Acute periodontal lesionsDAVID HERRERA, BETTINA ALONSO, LORENZO DE ARRIBA,ISABEL SANTA CRUZ, CRISTINA SERRANO & MARIANO SANZ

Acute lesions in the periodontium, such as abscessesand necrotizing periodontal diseases, are among thefew clinical situations in periodontics where patientsmay seek urgent care, mostly because of the associ-ated pain. In addition, and in contrast to most otherperiodontal conditions, rapid destruction of peri-odontal tissues may occur during the course of theselesions, thus stressing the importance of prompt diag-nosis and treatment. In spite of this, the available sci-entific knowledge on these conditions is limited andis based on somewhat outdated literature. This lackof contemporary data makes it rather challenging todevise evidence-based therapeutic guidelines. Hence,an update is imperative, although it must be confinedto an evaluation of narrative reviews and expertopinions.

Other gingival and periodontal lesionsmay also showan acute presentation, including different infectiousprocesses not related to oral bacterial biofilms, muco-cutaneous disorders, or traumatic and allergic lesions.

This article provides an overview and updates ofexisting information on acute conditions affecting theperiodontal tissues, including abscesses in the peri-odontium, necrotizing periodontal diseases and otheracute conditions.

Abscesses in the periodontium

Definition of periodontal abscess

Abscesses in the periodontium are odontogenic infec-tions that may be caused by pulp necrosis, periodon-tal infections, pericoronitis, trauma or surgery (109).Odontogenic or dental abscesses are classified,according to the source of infection, into periapical(dentoalveolar) abscess, periodontal abscess and pe-ricoronal abscess (327).

A periodontal abscess has been defined as a local-ized purulent infection in the periodontal tissues

(210). A more comprehensive definition has also beenproposed: ‘a lesion with an expressed periodontalbreakdown occurring during a limited period of time,and with easily detectable clinical symptoms, includ-ing a localized accumulation of pus located withinthe gingival wall of the periodontal pocket’ (130)(Fig. 1).

Classification of periodontal abscesses

Different criteria have been used to classify periodon-tal abscesses.

Location

Abscesses can be classiffied as gingival or periodontalabscesses (110). A gingival abscess is a localized pain-ful swelling that affects only the marginal and inter-dental gingiva and is normally associated withsubgingivally impacted foreign objects. These condi-tions may occur in a previously healthy gingiva (7). Aperiodontal abscess is a localized painful swelling thataffects deeper periodontal structures, including deeppockets, furcations and vertical osseous defects, andis usually located beyond the mucogingival line. His-tologically, both lesions are identical, but a gingivalabscess affects only the marginal soft tissues of previ-ously healthy sites, whilst a periodontal abscessoccurs in a periodontal pocket associated with a peri-odontitis lesion (76).

Course of the lesion

The course of the lesion can be acute and chronic.An acute periodontal abscess usually manifests symp-toms such as pain, tenderness, sensitivity to palpationand suppuration upon gentle pressure. A chronicabscess is normally associated with a sinus tract andit is usually asymptomatic, although the patient canexperience mild symptoms (250). A localized acuteabscess may become a chronic abscess when drain-age is established through a sinus or through the

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sulcus. Similarly, a chronic abscess may have an acuteexacerbation.

Number of abscesses

The number of periodontal abscesses (single andmultiple) has also been used for classification pur-poses (321). A single periodontal abscess is usuallyassociated with local factors, which contribute to theclosure of the drainage of a periodontal pocket. Multi-ple periodontal abscesses have been reported inuncontrolled diabetes mellitus, in medically compro-mised patients and in patients with untreated peri-odontitis after systemic antibiotic therapy for nonoralreasons (125, 126, 321). Multiple abscesses have alsobeen described in a patient with multiple externalroot resorptions (339).

Type of etiological factors

A periodontal abscess is usually associated with apreviously existing periodontal pocket, although itcan also develop in the absence of a pocket (130).Thus, different types of abscesses may be consid-ered, as related to their etiological factors; this clas-sification will be described in the section onetiology.

International Workshop for a Classification ofPeriodontal Diseases and Conditions

According to the International Workshop for a Classi-fication of Periodontal Diseases and Conditions (year1999), abscesses in the periodontium include gingival,periodontal, pericoronal and periapical abscesses (210).A gingival abscess is defined as ‘a localized, painful,rapidly expanding lesion involving the marginal gin-giva or interdental papilla sometimes in a previously

disease-free area’. A periodontal abscess (which canbe acute or chronic) is defined as ‘a localized accu-mulation of pus within the gingival wall of a peri-odontal pocket resulting in the destruction of thecollagen fibre attachment and the loss of nearby alve-olar bone’. A pericoronal abscess is ‘a localized accu-mulation of pus within the overlying gingival flapsurrounding the crown of an incompletely eruptedtooth’ (Fig. 2).

Clinical significance of periodontalabscess

A common periodontal emergency

Periodontal abscesses represented ca. 14% of all den-tal emergencies in a study in the USA (7). In generalpractices in the UK, 6–7& of the patients treated in1 month suffered from a periodontal abscess, whichwas the third most prevalent infection that demandedemergency treatment, after dentoalveolar abscesses(14–25&) and pericoronitis (10–11&) (177). In anarmy dental clinic, 3.7% of the patients had periodon-titis and, among these, 27.5% had a periodontalabscess, with clear differences between patientsundergoing active periodontal treatment (13.5%) anduntreated patients (59.7%) (117). Among patients insupportive periodontal therapy, a periodontal abscesswas detected in 37% of the patients and in 3.7% of theteeth followed for 5–29 years (mean 12.5 years) (209);in the Nebraska prospective longitudinal study, 53%of the patients followed for 7 years had a periodontalabscess, and 85% of these abscesses were associatedwith teeth treated only with coronal scaling. Sixteenout of 27 abscess sites had initial probing pocketdepths deeper than 6 mm, and in eight sites probing

Fig. 2. Pericoronal abscess associated with the right man-dibular third molar.

Fig. 1. A periodontal abscess, manifesting as a localizedpurulent lesion within the gingival wall of the periodontalpocket.

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pocket depths were 5–6 mm (156). Abscesses occurmore often in molar sites, representing more than50% of all sites affected by abscess formation (128,209, 300), probably because of the presence of furca-tion, and complex anatomy and root morphology.However, one case series suggested that the mandi-bular anterior incisors were the most frequentlyaffected teeth (149).

Tooth loss

Periodontal abscesses may lead to tooth loss, espe-cially if they affect teeth with pre-existing moderateto severe attachment loss, as occurs during sup-portive periodontal therapy in patients with severechronic periodontitis. In fact, periodontal abscesshas been considered as the main cause for toothextraction during supportive periodontal therapy(55, 209, 294, 300). Similarly, teeth with repeatedabscess formation were considered to have a hope-less prognosis (36), and 45% of teeth with a peri-odontal abscess during supportive periodontaltherapy were extracted (209). The main reason fortooth extraction in teeth with a questionable prog-nosis, followed for 8.8 years, was a periodontalabscess (55). Taking these reports into account, ithas been suggested that when a periodontalabscess is encountered in patients receiving sup-portive periodontal therapy, early diagnosis andadequate therapy are crucial to preserve the prog-nosis of the affected tooth (294).

Association with systemic dissemination of alocalized infection

Numerous case reports have described the occur-rence of systemic infections from a suspected sourcein a periodontal abscess, either through dissemina-tion during therapy or related to an untreatedabscess. During the treatment of an abscess, the con-comitant bacteremia may lead to colonization ofpathogenic microorganisms in other body sites andto the development of different infections, such aspulmonary actinomycosis (315), a brain abscesscontaining Prevotella melaninogenica and otherPrevotella spp. (103), or a total knee arthroplastyinfection (330). It has been suggested that the risk ofbacteremia during abscess drainage may be reducedif a needle aspirate of the abscess contents isobtained before the procedure (99, 265).

There are also case reports of bacteremia originat-ing from untreated abscesses, such as cellulitis inbreast-cancer patients (198), a cervical necrotizingfasciitis (57), a necrotizing cavernositis containingPeptostreptococcus spp. and Fusobacterium spp.

(245), or a sickle-cell crisis in a patient with sickle-cellanemia (255).

Etiology, pathogenesis andhistopathology of periodontal abscess

Periodontal abscesses may develop in periodontitis-affected sites (with a pre-existing periodontalpocket) or in healthy sites (without a pre-existingpocket).

In periodontitis, a periodontal abscess may repre-sent a period of disease exacerbation that isfavored by the existence of tortuous pockets, thepresence of furcation involvement (Fig. 3) or a ver-tical defect, in which marginal closure of the pocketmay lead to spread of the infection into the sur-rounding periodontal tissues (76, 158, 224). Also,changes in the composition of the subgingivalmicrobiota, with an increase in bacterial virulence,or a decrease in the host defence, could result ina diminished capacity to drain the increasedsuppuration. Among periodontal abscesses in peri-odontitis patients, different subgroups can bedistinguished:� after nonsurgical periodontal therapy. After scal-

ing or professional prophylaxis, dislodged calculusfragments can be pushed into the tissues (74), orinadequate scaling may allow calculus to remainin deep pockets, whilst the coronal part willocclude the normal drainage (156).

� after surgical periodontal therapy – associatedwith the presence of foreign bodies, such as mem-branes for regeneration or sutures (106).

� acute exacerbation of an untreated periodontitis(74) (Fig. 4).

� acute exacerbation in refractory periodontitis (97).� acute exacerbation in supportive periodontal ther-

apy, as described previously (55, 209, 294).

Fig. 3. Periodontal abscess with the presence of furcationinvolvement.

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� systemic antimicrobial intake without subgingivaldebridement. In patients with severe periodontitisthis may also cause abscess formation (125, 126,321), probably related to an overgrowth of oppor-tunistic bacteria (125).

Periodontal abscesses can also occur in previouslyhealthy sites (i.e. nonperiodontitis periodontalabscesses) owing to impaction of foreign bodies or toalteration of the root surfaces:� different foreign bodies have been described to be

associated with the development of a periodontalabscess, for example: an orthodontic elastic (250);a piece of dental floss (5); a dislodged cementaltear (124); a piece of a toothpick (100); or pieces ofnails in subjects with nail-biting habits (304). Theterm ‘oral hygiene abscesses’ has been proposedfor abscesses caused by the impaction of foreignbodies that are oral hygiene aids (110).

� the root surface may be altered by different fac-tors: perforation by an endodontic instrument (4);cervical cemental tears (124, 146); external rootresorption (339); an invaginated tooth (60); or acracked tooth (116).

In the development of a periodontal abscess, the firststep may be the invasion of bacteria into the soft tis-sues surrounding the periodontal pocket, which willdevelop an inflammatory process through the che-motactic factors released by bacteria that attractinflammatory cells and lead to the destruction of theconnective tissues, the encapsulation of the bacterialinfection and the production of pus. Once the abscessis formed, the rate of destruction within the abscesswill depend on the growth of bacteria inside thefocus, their virulence and the local pH (an acidic envi-ronment will favor the activity of lysosomal enzymes)(76).

The histopathology of periodontal abscess lesionswas described following evaluation of biopsies

retrieved from 12 abscesses (76), observing thefollowing areas from the outside to the inside of thelesion:� a normal oral epithelium and lamina propria.� an acute inflammatory infiltrate.� an intense focus of inflammation, with neutroph-

ils and lymphocytes present in an area ofdestroyed and necrotic connective tissue.

� a destroyed and ulcerated pocket epithelium.In seven biopsies analyzed using electron micro-scopy, gram-negative bacteria were found to invadethe pocket epithelium, and the affected connectivetissue formed a mass of granular, acidophilic andamorphous debris.

Microbiological findings

Purulent oral infections are usually polymicrobial andare caused by commensal bacteria (317). In microbio-logical reports on periodontal abscesses, gram-negative bacteria predominated over gram-positivebacteria, and rods predominated over cocci (224),with large proportions of strict anaerobes (128, 224,321).

The most prevalent bacterial species identified inperiodontal abscesses, using culture-based or molec-ular-based diagnostic techniques, is Porphyromonasgingivalis, with a range in prevalence of 50–100%(82, 123, 128, 149, 224, 321, 327) (Fig. 5). Other strictanaerobes frequently detected include Prevotellaintermedia, Prevotella melaninogenica, Fusobacteriumnucleatum, Tannerella forsythia, Treponema spp.Parvimonas micra, Actinomyces spp. and Bifidobacte-rium spp. Among the facultative anaerobic gram-neg-ative bacteria, Campylobacter spp., Capnocytophagaspp. and Aggregatibacter actinomycetemcomitanshave been reported (123), as well as gram-negativeenteric rods (149).

Fig. 4. Periodontal abscess in untreated periodontitis. Fig. 5. Microbiological sampling in a periodontal abscess.

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In summary, previous studies have shown thatthe microbiota of periodontal abscesses is not differ-ent from the microbiota of chronic periodontitislesions. It is polymicrobial and dominated by non-motile, gram-negative, strictly anaerobic, rod-shapedspecies. Among these bacteria, P. gingivalis is prob-ably the most virulent and relevant microorganism.Although it is not clearly mentioned, these studiesdescribed the microbiology of abscesses in patientswith periodontitis. Conversely, there is limitedinformation on the microbiota of other types ofabscesses, except for those associated with systemicantibiotic intake for nonoral reasons in patients withperiodontitis (125, 126, 321): in these abscesses,similarly to other abscesses in periodontitis, period-ontal pathogens were present, although opportunis-tic bacteria were also detected, especiallyStaphylococcus aureus, leading the authors to sug-gest that this type of abscess could be considered asa superinfection.

Diagnosis of a periodontal abscess

The diagnosis of a periodontal abscess should bebased on the overall evaluation and interpretation ofthe patient′s symptomatology, together with the clini-cal and radiological signs found during the oral exam-ination (67).

A series of symptoms (ranging from light discom-fort to severe pain, tenderness of the gingiva, swelling,tooth mobility, tooth elevation and sensitivity of thetooth to palpation) has been described to be associ-ated with an abscess (7, 128, 145).

The most prominent sign during the oral exami-nation is the presence of an ovoid elevation in thegingiva along the lateral part of the root, althoughabscesses located deep in the periodontium may bemore difficult to identify and may be found as adiffuse swelling or simply as a red area. Anothercommon finding is suppuration, either through afistula or, most commonly, through the pocketopening (Fig. 6), which may be spontaneous oroccur after applying pressure on the lesion. Theabscess is usually found at a site with a deep peri-odontal pocket, and signs of periodontitis, includingbleeding on probing or increased tooth mobility(123, 128, 300).

The radiographic examination may reveal a normalappearance, or some degree of bone loss (as mostabscesses will occur in a pre-existing periodontalpocket).

Periodontal abscesses may be associated with ele-vated body temperature, malaise and regional lymph-

adenopathy (128, 145, 300), and 30% of the patientsmay have elevated numbers of blood leukocytes(128).

The anamnesis may also provide relevant informa-tion, especially in abscesses associated with previoustreatment – either dental or periodontal treatmentsor nonoral therapies, such as systemic antimicrobials.Moreover, in abscesses related to impaction of for-eign bodies, the interview with the patient may be ofgreat help.

Differential diagnosis is critical because periodontalabscesses may be similar to other oral conditions:� other abscesses in the mouth: periapical or dento-

alveolar or endodontic abscesses; lateral periapi-cal cyst; vertical root fractures; endoperiodontalabscess; and postoperative infection (7). A combi-nation of different factors, such as pulp vitality,the presence of dental caries, the presence of peri-odontal pockets, the location of the abscess and acareful radiographic examination, should beassessed in detail to reach an accurate diagnosis.

� other serious oral diseases may also have a similarappearance: osteomyelitis in patients with peri-odontitis (241); squamous cell carcinomas (162, 163,322); a metastatic carcinoma of pancreatic origin(289); a metastatic head and neck cancer (85); aneosinophilic granuloma (111); or a pyogenic granu-loma (237). Therefore, in patients not responding toconventional therapy, a biopsy and histopathologi-cal diagnosis should be recommended.

� self-inflicted gingival injuries: including trauma ofthe gingiva with a pencil (267) or with a safety pin(37), or a nail-biting habit (304). The anamnesis isthe key factor in the diagnosis of these lesions.

Treatment of a periodontal abscess

Treatment of a periodontal abscess should includetwo distinct phases: control of the acute condition

Fig. 6. Periodontal abscess demonstrating suppurationthrough the periodontal pocket.

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to arrest tissue destruction and control the symp-toms; and management of a pre-existing and/orresidual lesion, especially in patients with periodon-titis.

Control of the acute condition

Four therapeutic alternatives have been proposed:tooth extraction; drainage and debridement; systemicor local antimicrobials; and surgery.

If the tooth is severely damaged, and its prognosisis hopeless after the destruction caused by theabscess, the preferred treatment should be toothextraction (300).

The most logical treatment of a periodontalabscess, as in other abscesses in the body, shouldinclude drainage (through the pocket or through anexternal incision), compression and debridement ofthe soft-tissue wall, and the application of topicalantiseptics after drainage. If the abscess is associatedwith a foreign-body impaction, the object must beeliminated through careful debridement (5), althoughit may no longer be present.

Systemic antimicrobials may be used as the soletreatment, as initial treatment or as an adjunctivetreatment to drainage. Systemic antimicrobials asthe sole or as initial treatment may only be recom-mended if there is a need for premedication, if theinfection is not well localized or if adequate drainagecannot be ascertained (176). As an adjunctive treat-ment, systemic antimicrobials should be consideredif a clear systemic involvement is present (7, 176).The duration of therapy and the type of antibiotic isalso a matter for discussion, including the recom-mendation of shorter courses of therapy (176, 202).However, the available scientific evidence on theefficacy of these therapies is very limited, with onlytwo prospective case series and two randomizedclinical trials. Smith & Davies (300) evaluated inci-sion and drainage of the abscess, together withadjunctive systemic metronidazole (200 mg, threetimes daily for 5 days), followed by a delayed peri-odontal therapy, in 22 abscesses for up to 3 years.Hafstr€om et al. (123) proposed drainage through theperiodontal pocket, irrigation with sterile saline, su-pragingival scaling and tetracycline for 2 weeks (1 g/day), and tested this therapy in 20 abscesses, with 13followed for 180 days, highlighting the importance ofdrainage and the potential of regeneration. Herreraet al. (129) compared azithromycin (500 mg, onceper day for 3 days) vs. amoxicillin plus clavulanate(500 + 125 mg, three times daily for 8 days), withdelayed scaling (after 12 days), in 29 patients withabscesses followed for 1 month, and concluded that

both protocols were similarly effective. Eguchi et al.(82) compared irrigation with sterile physiologicalsaline and 2% minocycline hydrochloride ointmentvs. irrigation with sterile physiological saline withoutthe local antibiotic, in 91 patients for 7 days.

Surgical procedures have also been proposed,mainly for abscesses associated with deep verticaldefects (158) or in cases occurring after periodontaldebridement in which residual calculus is presentsubgingivally after treatment (74). A case series evalu-ating a combination of an access flap with deep scal-ing and irrigation with doxycycline is also availableand reports ‘good results’, but scientific data were notprovided (316).

After drainage and debridement the patient shouldbe recalled 24–48 h after treatment to evaluate theresolution of the abscess (Fig. 7A,B) and the durationof the intake of antimicrobials. Once the acute phasehas resolved, the patient should be scheduled for afollow-up therapeutic phase.

In summary, numerous treatment protocols havebeen proposed, but sufficient scientific evidence isnot available to recommend a definitive approach.It is, however, clear that drainage and debridementshould be established when the systemic conditionand the access to the abscess is adequate. Whenimmediate drainage is not possible or a systemicaffect is evident, therapy with systemic antimicrobials

A

B

Fig. 7. (A) Periodontal abscess before treatment. (B) Peri-odontal abscess, 12 days later, after treatment with azi-thromycin.

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should be considered. The drug with the most appro-priate profile is metronidazole (normally prescribedfor acute conditions at 250 mg, three times daily).Azithromycin (500 mg, once per day) and amoxicillinplus clavulanate (500 + 125 mg, three times daily)have also shown good clinical results. The duration ofthe therapy should be restricted to the duration of theacute lesion, which is normally 2–3 days.

Management of a pre-existing and/or a residuallesion

As most periodontal abscesses occur in a pre-existingperiodontal pocket, periodontal therapy should beevaluated after resolution of the acute phase. In caseswhere the patient has not been treated previously,the appropriate periodontal treatment should be pro-vided. If the patient is already within the active phaseof therapy, the periodontal therapy should be com-pleted once the acute lesion has been treated. Inpatients receiving supportive periodontal therapy,careful evaluation of the recurrence of the abscessshould be made, as well as assessment of the tissuedamage and how this affects tooth prognosis.

Summary

Abscesses in the periodontium are important becausethey are a relatively frequent dental emergency, theycan compromise the periodontal prognosis of theaffected tooth and because the bacteria within theabscess can spread and cause infections in otherbody sites.

Although histologically all abscess lesions are simi-lar, different types of abscess have been identified,mainly classified by their etiological factors becausethere are clear differences between those affecting apre-existing periodontal pocket and those affectinghealthy sites.

For the management of this condition, rapid andaccurate diagnosis (mainly based on clinical features)and provision of early therapy are mandatory. Ther-apy for the acute condition should be based on drain-age and debridement, with evaluation of the need ofsystemic antimicrobial therapy based on local andsystemic factors. When the supporting tissues havebeen destroyed to the extent of compromising thetooth prognosis, tooth extraction may be the onlyvalid alternative. The definitive treatment of the pre-existing condition should be accomplished after theacute phase has been controlled, as most abscessesare found in patients with untreated periodontitis,thus needing periodontal therapy.

Necrotizing periodontal diseases

Definition

Necrotizing periodontal diseases are a group of infec-tious diseases that include necrotizing ulcerative gin-givitis, necrotizing ulcerative periodontitis andnecrotizing stomatitis. However, it has also been sug-gested that these conditions may represent differentstages of the same disease because they have similaretiologies, clinical characteristics and treatment,although they vary in disease severity (138, 140).These diseases share common clinical features con-sisting of an acute inflammatory process and thepresence of periodontal destruction (Fig. 8).

Necrotizing ulcerative gingivitis has been diagnosedfor centuries but referred to by various names, such asVincent’s disease, trench-mouth disease, necrotizinggingivo-stomatitis, fuso-spirochaetal stomatitis, ulcer-ative membranous gingivitis, acute ulcerative gingivi-tis, necrotizing ulcerative gingivitis and acutenecrotizing ulcerative gingivitis (21, 138, 152, 269).Necrotizing ulcerative periodontitis was defined bothin the 1989 World Workshop (54) and in the 1993 Euro-pean Workshop (26). At the International Workshopfor a Classification of Periodontal Diseases and Condi-tions in 1999 (22), the new category of ‘necrotizingperiodontal diseases’ was introduced, which includesnecrotizing ulcerative gingivitis and necrotizing ulcera-tive periodontitis. More recently, the terms necrotizinggingivitis and necrotizing periodontitis have been usedinstead of the terms necrotizing ulcerative gingivitisand necrotizing ulcerative periodontitis (138). Thesimpler terms necrotizing gingivitis and necrotizingperiodontitis adequately describe these diseases andthese terms will be used in the rest of the text.

Fig. 8. Multiple gingival crater formation. The clinical sce-nario includes rapid progression and severe periodontaldestruction.

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Classification of necrotizing periodontaldiseases

According to the location of the tissue affected by theacute disease process, necrotizing periodontal dis-eases can be classified as (138, 140):� necrotizing gingivitis: when only the gingival tis-

sues are affected.� necrotizing periodontitis: when the necrosis pro-

gresses into the periodontal ligament and thealveolar bone, leading to attachment loss.

� necrotizing stomatitis: when the necrosis pro-gresses to deeper tissues beyond the mucogingivalline, including the lip or cheek mucosa, the ton-gue, etc.

Clinical significance of necrotizingperiodontal diseases

Necrotizing periodontal diseases are considered to beamong the most severe inflammatory conditionsassociated with oral biofilm bacteria (138). Therefore,it is important to control predisposing factors, andonce the disease has developed, to act quickly inorder to limit its progression and exacerbation.

The prevalence of necrotizing periodontal diseasesin systemically healthy populations has not beenadequately established because most studies havefocused on a specific group of patients with clearpredisposing factors, such as military personnel(141, 248), students (108, 188, 307), patients positivefor HIV (136, 137) or subjects with severe malnutri-tion (88, 234). In addition, data from these condi-tions originate from hospitals or dental clinicsettings, which may overestimate the true epidemio-logic information. A high prevalence of necrotizinggingivitis (14%) was observed in different popula-tions (including military groups) during the SecondWorld War (12, 138) and a moderately high rate(2.2%) was observed in populations in North Amer-ica in the 1950s (122). After the Second World War,the prevalence clearly decreased in developed coun-tries and currently the prevalence is low.

Necrotizing periodontal diseases have beendescribed in young people from both developed anddeveloping countries (12). In North America and Eur-ope, these diseases have been studied mostly ingroups of subjects in their late teens to mid-20s. In326 North-American students in the 1960s (108), theprevalence of necrotizing periodontal diseases rangedfrom 2.5% to 6.7%. The current estimates in devel-oped countries are 0.5% or less (33, 141), with 0.001%reported in young Danish army recruits (138).

In developing countries, the reported prevalence ofnecrotizing periodontal diseases is higher than indeveloped countries, especially in children (12). InChile, among 9,203 students, 6.7% presented at leasta papilla with necrosis. In India, 54–68% of the caseswere observed in children younger than 10 years ofage (249). In South Africa, 3.3% of subjects 3–48 yearsof age, presented with necrotizing gingivitis; 73% ofthese subjects were 5–12 years of age and most wereof a low socio-economic class (20). In Nigeria, theprevalence of necrotizing gingivitis ranged between1.7% and 15% in children of 2–6 years of age, and was27.2% in children with severe malnutrition (12, 88,292). In Kenya, 0.15% of patients who attended theNairobi Hospital during one year were diagnosedwith necrotizing gingivitis and 58.5% were youngerthan 11 years of age (155). In spite of these figures,subjects of any age may be affected.

Necrotizing periodontitis is less frequent than nec-rotizing gingivitis and it has been most frequentlyreported in HIV-positive patients, with a prevalenceof 0–11% (40, 136, 261, 338). The prevalence is lowerin studies performed outside hospitals or dental clin-ics. In HIV-positive patients under anti-retroviraltherapy (204, 272, 318), the prevalence of necrotizingperiodontitis may not differ from that in the generalpopulation.

Necrotizing periodontal diseases can progress rap-idly and cause severe tissue destruction. It is thereforeimportant for these conditions to be managedpromptly because there is evidence proving that nec-rotizing periodontal diseases can be controlled byadequate periodontal treatment combined with effec-tive oral-hygiene measures and control of predispos-ing factors (152). However, patients with necrotizinggingivitis are frequently susceptible to future diseaserecurrence, mostly as a result of the difficulties incontrolling predisposing factors as well as the diffi-culty in achieving proper supragingival biofilm con-trol, in part because of the sequelae of these diseases,including the presence of gingival craters (196).

Necrotizing gingivitis can heal without clinicalsequelae (38), but often the necrotizing lesion extendslaterally from the papilla to the gingival margin,affecting both the buccal and lingual sites, and pro-gresses to other sites in the mouth, evolving from alocalized disease into a generalized disease (Fig. 9).Necrotizing gingivitis may also progress apically,evolving into necrotizing periodontitis (Fig. 10). Infact, necrotizing periodontitis can be the result of oneor various episodes of necrotizing gingivitis, or it canbe the result of a necrotizing periodontal diseaseaffecting a site with pre-existing periodontitis (227).

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Necrotizing periodontal diseases can also becomechronic, with a slow reduction in their symptomatol-ogy and progression, and ensuing destruction,although at a slower rate (138, 248). Some authorsbelieve that these conditions remain acute and maybe ‘recurrent’ (152).

In cases of severe systemic involvement, such as inpatients with AIDS or with severe malnutrition, nec-rotizing gingivitis and necrotizing periodontitis canprogress further with rapid involvement of the oralmucosae. The severity of these lesions are normallyrelated to the severity of the systemic condition andto the compromised host immune response, leadingto extensive bone destruction and the presence oflarge osteitis lesions and oral–antral fistulae (335).Necrotizing stomatitis has common features withcancrum oris or Noma. Some investigators suggestthat Noma is a progression of necrotizing stomatitisaffecting the skin, whereas others believe that necro-tizing stomatitis and Noma are two distinct clinicalentities. Noma is a destructive gangrenous diseaseaffecting the facial tissues. It is associated with high

rates of mortality and morbidity (32, 89, 91), and it isalmost exclusively observed in developing countries,especially in children suffering from systemic dis-eases, including severe malnutrition. Noma is nor-mally preceded by measles, malaria, severe diarrheaand necrotizing gingivitis, which highlights theimportance of prevention, early detection and treat-ment during the first stages of the disease (269).

Etiology, pathogenesis andhistopathology of necrotizing periodontaldiseases

Necrotizing periodontal diseases are caused by infec-tious agents, although predisposing factors, such as acompromised host immune response, are the mainfactors facilitating bacterial pathogenicity. This bacte-rial etiology was already demonstrated by Plaut in1894 and by Vicent in 1896 (269), as microscopic exam-ination of plaque samples retrieved from affected sub-jects clearly showed the presence of spirochetes andfusiform bacteria, even within the tissues. Moreover,clinical resolution was observed after mechanicaldebridement and antimicrobial treatments (302).However, knowledge of the pathogenesis of these dis-eases is limited because it is not clear whether thesebacteria observed in the lesions are the cause or theconsequence, as secondary bacterial colonization mayensue after periodontal destruction since the necrotictissues are the perfect environment for bacterial colo-nization and tissue invasion (138, 269).

The spirochetes and fusiform bacteria described inthe necrotic lesions have the capacity to invade theepithelium (131) and the connective tissue (181), aswell as to release endotoxins that may cause peri-odontal tissue destruction through the activation ormodification of the host response.

Necrotizing gingivitis lesions show a distinctpathology under light microscopy (181), with thepresence of an ulcer within the stratified squamousepithelium and the superficial layer of the gingivalconnective tissue surrounded with a nonspecificacute inflammatory reaction. Four areas have beendescribed within these lesions:� the bacterial area with a superficial fibrous mesh

composed of degenerated epithelial cells, leuko-cytes, cellular rests and a wide variety of bacterialcells, including rods, fusiforms and spirochetes.

� the neutrophil-rich zone, composed of a highnumber of leukocytes, especially neutrophils, andnumerous spirochetes of different sizes and otherbacterial morphotypes located between the hostcells.

Fig. 9. Necrotic area in a localized papilla: necrotizing gin-givitis starts at the interdental papilla and differentdegrees of destruction can be observed in different areasof the same mouth.

Fig. 10. Necrotizing periodontitis: it can occur afternumerous episodes of necrotizing gingivitis, or as a necro-tizing disease over a pre-existing periodontitis.

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� the necrotic zone, containing disintegrated cells,together with medium- and large-size spirochetesand fusiform bacteria.

� the spirochetal infiltration zone, where the tissuecomponents are adequately preserved but areinfiltrated with large- and medium-size spiro-chetes. Other bacterial morphotypes are notfound.

Microbiology of necrotizing periodontaldiseases

A similar composition of the microbiota associated tonecrotizing periodontal diseases has been observedin different studies, including Treponema spp., Sele-nomonas spp., Fusobacterium spp. and P. intermedia.Other microorganisms have also been described,although these were defined as ‘variable’ flora andwere not present in all cases (187). As this typicalmicrobiological description can also be detected inhealthy, gingivitis or periodontitis sites, the use ofmicrobiological testing does not provide relevantdiagnostic information (67, 152).

In HIV-positive patients with necrotizing periodon-tal diseases the microbiological findings are also non-specific (204, 266, 338), except in regard to the countsof yeasts (namely, Candida albicans), the presence ofherpes viruses (62, 272, 338, 340) or the detection ofsuperinfecting bacterial species, such as enteric bacte-ria including Enterococcus avium, Enterococcus faecal-is, Clostridium clostridioforme, Clostridium difficile,Mycoplasma spp. and Klebsiella pneumoniae (258,340). Most recently, with the use of molecular technol-ogies (PCR), some bacterial species (including Eubac-terium saphenus, Eubacterium sabbureum, Filifactoralocis, Dialister spp. and Porphyromonas endodontal-is) were found to be frequently associated with necro-tizing periodontal disease lesions, whilst the typicalperiodontitis-associated pathogens P. gingivalis andT. forsythia were less frequently found (243).

Some researchers have pointed out the possible eti-ological role of viruses (including human cytomegalo-virus) in necrotizing periodontal diseases (78, 273). Inchildren with necrotizing gingivitis in Nigeria, in addi-tion to the presence of cytomegalovirus in the lesions,other viruses were detected, including Epstein–Barrvirus type 1 and herpes simplex virus (64).

Predisposing factors for necrotizingperiodontal diseases

The most common predisposing factors for necrotiz-ing periodontal disease are those that alter the host

immune response, although usually more than onefactor is necessary for initiating the disease (138). In astudy in the USA, the most important factor was HIVinfection. In non-HIV patients, the most importantfactors were a previous history of necrotizing peri-odontal disease, poor oral hygiene, inadequate sleep,unusual psychological stress, poor diet, recentsystemic diseases, alcohol abuse, tobacco smoking,Caucasian ethnicity and age below 21 years (140).

Systemic conditions

Conditions that impair the host immune responsefavor necrotizing periodontal diseases. Infection withHIV or with diseases affecting leukocytes (e.g. leuke-mia) are among the most important predisposing fac-tors. Other systemic conditions that have shown apositive association with necrotizing periodontal dis-eases include malnutrition, measles, chickenpox,tuberculosis, herpetic gingiva-stomatitis, malaria, oreven diabetes, which was identified in a study of Chil-ean adolescents (188).

Among predisposing systemic conditions, HIVinfection and malnutrition have been studied in moredepth:� in HIV-positive patients, necrotizing periodontal

diseases are more frequent and show faster pro-gression, although no differences have beendetected between the characteristics of the diseasein HIV-negative and HIV-positive patients. It hasbeen suggested that HIV-positive patients have ahigher tendency for recurrence and a diminishedresponse to both mechanical and/or pharmaco-logical periodontal treatment (227). In HIV-posi-tive patients, the reduction in the counts ofperipheral CD4 lymphocytes has been correlatedwith necrotizing gingivitis and necrotizing peri-odontitis (113, 303) and therefore the diagnosis ofnecrotizing periodontal disease should promptthe likelihood that the patient may have an HIVinfection, and therefore the affected subjectsshould be screened for HIV (138, 139).

� malnutrition has also been reported as a predis-posing factor for necrotizing periodontal diseases(269), especially in developing countries (88, 90,234). The basis for this interaction has beentermed ‘protein-energy malnutrition’, implying amarked reduction in key antioxidant nutrients andan altered acute-phase response against infection.Other consequences are an inversed proportion inthe ratio of helper T-lymphocytes/suppressorT-lymphocytes, histaminemia, increased free corti-sol in blood and saliva and defects in mucosalintegrity (90).

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Psychological stress and insufficient sleep

Acute psychological stress and situations of acutestress have been associated with necrotizing gingivi-tis (140, 152, 291). Certain situations may predisposeindividuals to necrotizing periodontal disease, suchas military personnel in wartime, new recruits formilitary services, drug-abusers during abstinencesyndrome, students during examination periods andpatients with depression or other psychological con-ditions (108, 122, 248). During these stress periods,not only is the immune response altered, but alsothe subject’s behavior, leading to inadequate oralhygiene, poor diet or increased tobacco consump-tion. The proposed mechanisms to explain this asso-ciation are based on reductions of the gingivalmicrocirculation and salivary flow and increases inthe serum and urine levels of 17-hydroxycorticoster-oid, which are associated with an alteration in thefunction of polymorphonuclear leukocytes and lym-phocytes, or even with an increase in the levels ofperiodontal pathogens, such as P. intermedia (187).Higher urinary levels of 17-hydroxycorticosteroidhave been reported in patients with necrotizing gin-givitis than in healthy or treated patients; in addi-tion, the former group demonstrated statisticallysignificant higher levels of anxiety, depression oremotional alteration (138). Patients with necrotizinggingivitis also had polymorphonuclear leukocyteswith altered functions because their bactericidal,phagocytic and chemotactic capacities weredepressed (63).

Inadequate oral hygiene, pre-existing gingivitis andprevious history of necrotizing periodontal disease

Plaque accumulation has been considered a predis-posing factor for necrotizing periodontal disease (140,152), although it may also be a consequence of thepresence of ulcers and crater lesions that may limittoothbrushing as a result of pain. Necrotizing peri-odontal disease usually occurs over a pre-existingperiodontal disease, usually chronic gingivitis (248)(Fig. 11). In one study, 28% of the patients with nec-rotizing periodontal disease reported a history ofpainful gingival inflammation and 21% showedlesions compatible with previous necrotizing peri-odontal disease (140).

Alcohol and tobacco consumption

Smoking is a risk factor for necrotizing periodontaldisease (152, 153, 264) and, in fact, most HIV-negativepatients diagnosed with necrotizing periodontal dis-ease were smokers (108, 248, 307). The mechanisms

explaining this association are probably related to theeffect of smoking on inflammation and the tissueresponse, because smoking interferes with both poly-morphonuclear leukocyte and lymphocyte functionand nicotine induces vasoconstriction in gingivalblood vessels.

Alcohol consumption has also been associated withthe physiological and psychological factors favoringnecrotizing periodontal disease (139).

Young age and ethnicity

In developed countries, young people, mostly between21 and 24 years of age, are more prone to suffer necro-tizing periodontal disease, usually combined withother predisposing factors, such as smoking and stress(139, 140, 307). In developing countries, necrotizingperiodontal disease affects even younger people, withmalnutrition and the occurrence of infections beingthe most frequent predisposing factors (89, 90, 269).Studies in North America have reported that up to95% of cases of necrotizing periodontal disease occurin Caucasian patients (33, 140, 307), although morestudies are needed to confirm this finding.

Diagnosis of necrotizing periodontaldiseases

The diagnosis of necrotizing periodontal diseases isbased mainly on the clinical findings (67, 269).Although the reported histology and the typical mic-robiota associated with these lesions have a distinc-tive character, neither biopsy nor microbiologicalsampling are usually essential diagnostic tools inthese diseases (67). The different stages of necrotizingperiodontal disease share clinical features, but also

Fig. 11. Plaque and calculus accumulation in a patientwith chronic gingivitis: necrotizing periodontal diseasesaffect tissues with pre-exisitng chronic periodontal condi-tions.

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distinct findings, depending on the extent and sever-ity of the lesions (1, 67, 138, 152, 269).

Necrotizing gingivitis

The diagnosis is based on the presence of necrosisand ulcers in the free gingiva. These lesions usuallystart at the interdental papilla and have a typical‘punched-out’ appearance. In addition, a marginalerythema, named ‘lineal erythema’, may be present,separating the healthy and the diseased gingiva.These necrotic lesions can progress to the marginalgingiva. The most typical location is the anteriorteeth, especially in the mandible (Fig. 12). In necro-tizing gingivitis, gingival bleeding is a frequent find-ing, and it is usually spontaneous or occurs afterminimal contact (Fig. 13). Pain normally has a rapidonset and occurs with different degrees of severity,depending on the severity and extent of the lesions.The bouts of pain increase with eating and with oral

hygiene practices and is normally the reason for thepatient’s consultation.

Other less common findings include the presenceof:� pseudomembrane over the necrotic area. The

pseudomembrane consists of a whitish/yellow-colored meshwork, composed of necrotic tissue,fibrin, erythrocytes, leukocytes and bacterial cells.When this ‘membrane’ is removed, the underlyingconnective tissue becomes exposed and bleeds.

� halitosis, although this is not an exclusive sign ofnecrotizing gingivitis.

� adenopathies, which are usually found in the mostsevere cases of disease. If present, submandibularlymph nodes are more affected than those in thecervical area (150, 151).

� fever and a general feeling of discomfort.

Necrotizing periodontitis

The same clinical picture described in necrotizinggingivitis occurs in necrotizing periodontitis, but inaddition, in necrotizing periodontitis the followingcharacteristics may be present:� necrosis affects the periodontal ligament and the

alveolar bone, leading to loss of attachment. Asthere is concomitant necrosis of the soft tissue,the presence of pockets is not an usual finding(Fig. 14).

� as the disease progresses (Fig. 15), the interdentalpapilla is divided into a buccal part and a lingual/palatal part, with a necrotic area in the middle,known as the interproximal crater. If the cratersare deep, the interdental crestal bone becomesexposed and denudated. In addition, crater for-mation favors disease progression by allowing theaccumulation of more bacteria. Interproximalnecrotic areas spread laterally and merge with the

Fig. 12. Necrotizing gingivitis affects more frequently themandibular anterior sextant.

Fig. 13. Bleeding observed in necrotizing gingivitis: it canoccur spontaneously or after minimal stimulus.

Fig. 14. Papilla destruction in necrotizing gingivitis:no pocket formation is observed following the loss of softtissues.

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neighboring areas, creating an extensive zone ofdestruction.

� in severe cases, especially in immune-compro-mised patients, bone sequestrum (necrotic bonefragments within the tissues but separated fromthe healthy bone) may occur, mainly interdentally,but also in the buccal or lingual/palatal parts ofthe alveolar bone.

Necrotizing stomatitis

When bone denudation extends through the alveolarmucosa, larger bone sequestra may occur, with largeareas of osteitis and oral–antral fistulae. These lesionsare of greater severity in patients with severe systemiccompromise, including patients with AIDS andpatients with severe malnutrition (335).

Management of necrotizing periodontaldiseases

Owing to the (previously listed) specific features ofnecrotizing periodontal disease (tissue destruction,acute course and pain), diagnosis and treatment haveto be performed as soon as possible, and conven-tional periodontal therapies may need adjunctivetherapeutic measures (2, 152).

The treatment should be organized in successivestages: treatment of the acute phase; treatment ofthe pre-existing condition and corrective treatmentof the disease sequelae; supportive or maintenancephase.

Treatment of the acute phase

There are two main objectives of therapy: to arrestthe disease process and tissue destruction; and tocontrol the patient′s general feeling of discomfort andpain that is interfering with nutrition and oral hygienepractices (138). The first task should be a carefulsuperficial debridement to remove the soft and min-eralized deposits. Power-driven debridement devices(e.g. ultrasonics) are usually recommended, exerting

minimal pressure over the ulcerated soft tissues. Thedebridement should be performed daily, becomingdeeper as the tolerance of the patient improves, andlasting for as long as the acute phase lasts (normally 2–4 days). Mechanical oral hygiene measures shouldbe limited because brushing directly in the woundsmay impair healing and induce pain. During this per-iod the patient is advised to use chemical plaque-con-trol formulations, such as chlorhexidine-basedmouthrinses (0.12–0.2%, twice daily). Other productshave also been suggested, such as 3% hydrogen per-oxide diluted 1:1 in warm water, and other oxygen-releasing agents, which not only contribute to themechanical cleaning of the lesions but also providethe antibacterial effect of oxygen against anaerobes(333). Other oxygen therapies have also been evalu-ated, such as local oxygen therapy, which may help toreduce, or even eradicate, microorganisms, resultingin faster clinical healing with less periodontal destruc-tion (101).

In cases that show unsatisfactory response todebridement or show systemic effects (fever and/ormalaise), the use of systemic antimicrobials may beconsidered. Metronidazole (250 mg, every 8 h) maybe an appropriate first choice of drug because it isactive against strict anaerobes (187). Other systemicdrugs have also been proposed, with acceptableresults, including penicillin, tetracyclines, clindamy-cin, amoxicillin or amoxicillin plus clavulanate. Con-versely, locally delivered antimicrobials are notrecommended because of the large numbers of bac-teria present within the tissues, where the local drugwill not be able to achieve adequate concentrations.

These patients have to be followed up very closely(daily, if possible) and as the symptoms and signsimprove, strict mechanical hygiene measures shouldbe enforced, as well as complete debridement of thelesions.

Treatment of the pre-existing condition

Necrotizing periodontal diseases normally occurs overa pre-existing chronic gingivitis or periodontitis infec-tion. Once the acute phase has been controlled, treat-ment of the pre-existing chronic condition should bestarted, including professional prophylaxis and/orscaling and root planing. Oral hygiene instructionsand motivation should be enforced. Existing predis-posing local factors, such as overhanging restorations,interdental open spaces and tooth malposition,should be carefully evaluated and treated (140). Atthis stage, and also during the acute phase, attentionshould be paid to the control of the systemic predis-posing factors, including smoking, adequate sleep,

Fig. 15. Crater formation and bleeding in a posterior area.

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reduction of stress or treatment of involved systemicconditions.

Corrective treatment of disease sequelae

The correction of the altered gingival topographycaused by the disease should be considered (Fig. 16)because gingival craters may favor plaque accumula-tion and disease recurrence. Gingivectomy and/orgingivoplasty procedures may be helpful for treat-ment of superficial craters; periodontal flap surgery,or even regenerative surgery, are more suitableoptions for deep craters (138).

Supportive or maintenance phase

During supportive or maintenance phases, the maingoal is compliance with the oral hygiene practices(Fig. 17) and control of the predisposing factors.

Specific considerations for HIV-positive patients

HIV-positive patients may not be aware of their sero-logic status. The occurrence of necrotizing periodon-tal disease in systemically healthy individuals issuggestive of HIV infection and, therefore, the affectedindividuals should be screened for HIV (138, 140).The specific management of necrotizing periodontaldisease in HIV-positive patients includes debride-ment of bacterial deposits combined with irrigationof the site with iodine-povidone, based on its hypo-thetic anesthetic and bleeding control effects (338),although no scientific studies are available to supportthis protocol (271, 336, 338). Careful considerationshould be made regarding the use of systemic antimi-crobials because of the risk of overgrowth of Candidaspp. Metronidazole has been recommended for itsnarrow spectrum and limited effects on gram-positivebacteria, which prevent Candida spp. overgrowth(272, 336, 338), although HIV-positive patients maynot need antibiotic prophylaxis for the treatment ofnecrotizing periodontal disease (194). In nonrespond-ing cases, the use of antifungals may be beneficial,including clotrimazole lozenges, nystatin vaginal tab-lets, systemic fluoconazole or itraconazole, mainly incases of severe immune suppression (272, 338). InHIV-positive patients, the systemic status should beclosely monitored, including the viral load and thehematologic and immune conditions, leading todevelopment of a customized periodontal treatmentplan (266, 272, 338).

Summary

Necrotizing periodontal disease includes necrotizinggingivitis, necrotizing periodontitis and necrotizingstomatitis, and these may be considered as differentstages of the same pathologic process. This group ofdiseases always presents three typical clinical features– papilla necrosis, bleeding and pain – which makesthem different from other periodontal diseases.Although their prevalence is not high, their impor-tance is clear because they represent the most severebiofilm-related periodontal conditions, leading torapid tissue destruction. In their etiology, togetherwith bacteria, numerous factors that alter the hostresponse may predispose to these diseases, includingHIV infection, malnutrition, stress or tobaccosmoking.

Owing to their acute presentation, together withthe associated pain and tissue destruction, treatmentshould be provided immediately upon diagnosis; thisshould include superficial debridement, careful

Fig. 16. Gingival craters are important sequelae becausethey can limit mechanical plaque control.

Fig. 17. Esthetic consequences of necrotizing periodontaldiseases.

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mechanical oral hygiene, rinsing with chlorhexidineand daily revisions. Systemic antimicrobials may beused adjunctively in severe cases or in nonrespondingconditions, and the best option is metronidazole.Once the acute disease is under control, definitivetreatment should be provided, including adequatetherapy for the pre-existing gingivitis or periodontitisas well as adequate oral hygiene practices and sup-portive therapy. Surgical treatment of the sequelaeshould be considered based on the needs of the indi-vidual case.

Other acute conditions in theperiodontium

This group of acute gingival lesions includes lesionsmanifesting initially as acute conditions or as acuteepisodes of a chronic condition. They can appear asisolated lesions or as part of complex clinical picturesand they are frequently responsible for emergencyconsultations.

The clinical lesion is usually an ulcer or erosion,which may be the primary lesion or secondary to avesicle-bullous lesion. The most frequent symptom islocalized pain, which initiates with the lesion or mayprecede it, although it may also occur in conjunctionwith pain in the pharynx or dysphagia. To establishthe proper diagnosis, a clinical history, anamnesisand careful examination are mandatory because fre-quently there is a direct and recent relationship withthe cause (68). In the following discussion, the lesionsare classified according to their etiology because theirclinical appearance is similar and a careful differentialdiagnosis is key to their therapy (22, 134, 326).

Gingival diseases of infectious origin

Gingival lesions of specific bacterial origin

Specific bacterial infections localized in the oralmucosa are uncommon. They may be caused by bac-teria normally present in the oral cavity that eventu-ally become pathogenic, and also by bacteriaexogenous to the oral cavity, such as gonococci, tula-remia or anthrax. In addition, the lesions present inthe oral cavity may be a secondary location of gener-alized infectious disease, as in scarlatina, diphtheria,syphilis or tuberculosis.

Both staphylococci and streptococci may cause oralinfections with gingival involvement, leading to alesion with a nonspecific appearance (usually ery-thematous or erosive) (102, 201). Group B streptococ-cal infections frequently result in pharynx-amigdalitis

that affects all oral mucosae and may be associatedwith fever and malaise. Treatment includes rehydra-tion, rest and the prescription of systemic antimicro-bials (154, 157, 160, 183). Stomatitis associated withS. aureus is characterized by bullous generalized der-matitis, with vesicles and desquamation, whichaffects the lips, oral mucosa and other mucosae. Itsappearance is similar to multiform erythema or impe-tigo and it is usually treated with systemic antimicro-bials (102, 299).

Despite the presence of the oral epithelium as aprotective barrier against infection with Neisseriagonorrhoeae, gonococcal lesions may develop as aresult of direct contact. In the newborn, N. gonor-rhoeae infection may occur through contact whenpassing through the birth canal. In adults, transmis-sion may be bucco-genital and superficial lesions arefound as white/yellowish plaques or pseudomem-branes that, when removed, result in a bleeding ulcer.Salivary flow may be reduced and saliva can be den-ser. The clinical history is crucial and treatmentshould consist of the administration of systemic anti-microbials (61, 92, 293, 332).

Among generalized infectious diseases, syphilismay often affect the gingival tissues. Syphilis iscaused by Treponema pallidum and may be difficultto diagnose because of similarities with other sys-temic conditions (96, 172, 256). Syphilis can be con-genital or acquired. In acquired syphilis, theincubation period may vary from 12 to 40 days, andthe lesions may follow different stages. In primarysyphilis, the lesion is located at the point of transmis-sion, normally as a chancre that may be located onthe lips, tongue or tonsils (11). The gingiva may beaffected by secondary syphilis after 6–8 weeks, oreven 6 months, with the presence of a plaque (ele-vated papule with central erosion) that may last forweeks or even a year (18, 168, 193, 197, 257, 268). Ter-tiary syphilis is uncommon and, when present in theoral cavity, it may affect the palate and the tongue(171). Differential diagnosis is critical and sometimesdifficult. Treatment consists of the administration ofspecific systemic antimicrobials (96, 197).

Viral infections

Different viruses may cause lesions in the oral cavity,with or without concomitant skin involvement (215).The most frequently associated viruses causing gingi-val and periodontal lesions are from the Herpesviri-dae family (herpes simplex virus type 1, the causalagent of oral and labial herpes lesions; herpes simplexvirus type 2, associated with genital herpes; and vari-cella-zoster virus, responsible for varicella and herpes

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zoster) (64–66, 119, 137, 211, 240, 298). Herpesvirusesadapt easily to the host, and after the primary infec-tion they remain inside the infected cells in a latent orsilent state; they show tropism for epithelial and neu-ral cells, and the preferred site for latency of herpessimplex viruses and varicella-zoster virus is ganglionsin the nervous system (66, 83, 84, 324, 337).

Varicella is the outcome of an infection with vari-cella-zoster virus and occurs after the initial contactwith the virus. It results in a generalized condition,especially in children, with vesicle eruptions in skinafter an incubation period of 1–3 weeks. Before orafter appearance of the skin lesions, vesicles can beevident in the oral cavity, including the gingiva, andthey break easily, forming ulcers surrounded by anerythematous halo. The result of the re-activation ofthe varicella-zoster virus from the regional sensitiveganglia is herpes zoster, which occurs especially inthe elderly or associated with immune-depression. Itmay affect the trigeminal ganglion, with clinicalmanifestation preceded by pain or an itching feeling.Clinical lesions are vesicles surrounded by an ery-thematous halo, with a unilateral distribution; thevesicles break easily, forming erosive areas (214, 262,312). Primary herpetic infection with herpes simplexvirus type-1 is normally asymptomatic, but it is some-times very evident in the form of generalized gingivo-stomatitis, with dysphagia, fever, malaise andsubmandibular adenopathy. It is more frequentlyobserved in children 2–5 years of age, with orallesions in the form of ulcers or erosions, after the vesi-cles have broken (Fig. 18). Treatment may includeantiviral agents and adequate nutritional support,mostly when pain compromises eating (66, 84, 216,287, 324).

Recurrent herpetic infection with herpes simplexvirus type-1 may be either intraoral or labial. Initialsymptoms include local discomfort in the form ofitching or stinging. The lesions develop as an ery-thema, and then a variable number of grouped vesi-cles break, forming an erosion in the oral mucosae,gingiva or the lip (Fig. 19). Lesions normally last for 7–10 days and heal without scarring. Differential diag-nosis with other conditions showing ulcers, such asrecurrent aphthous stomatitis, is important, althoughthe latter lesions will not affect keratinized tissues(178, 252, 254, 284, 341). As the condition is self-limit-ing, no treatment is usually required, although if pres-ent in immune-compromised patients, antiviralagents should be prescribed (216, 287, 311, 337).

Other viruses, such as Epstein–Barr virus, cytomeg-alovirus and Coxsackie virus, are frequently transmittedvia saliva and may result in specific oral manifesta-

tions: infectious mononucleosis (Epstein–Barr virus)or hand, foot and mouth disease (Coxsackie virus).Sometimes they may also cause unspecific condi-tions, including acute stomatitis with oral ulcers andmalaise and adenopathy. These conditions can beimportant in immune-compromised patients (25,127, 189, 218, 231).

In addition to the acute conditions already dis-cussed, viruses are associated with chronic conditionsthat may require emergency attention for complica-tions during their development, trauma or unex-pected findings, including viral warts or condylomaacuminata.

Fungal infections

Many fungal species are part of the resident flora ofthe mouth, but they may cause pathology when localor systemic factors trigger their overgrowth (114, 207,222). Among these opportunistic fungal infections,candidiasis is the most frequent, normally affectingimmune-compromised subjects, especially HIV-posi-tive patients, or during infancy and in the elderly (49,118, 133, 229, 278, 328). Although their localized formsare usually not severe, it may spread and lead to moresevere infections, such as esophagic or systemic

Fig. 18. Herpetic gingivo-stomatitis: painful gingivitis withgeneralized vesicles in primary herpetic infection.

Fig. 19. Recurrent herpetic infection: vesicles break, lead-ing to erosive lesions. Gingival location is not infrequent.

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candidiasis. Among Candida spp., C. albicans is themost relevant for oral infections (263).

Multiple factors are associated with the pathogen-esis of oral candidiasis (Fig. 20), and these may bedivided into host-related factors and local and envi-ronmental factors (49, 134, 275, 278, 314). Among thehost-related factors are the presence of concomitantsystemic diseases (such as diabetes) or debilitatingconditions leading to a reduced host response. Themost common local and environmental factorsinclude removable prostheses, systemic antimicrobi-als, corticosteroids and tobacco smoking (9, 49, 104,114, 118, 134, 207, 275, 278, 314).

Acute candidiasis can present as pseudomembra-nous or erythematous candidiasis, with itching orstinging being. The diagnosis is mainly clinical (28,135). Treatment includes antifungal agents, such asnystatin, amphotericin B or miconazole, in solutionsor gels. In severe cases, or in immune-compromisedpatients, the treatment of choice is systemic fluconaz-ole. It is also mandatory to evaluate and control theassociated predisposing/adjunctive local and/or sys-temic factors (9, 43, 104, 319).

Gingival manifestations of systemicconditions

Mucocutaneous disorders

Mucocutaneous disorders represent a group ofchronic autoimmune diseases that are characterizedby the presence of vesicle-bullous lesions, with liquidcontent (either serum or hemorrhagic). Although theevolution of these diseases is chronic, acute boutsmay occur and affect an intraoral location, and alsothe skin or other mucosae (50, 310, 331).

Vesicle-bullous diseases usually present in thegingival tissues as desquamative gingivitis. This mani-festation reflects the presence of epithelial desqua-

mation and erythematous, vesicle-bullous or erosivelesions in the gingiva. Although it is normally part of achronic process, painful acute phases can also occur,with intense and diffuse redness in the attached andfree gingiva. The epithelium is fragile and easilydetached, leaving a reddish surface, which bleedsafter minimal stimulus (313). When the lesions arelimited to the gingival tissues, they are more fre-quently located in dentate areas at buccal sites(Fig. 21). Women in the fourth to fifth decades of lifeare more prone to present these lesions (172, 184,185, 199, 310, 325). Therapy is usually based on treat-ment with topical or systemic corticoids (51, 52, 95,115, 191, 226).

Lichen planus is a chronic inflammatory diseaseaffecting the skin and the mucosae, and is the mostcommon noninfectious disease of the oral cavity. Theoral manifestation is very common, mostly in adultwomen (30–50 years) of Caucasian ethnicity (186,213, 280). The oral lesions usually precede the skinlesions or are the only lesion (Fig. 22). Clinical mani-festations range from the typical reticular form,affecting the buccal and cheek mucosae, to erosiveforms, usually located in the tongue and gingiva, thatcause pain and tenderness, as well as bleeding. When

Fig. 20. Oral candidiasis: one of the predisposing factors isa removable prosthesis, and erythematous lesions areamong the most frequent lesions.

Fig. 21. Mucocutaneous disorders: most of them may haveoral and gingival lesions, normally with a chronic evolu-tion but also with acute periods.

Fig. 22. Lichen planus: gingival involvement includes ero-sive lesions and reticular whitish lesions.

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present in the gingiva, the lesions are usuallyobserved as a desquamative gingivitis affecting theattached gingiva. The diagnosis is both clinical (bilat-eral and symmetric lesions, whitish reticular lesionsor red lesions, not disappearing after scraping) andhistological (53, 186, 213, 281). If some of the diagnos-tic criteria are not met, the lesions will be defined aslichenoid reactions (Fig. 23), normally associatedwith restorative materials, pharmaceutical drugs,graft vs. host disease or some systemic conditions (10,75, 80, 147, 169, 233, 246).

Pemphigus is a severe, autoimmune mucocutane-ous disease, with a chronic and aggressive progres-sion, characterized by the destruction of theintercellular adhesion systems between keratinocytes,leading to intra-epithelial bulla formation (39, 170,221, 288). Among the different clinical forms, only thevulgaris and the vegetans can affect the oral mucosae,although the latter is very infrequent. Pemphigus vul-garis is more frequent in women, 40–60 years of age,with a Mediterranean or Jewish background. Skinlesions are more common, but in 50% of the casesoral lesions may precede the skin lesions (295). Intra-oral lesions, if affecting the gingiva, appear as desqua-mative gingivitis (86). Diagnosis may be difficult andwill be based on histology and immune-fluorescence(48, 87, 212, 230, 282, 286, 288, 296).

Pemphigoid includes a group of autoimmunemucocutaneous diseases that affect either the skin(bullous pemphigoid and gestational herpes) or themucosae (mucous membrane pemphigoid or cicatri-cial pemphigoid). In the latter, the autoimmune reac-tion affects the basal membrane (subepithelial bulla)and frequently occurs in women older than 50 yearsof age, presenting oral lesions in more than 90% ofthe cases. These lesions are usually located in the gin-

giva, later spreading to neighboring tissues or to othersites. Gingival tissues are affected in 40–100% of thecases as desquamative gingivitis, including periods ofexacerbation and remission (19, 31, 170, 239, 274,285).

Other mucocutaneous conditions, characterized asvesicle-bullous conditions, include linear IgA disease,bullous epidermolisis, erythema multiforme andlupus erythematosus. When affecting the gingiva,they manifest as desquamative gingivitis and the dif-ferential diagnosis should be based on histologic orlaboratory evidence, as well as the involvement ofother body sites or organs (13, 50, 94, 200, 225, 310,323, 331).

Allergic reactions

Allergy is an abnormal reaction of the human body:an exaggerated response to a contact with a foreignsubstance or product (allergen) that does not neces-sarily induce a similar reaction in other individuals(3, 27, 44, 72, 195, 228). Food products, includingfruits, seafood, nuts or some vegetables, inducemost allergic reactions; however, some medicines,including antibiotics (e.g. penicillin) or nonsteroidalanti-inflammatory drugs (e.g. acetylsalicylic acid)can also be responsible for allergic reactions (15, 17,23, 42, 46, 70, 72, 112, 179, 228, 235). Other poten-tially allergenic products are haptens, which need tobe linked to proteins in order to become allergens,and are very relevant in dentistry because they arepresent in some metals and dental materials (3, 41,72, 73, 164, 169, 173, 203, 217), in topical anesthesia,in oral hygiene products (161), as well as in rubberdams, latex examination gloves and cosmetics (16,45, 79, 169, 180, 208, 277, 297). Allergies in themouth may have different clinical manifestations,ranging from the typical urticarial reaction to an-gioedema, although they do not normally affect thegingival tissues (27, 159, 205).

Erythema multiforme is a disseminated hypersensi-tivity reaction, which may affect the majority ofhuman systems and even compromise the patient’slife (3, 24, 29, 34, 47, 58, 81, 93, 98, 107, 167, 260, 270,279, 306). An inductor or precipitating factor is nor-mally present; these include herpes simplex virusinfections; drugs such as sulfamide, penicillin or salic-ylate; or gastrointestinal conditions, including Cro-hn’s disease and ulcerative colitis (29, 190, 270).Clinically, exudative erythema multiforme may affectthe skin and mucosae, presents as minor and major(also known as Stevens–Johnson syndrome) formsand is characterized by bullae formation (24, 34, 47,93, 132, 143, 190, 223, 260). The diagnosis is mainly

Fig. 23. Liquenoid lesions: identical to lichen planuslesions, but clearly associated with a causative factor (suchas amalgam fillings); these lesions disappear after elimina-tion of the causative factor.

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clinical and, when affecting gingival tissues, differen-tial diagnosis with other conditions that manifest asdesquamative gingivitis should be considered (24, 47,144). In mild cases, topical corticoids, analgesics anda soft diet may be sufficient. In severe cases, systemiccorticoids are the first option, and in refractory casesthe treatment is with azathioprine or dapsone (144,192, 223, 232).

Contact allergy of an intraoral location is an ill-de-fined entity (3, 27, 72, 73) and is normally associatedwith drugs (antimalarial, nonsteroidal anti-inflamma-tory, antihypertensive or antidiabetic medications) ormetals (especially amalgam (41, 169, 208), gold (334)or nickel (73)), or with other dental materials, includ-ing acrylic resins or dental composites (6, 164, 173,203, 217, 277) (Fig. 24). Contact allergies associatedwith toothpastes, mouthrinses or chewing gums arerare (16, 79, 161, 180, 297). The lesions are usually notclinically distinguishable from a tooth-related irrita-tion or trauma (73, 305, 329). Symptoms includeburning, itching or stinging, and the lesion is oftendefined as a liquenoid reaction (165, 206). The clinicalaspect of intraoral contact allergies includes erythem-atous and edematous gingival tissues, sometimeswith ulcers and whitish areas. The same lesions canbe observed on the lip, buccal or lingual mucosae.Therefore, diagnosis is often difficult, with a need tofind a direct association between the clinical lesionsand the exposure to allergens. The most importanttherapeutic measure is to remove the allergen,although this is not always easy and sometimes it willnot solve the case, including cases of incorrect diag-nosis (16, 79, 161, 180, 297).

Traumatic lesions

The clinical presentation of lesions associated withphysical and chemical agents will depend on wether

the action of the agent is direct or indirect. The effectof a direct action depends on the type of agent, thelength of exposure to the agent and the amount ofsurface of mucosa affected. Indirect effects appear ascolor alteration, erythema, erosion, ulcer, gingivalenlargement, hemorrhage or dysgeusia (59, 236, 259).

Among traumatic lesions, iatrogenic lesions are rel-evant in dentistry because they are produced duringtherapeutic intervention or as a result of the therapy(Fig. 24). They are normally considered as treatmentcomplications because dental instruments and chem-ical products can cause injuries or burns, includinglesions in the gingival tissues (8, 59, 71, 105, 112, 220,236, 247, 251, 259, 276, 277, 290, 305).

Physical (mechanical and thermal) injury

Physical mechanical injuries may appear as erosionsor ulcers, associated with gingival recession. How-ever, they can also present as hyperkeratosis, vesiclesor bullae, sometimes in combination with other orallesions on the lips, tongue or teeth; they may beasymptomatic, but they can also induce intense,localized pain at the area of the lesion. The correctdiagnosis is based not only on the clinical aspect, butalso in the identification of the noxious agent, and forthat, patient collaboration is crucial (148, 182, 236,259, 305).

Physical mechanical injuries are most frequentlycaused by traumatic accidents, but they can also berelated to incorrect oral hygiene habits and parafunc-tions (182, 238, 242, 301). If the physical trauma islimited, but continuous over time, the gingival lesionwill be frictional hyperkeratosis that may lead to aleukoplakic lesion. If the physical trauma is moreaggressive, superficial laceration or more severe tis-sue loss can occur, eventually resulting in gingivalrecession (Fig. 25). For example, the use of an abra-

Fig. 24. Iatrogenic lesions: gingival erosions.

Fig. 25. Traumatic lesions: often self-inflicted, or associ-ated with traumatic toothbrushing or incorrect oralhygiene habits.

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sive dentifrice and vigorous horizontal brushing willresult in an ulcer or an erosion in the gingiva, fre-quently leading to tooth abrasion (182, 301). The useof dental floss can also result in gingival ulceration orinflammation, especially at the most coronal part ofthe interdental papilla (142).

Some physical traumatic lesions are self-inducedand they are termed self-induced gingitivis, patomi-mias, factitious lesions or artifacts (14, 30, 37, 77, 120,121, 244, 308, 309). Lesions present as ulcers in thegingival margin and are associated with gingivalrecession; patients are frequently children or teenag-ers, sometimes with psychological conditions. Thereis a clear tendency for recurrence, and the traumaticagent can be the fingers, nails or different instru-ments (pencil, pen, etc.) (69, 166, 253, 259).

Another group of physical traumatic lesions arerelated to dental fractures or broken teeth, orthodon-tic or prosthetic appliances and oral piercings (56,148, 174, 175). Normally, they are observed as ulcersor erosions, but dental or periodontal abscesses canbe triggered, as well as chronic infections such assubprosthesis palatitis or lesions such as as fissuredepulis. Frictional hyperqueratosis can also occur. Inaddition, the risk of precancerous or carcinomalesions is present, especially if other factors (infection,irritation, chemicals, etc.) also act over the trauma-tized area.

Ionizing radiation may cause physical injuries tothe gingival tissues (320). This type of lesion isobserved after irradiation therapy as part of the head-and-neck cancer treatment. The gingival tissues showmucositis, with erythema, followed by epithelialnecrosis with whitish plaques, which results in bleed-ing surfaces after dislodging (283).

Relevant lesions related to hot, cold or electricaltrauma are uncommon, although burns caused byvery hot food or liquids may need emergency consul-tation (35, 219, 220, 236). The patient will feel pain inthe affected area, which appears with erythema or isdesquamated, sometimes with vesicles, erosions orulcers. Normally, diagnosis is straightforward (Fig. 26).

Chemical and pharmacological injury

Numerous agents can induce chemical injury; theseinclude acids and bases, medicines, alcohol andtobacco, and also lesions associated with the use ofmouthrinses and dentifrices. Lesions may appearafter direct contact of the agent over the mucosa,leading to a maculae, vesicles, erosions or ulcers, withdifferent relevance, depending on the causal agent,the size of the lesion and the duration of contact (8,71, 105, 112, 276, 290).

Summary

This is a group of periodontal lesions, with acuteonset, which are not etiologically associated with oralbiofilm microorganisms. However, they result in painand in difficulties with oral hygiene practices. Infec-tious diseases, mucocutaneous diseases and trau-matic or allergic lesions can be included among theseconditions.

In most cases, the gingival involvement is notsevere, but it is important to be familiar with theselesions because they are common and may be areason for emergency dental consultations. In addi-tion, some may represent the first lesion of a severesystemic disease, as in mucocutaneous diseases, andthey usually manifest with the characteristic gingivallesion of desquamative gingivitis.

Many of these conditions have the appearance ofan erythematous lesion, sometimes erosive, with paininduced by toothbrushing or chewing. The differen-tial diagnosis is crucial with special focus on theanamnesis and clinical history and progression of thelesions. Erosive lesions may be the result of directaggressions, such as trauma, or indirect reactivelesions related to dental or iatrogenic interventions.The proper differential diagnosis will lead to theappropriate therapeutic intervention.

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