters, such as bleeding and periodontal probing

depth, were also significantly reduced. Short-term mi-

crobiological results demonstrated a reduction of the

microbiota in the abscess, as well as the number of

selected periodontal pathogens (Herrera et al. 2000c).

However, none of the antibiotic therapies were able to

entirely resolve the infection. This implies that me-

chanical debridement, sometimes including surgical

means, is an essential measure in the definitive treat-

ment of a periodontal abscess.

Table 11-1 shows a number of different antibiotics

that may be used in the treatment of a periodontal

abscess. Doses and regimes recommended may differ

between different countries. In principle, a high dose

of the antibiotic delivered during a short period of

time, is recommended. If the patient is recovering

properly, the antibiotic regimen may not be extended

over a 5-day period.

266 • CHAPTER II

COMPLICATIONS

Tooth loss

Periodontal abscesses have been suggested as the

main cause for tooth extraction during the phase of

supportive periodontal therapy (SPT) (Chace & Low

1993). A tooth with a history of repeated abscess for-

mation is considered as a tooth with a questionable

prognosis (Becker et al. 1984). In a retrospective study,

45% of teeth with periodontal abscesses in a SPT

population were extracted (McLeod et al. 1997). An-

other retrospective study including 455 teeth with a

questionable prognosis, showed that 55 (12%) were

lost after a mean of 8.8 years, and that the main reason

for tooth extraction was periodontal abscess forma-

tion (Chace & Low 1993). Smith & Davies (1986) evalu-

ated 62 teeth with abscesses; 14 (22.6%) teeth were

extracted as initial therapy, and 9 (14.5%) after the

acute phase. Out of the 22 teeth treated and sub-

sequently monitored, 14 had to be extracted during

the following 3 years.

Dissemination of the infection

A number of publications, mainly case reports, have

described different systemic infections in different

parts of the body, in which the suspected source of

infection was a periodontal abscess. Two possibilities

have been described: the dissemination of the bacteria

inside the tissues during therapy; or bacterial dissemi-

nation through the blood stream due to bacteremia

from the untreated abscess.

Dento-alveolar abscesses of endodontic origin are

more often associated with complications such as bac-

terial spread than periodontal abscesses. Cellulitis,

subcutaneous infection, phlegmone and mediastinitis

can result from odontogenic infections but are very

uncommon with periodontal abscesses. However, a

periodontal abscess can function as a focus for a non-

oral infection. A periodontal abscess may be the focus

from which bacteria and bacterial products dissemi-

nate from the oral cavity to other body sites and may

result in a variety of different infectious disorders.

Mechanical treatment of a periodontal abscess may

result in bacteremia (Flood et al. 1990, Roberts & Sher

-riff 1990) which, in patients with, for example, endo-

prosthesis (Van Winkelhoff et al. 1993, Van Waldman

et al. 1997) or in immuno-compromised states, can

result in non-oral infections.

The lungs may act as a mechanical barrier where

periodontal bacteria can be trapped and subsequently

may cause disease (Suzuki & Delisle 1984, Kuijper et

al. 1992). Occasionally dissemination of periodontal

bacteria can result in a brain abscess (Gallaguer et al.

1981). A number of case reports on periodontal patho-

gens that have been retrieved from brain abscesses are

available. P. micros, F. nucleatum, black-pigmented an-

aerobic rods and

Actinomyces

spp. are among the strict

anaerobic periodontal species that have been isolated

from intra-cranial abscesses (Van Winkelhoff & Slots

1999). Other infections related with periodontal ab-

scesses are: cervical necrotizing fascitis (Chan &

McGurk 1997), and cellulites in breast cancer patients

(Manian 1997).

Table 11-1. Antimicrobial agents that may be used in the treatment of periodontal abscesses

THE PERIODONTAL ABSCESS • 267

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268 • CHAPTER 11

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CHAPTER 12

Non-Plaque Induced

Inflammatory

Gingival Lesions

PALLE HOLMSTRUP AND DANIEL VAN STEENBERGHE

Gingival diseases of specific bacterial origin

Gingival diseases of viral origin Gingival

diseases of fungal origin

Gingival lesions of genetic origin

Gingival diseases of systemic origin

Traumatic lesions

Gingival inflammation, clinically presenting as gingi-

vitis, is not always due to accumulation of plaque on

the tooth surface, and non-plaque induced inflamma-

tory gingival reactions often present characteristic

clinical features (Holmstrup 1999). They may occur

due to several causes, such as specific bacterial, viral

or fungal infection without an associated plaque-re-

lated gingival inflammatory reaction. Gingival lesions

of genetic origin are seen in hereditary gingival fibro-

matosis, and several mucocutaneous disorders mani-

fest as gingival inflammation. Typical examples of

such disorders are lichen planus, pemphigoid, pem-

phigus vulgaris and erythema multiforme. Allergic

and traumatic lesions are other examples of non-

plaque induced gingival inflammation. Dentists, and

especially specialists in periodontology, are the key

persons in the diagnostic unraveling and treatment of

patients affected by such lesions.

This chapter focuses on those non-plaque induced

inflammatory gingival lesions of the gingival tissues,

which are most relevant, either because they are com-

mon or because they are important examples for the

understanding of the variety of tissue reactions that

take place in the periodontium. For further informa-

tion the reader is referred to other textbooks (Piette &

Reychler 1991, Pindborg 1992, Newman et al. 1993,

Porter & Scully 1994a,b). The modifying factors of

plaque-related gingivitis such as smoking, sexual hor-

mones and metabolic anomalies (diabetes) are dealt

with in Chapter 6 and tumors and cysts are reviewed

in Chapter 13.

GINGIVAL DISEASES OF SPECIFIC

BACTERIAL ORIGIN

Infective gingivitis and stomatitis may occur on rare

occasions in both immunocompromised and non-im-

munocompromised individuals, when non-plaque re-

lated pathogens overwhelm innate host resistance (

Rivera-Hidalgo & Stanford 1999). The lesions may be

due to bacteria and may not be accompanied by le-

sions elsewhere in the body. Typical examples of such

lesions are due to infections with

Neisseria gonorrhea

(

Scully 1995, Siegel 1996), Treponema pallidum (Scully

1995, Ramirez-Amador et al. 1996, Siegel 1996, Rivera

-Hidalgo & Stanford 1999), Streptococci, Mycobacterium

chelonae (Pedersen & Reibel 1989) or other organisms

(Blake & Trott 1959, Littner et al. 1982). The gingival

lesions manifest as fiery red edematous painful ul-

cerations, as asymptomatic chancres or mucous

patches, or as atypical non-ulcerated, highly inflamed

gingivitis. Biopsy supplemented by microbiologic ex-

amination reveals the background of the lesions.

GINGIVAL DISEASES OF VIRAL

ORIGIN

Herpes virus infections

A number of viral infections are known to cause gin-

givitis (Scully et al. 1998b). The most important are the

270 • CHAPTER 12

Fig. 12-1. Herpetic gingivostomatitis in a 3-year-old

child. Erythematous swelling of attached gingiva with

sero-fibrinous exudate along the gingival margin.

Fig. 12-2. Herpetic gingivostomatitis in a 43-year-old

woman. Ulceration along the gingival margin and rup-

tured vesicle in relation to second lower left premolar.

No affection on top of interdental papillae.

Fig. 12-3. Herpetic gingivostomatitis in a 38-year old

woman. Widespread ulceration of lower lip mucosa

and gingiva.

herpes viruses: herpes simplex viruses type 1 and 2

and varicella-zoster virus. These viruses usually enter

the human body in childhood and may give rise to oral

mucosal disease followed by periods of latency and

sometimes reactivation. Herpes simplex virus type 1 (

HSV-1) usually causes oral manifestations, whereas

herpes simplex virus type 2 (HSV-2) is mainly in-

volved in anogenital infections and only occasionally

is involved in oral infection (Scully 1989).

Primary herpetic gingivostomatitis

Herpes simplex infections are among the most coin-

Fig. 12-4. Same patient as shown in Fig. 12-3, 4 weeks

later. Healing without loss of tissue or scar formation.

mon viral infections. Herpes simplex is a DNA virus

with low infectiosity, which after entering the oral

mucosal epithelium, penetrates a neural ending and by

retrograde transport through the smooth endoplas-

matic reticulum (200—300 mm/day) travels to the

trigeminal ganglion where it can remain latent for

years. The virus has also been isolated in extraneural

locations such as the gingiva (Amit et al. 1992). Some-

times herpes simplex viruses may also play a role in

recurring erythema multiforme. It is presently un-

known whether the virus plays a role in other oral

diseases, but herpes simplex virus has been found in

NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS •

271

Fig. 12-5. Recurrent intraoral herpes infection. Rup

tured vesicles of right palatal gingiva and

mucosa.

gingivitis (Ehrlich et al. 1983), acute necrotizing gingi-

vitis (Contreras et al. 1997), and periodontitis (Parra &

Slots 1996).

When a baby is infected, sometimes from the par-

ent's recurrent herpes labialis, it is often wrongly di-

agnosed as "teething". With increased hygiene in the

industrialized society, more and more primary infec-

tions occur at higher ages, i.e. during adolescence or

even adulthood. It is estimated in the US that there are

about half a million cases per year (Overall 1982). The

primary herpetic infection may run an asymptomatic

course in early childhood, but may also give rise to

severe gingivostomatitis, which occurs mostly before

adolescence (Fig. 12-1). This manifestation includes

painful severe gingivitis with redness, ulcerations

with serofibrinous exudate and edema accompanied

by stomatitis (Figs. 12-2 and 12-3). The incubation

period is one week. A characteristic feature is the

formation of vesicles, which rupture, coalesce and

leave fibrin-coated ulcers (Scully et al. 1991, Miller &

Redding 1992). Fever and lymphadenopathy are other

classic features. Healing occurs spontaneously with-

out scarring in 10 to 14 days (Fig. 12-4). During this

period pain can render eating difficult.

The virus remains latent in the ganglion cell, prob-

ably through integration of its DNA in that of the

chromosomal DNA (Overall 1982). Reactivation of the

virus resulting in recurrent infections occurs in 20-40%

of individuals with the primary infection (Greenberg

1996) and usually presents in the form of herpes

labialis, but recurrent intraoral herpes infections are

also seen. Recurrent infections occur in general more

than once per year, usually at the same location as the

vermilion border and /or the skin adjacent to it, where

neural endings are known to be clustering. A large

variety of factors trigger reactivation of latent virus.

These are trauma, ultraviolet light exposure, fever,

menstruation and others (Scully et al. 1998b).

While recurrences at the vermilion border are well

recognized, recurrent intraoral herpes lesions often

remain undiagnosed because they are considered

aphtous ulcerations (Lennette & Magoffin 1973), irre-

spective of the fact that aphtous ulcers do not affect

keratinized mucosa. Recurrent intraoral herpes typi-

cally presents a less dramatic course than does the

primary infection. A characteristic manifestation is a

cluster of small painful ulcers in the attached gingiva

and hard palate (Yura et al. 1986) (Fig. 12-5). The

diagnosis can be made on the basis of the patient

history and clinical findings supported by isolation of

HSV from lesions. A reliable isolation of virus is best

obtained from intact vesicular lesions, for instance in

the form of an aspiration of the vesicle fluid with a

small syringe. Isolation and growth of herpes viruses

are elaborate because of their fragility. The virus must

be transferred to a special cell line in the laboratory

within 24 hours, or stored at -70°C. The herpes virus

is detected within 5 days, and while a positive viral

culture can be taken as evidence of viral infection, a

negative result does not rule out such an infection.

Laboratory diagnosis may also involve examination

of a blood sample for increased antibody titer against

herpes virus. However, this is most relevant in cases

of primary infection, because the antibody titer re-

mains elevated for the rest of the lifetime. The his-

topathologic features of cytologic smears from the

gingival lesions are not specific, but the presence of

giant cells and intranuclear inclusion bodies may in-

dicate intra-cellular activity of virus (Burns 1980).

Immunodeficient patients, such as HIV-infected in-

dividuals, are at increased risk of acquiring the infec-

tion (Holmstrup & Westergaard 1998). In the immu-

nocompromised patient the recurrence of herpes in-

fection, either gingival or elsewhere, may be severe

and even life-threatening.

The treatment of herpetic gingivostomatitis in-

cludes careful plaque removal to limit bacterial super-

infection of the ulcerations, which delays their heal-

ing. In severe cases, including patients with immu-

nodeficiency, the systemic use of antiviral drugs such

as acyclovir or valacyclovir is recommended (O'Brien

& Campoli-Richards 1989, Mindel 1991). Resistance to

272 • CHAPTER 12

Fig. 12-6. Herpes zoster of left palatal gingiva and mu-

cosa. Irregular fibrin coated ulcerations with severe

pain.

acyclovir, especially among immunodeficient patients

on long-term therapy, is a growing concern (Westheim

et al. 1987) and explain why other antiviral drugs may

be relevant.

Herpes zoster

Varicella-zoster virus causes varicella (chicken pox) as

the primary self-limiting infection. It occurs mainly in

children and later reactivation of the virus in adults

causes herpes zoster (shingles). Both manifestations

can involve the gingiva (Straus et al. 1988, Scully

1995). Chicken pox is associated with fever, malaise

and a skin rash. The intraoral lesions are small ulcers

usually on the tongue, palate and gingiva (Miller 1996,

Scully et al. 1998b). The virus remains latent in the

dorsal root ganglion from where it can be reactivated

years after the primary infection (Rentier et al. 1996).

Later reactivation results in herpes zoster, with unilat-

eral lesions following the infected nerve (Miller 1996).

The reactivation normally affects the thoracic ganglia

in elderly or immunocompromised patients. Reacti-

vation of virus from the trigeminal ganglion occurs in

20% of reported cases (Hudson & Vickers 1971). If the

second or third branch of the trigeminal nerve is in-

volved, skin lesions may be associated with intraoral

lesions, or intraoral lesions may occur alone (Eisen-

berg 1978), for instance affecting the palatal gingiva

(Fig. 12-6). Initial symptoms are pain and paraesthe-

sia, which may be present before lesions occur (Green

-berg 1996). The associated pain is usually severe. The

lesions, which often involve the gingiva, initiate as

vesicles. They soon rupture to leave fibrin-coated ul-

cers, which often coalesce to irregular forms (Millar &

Traulis 1994) (Fig. 12-6). In immunocompromised pa-

tients, including HIV-infected individuals, the infec-

tion can result in severe tissue destruction with tooth

exfoliation and necrosis of alveolar bone and high

morbidity (Melbye et al. 1987, Schwartz et al. 1989).

The diagnosis is usually obvious due to the unilateral

occurrence of lesions associated with severe pain.

Healing of the lesions usually takes place in 1-2

weeks.

Treatment consists of soft or liquid diet, rest,

atrau-

matic removal of plaque and diluted chlorhexidine

rinses. This may be supplemented by antiviral drug

therapy.

GINGIVAL DISEASES OF FUNGAL

ORIGIN

Fungal infection of the oral mucosa includes a range

of diseases such as aspergillosis, blastomycosis, can-

didosis, coccidioidomycosis, cryptococcosis, histo-

plasmosis, mucormycosis and paracoccidioidomy-

cosis infections (Scully et al. 1998b), but some of the

infections are very uncommon and not all of them

manifest as gingivitis. The present chapter focuses on

candidosis and histoplasmosis, both of which may

cause gingival infection.

Candidosis

Various

Candida

species are recovered from the mouth

of humans including C.

albicans, C. glabrata, C. krusei,

tropicalis, C. parapsilosis,

and C. guillermondii (Can-

non et al. 1995). C.

albicans

is by far the most common.

It is a normal commensal of the oral cavity but also an

opportunistic pathogen. The prevalence of oral car-

riage of C.

albicans

in healthy adults ranges from 3%

to 48% (Scully et al. 1995), the large variation being

due to differences in examined populations and the

procedures used. The proportion of C.

albicans

in the

total oral yeast population can reach about 50-80% (

Wright et al. 1985), and by far the most common

fungal infection of the oral mucosa is candidosis

mainly caused by the organism C.

albicans

(Scully et al

1998b), the proteinase-positive strains of which are

associated with disease (Negi et al. 1984, Odds 1985)

and invasion of keratinized epithelia such as that of

the gingiva. Invasion and increased desquamation is

due to the hyaluronidase production. Infection by C.

albicans

usually occurs as a consequence of reduced