Jan Lindhe. Clinical Periodontology

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NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS • 283

able in serum samples of most patients, but at the

initial stage of intraoral affection antiepithelial anti-

body may not be elevated (Melbye et al. 1987, Manton

& Scully 1988, Lamey et al. 1992, Lever & Schaum-

burg-Lever 1997). The background of bulla formation

in PV is damage to the intercellular adhesion caused

by autoantibodies to cadherin-type epithelial cell ad-

hesion molecules (desmoglein 1 and 3) (Nousari &

Anhalt 1995, Nishikawa et al. 1996). The mechanism

by which these molecules trigger the formation of

autoantibodies has not yet been established.

Immediate referral of patients with PV to a derma-

tologist or internal medicine specialist is important

because when recognized late the disease can be fatal,

although systemic corticosteroid therapy can pres-

ently solve most cases. Supplementary local treatment

consists of gentle plaque control and professional

cleaning as mentioned for the chronic inflammatory

oral mucosal diseases above. Sometimes, additional

topical corticosteroid application is needed to control

the intraoral disease activity.

Erythema multiforme

Erythema multiforme (EM) is an acute, sometimes

recurrent, vesiculobullous disease affecting mucous

membranes and skin. A general malaise often pre-

cedes the lesions, which involve skin and mucous

membranes in various degrees. Two forms of the dis-

ease have been described: a minor form with only

moderate involvement and a major form, also men-

tioned as Stevens-Johnson syndrome, with wide-

spread mucous membrane, i.e. oral, ocular and geni-

tal, in addition to skin lesions (Lozada-Nur et al. 1989,

Assier et al. 1995, Bystryn 1996). This latter multilocu-

lar entity has to be differentiated from other disorders

such as Reiter and Behcet's syndromes, which also

affect the eyes, the oral mucosa and often the genitalia.

The pathogenesis of EM remains obscure, but the

disease appears to be an immune reaction precipitated

by a wide range of factors including herpes simplex

virus (Lozada & Silverman 1978, Nesbit & Gobetti

1986, Ruokonen et al. 1988, Miura et al. 1992, Aurelian

et al. 1998), mycoplasma pneumoniae (McKellar &

Reade 1986, Stutman 1987) and various drugs (Bot-

tiger et al. 1975, Gebel & Hornstein 1984, Kauppinen

& Stubb 1984).

EM may occur at any age but most frequently af-

fects young individuals. It may or may not involve the

oral mucosa, but oral involvement occurs in as much

as 25-60% of cases (Huff et al. 1983) and sometimes is

the only involved site. The characteristic oral lesions

comprise swollen lips often with extensive crust for-

mation of the vermilion border (Fig. 12-37). The basic

lesions, however, are bullae that rupture and leave

extensive ulcers usually covered by heavy yellowish

fibrinous exudates sometimes described as

pseudomembranes (Figs. 12-38 and 12-39). Such le-

sions may also involve the buccal mucosa and gingiva

(Huff et al. 1983, Lozada-Nur et al. 1989, Scully et al.

1991, Barrett et al. 1993). The skin lesions are charac-

Fig. 12-37. Erythema multiforme with crust formation

of the vermilion border of the lower lip.

Fig. 12-38. Erythema multiforme with ulceration cov

ered by heavy fibrin exudate.

Fig. 12-39. Erythema multiforme with fibrin coated ul

ceration of palatal mucosa.

teristic due to the iris appearance with a central bulla

formation surrounded by a blanched halo within an

erythematous zone (Fig. 12-40). Similar intraoral le-

sions do occur but they are infrequent. The disease is

usually self-limiting but recurrences are common.

Healing of the lesions may require several weeks (Fab-

bri & Panconesi 1993).

The histopathology of EM shows intra- or subepi-

284 • CHAPTER 12

Fig. 12-40. Erythema multiforme. Skin lesion with char

acteristic iris appearance. Central bulla formation sur-

rounded by a blanched halo within an erythematous

zone.

thelial separation of epithelium from connective tis-

sue with non-specific inflammation (Reed 1985). Im-

munohistochemical findings are non-specific and in

most instances the diagnosis relies on the clinical find-

ings.

Although periodontal lesions are not the most fre-

quent intraoral manifestation, they can sometimes

pose a differential diagnostic problem. The typical

crusty ulcerations of the vermilion border and the

heavy fibrin exudates covering intraoral lesions are

indicative of erythema multiforme, sometimes there-

fore denoted erythema multiforme exudativum. The

mucosal ulcerations may take weeks to heal and they

are painful (Lozada-Nur et al. 1989).

As for any intraoral ulcerations, a gentle plaque

control and professional cleaning is mandatory. The

treatment often involves systemic corticosteroids, but

topical treatment may act in cases with minor lesions.

Lupus erythematosus

Lupus erythematosus (LE) is a group of autoimmune

connective tissue disorders in which autoantibodies

form to various cellular constituents including nu-

cleus, cytoplasma membrane and others. Women are

much more affected than men. The etiology of LE

remains unknown, but deposits of antigen-antibody

complexes appear to play a role in the tissue damage

characteristic of the disease (Schrieber & Maini 1984).

LE includes two major forms: discoid LE (DLE) and

systemic LE (SLE) which may involve a range of organ

systems including kidney, heart, central nervous sys-

tem, vascular system and bone marrow. The preva-

lence of LE has been estimated at 0.05% (Condemi

1987).

DLE is a mild chronic form, which involves skin

and mucous membranes, sometimes involving the

gingiva as well as other parts of the oral mucosa (

Schiodt 1984a,b). The typical lesion presents a central

atrophic area with small white dots surrounded by

irradiating fine white striae with a periphery of

telangiectasia (Fig. 12-41). The lesions can be ulcerated

or clinically indistinguishable from leukoplakia or

atrophic oral lichen planus (Fig. 12-42) (Schiodt

1984b). Sometimes patients present brownish gingival

lesions, which is a side effect of antimalarial drugs

prescribed to these patients as part of their treatment

(Fig. 12-43). Eight per cent of patients with DLE de-

velop SLE, and ulcerations may be a sign of SLE,

which, on the other hand, demonstrates oral lesions in

25-40% of the patients (Schiodt 1984a, Pisetsky 1986,

Johnsson et al. 1988). The characteristic bordeaux-col-

ored "butterfly" skin lesions are photosensitive, scaly,

erythematous macules located on the bridge of the

nose and the cheeks (Standefer & Mattox 1986). The

systemic type, which can still be fatal because of neph-

rological and hematological complications, also has

skin lesions on the face but they tend to spread over

the entire body.

The diagnosis is based on clinical and his-

topathological findings. The epithelial changes, char-

acteristic of oral LE lesions, are hyperkeratosis, keratin

plugging and variation in epithelial thickness, lique-

faction degeneration of basal cells and increased

width of the basement membrane. The subepithelial

connective tissue harbors inflammation, sometimes

resembling OLP but often with a less distinct band-

shaped pattern (Schiodt & Pindborg 1984). Immuno-

histochemical investigation reveals deposits of vari-

ous immunoglobulins, C3 and fibrin along the base-

ment membrane (Reibel & Schiodt 1986).

Systemic corticosteroid and other anti-inflamma-

tory treatment regimens are required for SLE. Addi-

tional topical treatment is sometimes needed for

symptomatic intraoral lesions to resolve.

Drug-induced mucocutaneous disorders

A number of drugs show reverse effects in the oral

mucosa. Best known in the periodontal field is gingi-

val hyperplasia related to intake of phenytoin, sodium

valproate, cyclosporine and dihydropyridines. Be-

cause these lesions to some extent are plaque depend-

ent, they are reviewed in Chapter 7. Other types of

drugs may give rise to EM as mentioned above.

Several other drugs may be associated with adverse

effects that include lesions of the oral mucosa. An

example is azathioprine, which is an antimetabolite

used for immunosuppression in the treatment of

autoimmune and other diseases and to prevent rejec-

NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS • 285

Fig. 12-41. Gingival discoid lupus erythematosus le-

sion. A central atrophic area with small white dots is

surrounded by delicate white striae.

Fig. 12-42. Atrophic gingival discoid lupus erythemato-

sus lesions may resemble plaque-induced gingivitis.

Areas of the gingival margin of normal color shows

that the lesions are not plaque-induced.

Fig. 12-43. Antimalarial drugs may result in brownish

gingival discoloration. This is a patient with discoid lu-

pus erythematosus receiving an antimalarial drug,

chloroquine, as part of the treatment regimen.

Fig. 12-44. Drug-induced stomatitis sometimes involve

the gingiva. This is a gingival lesion with ulceration

due to azathioprine, which is an antimetabolite used for

immunosuppression.

tion of transplants. Its mode of action is through inhi- idly proliferating tissues such as the bone marrow, the

bition of purine base synthesis, resulting in suppres- hair follicles, the gastrointestinal and the oral mucosa

sion of nucleic acid and protein synthesis, whereby the may thereby show side effects, oral ulceration being

immune response is inhibited at various stages. Rap- one such example. These ulcerations may include the

286 • CHAPTER 12

gingiva. Other examples of drugs frequently resulting

in adverse effects in the form of stomatitis are antineo-

plastic drugs used in cancer chemotherapy. Methotr-

exate is a cytostatic drug sometimes used in the treat-

ment of leukemia. Epithelial atrophy, superficial

sloughing, intense erythema and ulceration are char-

acteristic findings in the oral mucosa of patients with

adverse effects of the chemotherapeutic treatment (

Pindborg 1992) (Fig. 12-44). The ulcerative lesions are

frequent portals of entry for microorganisms from the

mouth, and thereby often sources of serious systemic

infection in patients with suppression of the bone

marrow and reduced defense systems against infec-

tion. Professional plaque removal, mouth rinsing with

0.1% chlorhexidine and prophylactic antibiotic regi-

men are important in such patients (Sonis 1998, Holm-

strup & Glick 2002).

Allergic reactions

Allergic manifestations in the oral mucosa are uncom-

mon. However, several mechanisms may be involved

in allergy, which are exaggerated immune reactions.

Oral mucosal reactions are type I reactions (immediate

type), which is mediated by IgE, or more often they

are type IV reactions (delayed type) mediated by T-

cells. The rare intraoral occurrence may be due to the

fact that much higher concentrations of allergen are

required for an allergic reaction to occur in the oral

mucosa than in skin and other surfaces (Amlot et al.

1985, Liiders 1987, Holmstrup 1999). This chapter in-

cludes allergies to dental restorative materials, tooth-

pastes, mouthwashes and food.

Dental restorative materials

The clinical manifestation of type IV allergy (contact

allergy) occurs after a period of 12 to 48 hours follow-

ing contact with the allergen. The oral mucosal affec-

tions have been denoted contact lesions and prior

contact with the allergen resulting in sensitization is

prerequisite for these reactions to occur (Holmstrup

1991). The oral mucosal reactions to restorative mate-

rials include reactions to mercury, nickel, gold, zinc,

chromium, palladium and acrylics (Ovrutsky & Uly-

anow 1976, Zaun 1977, Bergman et al. 1980, Council on

Dental Materials, Instruments and Equipment

Workshop 1984, Fisher 1987). The lesions, which may

sometimes affect the gingiva, have clinical similarities

with oral lichen planus affections, which is why they

are denoted OLL (see earlier in this chapter) or oral

leukoplakia (Fig. 12-45). They are reddish or whitish,

sometimes ulcerated lesions, but one of the crucial

diagnostic observations is that the lesions resolve after

removal of the offending material. Additional patch

testing to identify the exact allergen gives supplemen-

tary information, but for dental amalgam it has been

shown that there is no obvious correlation between the

result of an epicutaneous patch test and the clinical

result after removal of the fillings (Skoglund 1994). A

Fig. 12-45. Lichenoid contact lesion of left buccal mu-

cosa due to type IV hypersensitivity to mercury. The le-

sion is confined to the zone of contact with the amal-

gam fillings. These lesions usually recover after replace-

ment of the mercury containing fillings with compos-

ites or other materials devoid of allergy provoking com-

ponents.

clinical manifestation confined to the area of contact

with the offending restorative material and the result

after replacing this material reveals the diagnosis (

Holmstrup 1999).

Reactions to oral hygiene products, chewing gum

and food

Toothpastes, mouthwashes and chewing gum

Contact allergy rarely occurs after the use of tooth-

pastes (Sainio & Kanerva 1995, Skaare et al. 1997,) and

mouthwashes (Sainio & Kanerva 1995). The constitu-

ents responsible for the allergic reactions may be fla-

vor additives, for instance carvone and cinnamon (

Drake & Maibach 1976) or preservatives (Duffin &

Cowan 1985). The flavoring constituents maybe used,

also, in chewing gum and result in similar forms of

gingivostomatitis (Kerr et al. 1971). The clinical mani-

festations of allergy include a diffuse fiery red edema-

tous gingivitis sometimes with ulcerations or whiten-

Fig. 12-46. Diffuse gingivitis and cheilitis due to contact

allergy to flavor additive in dentifrice.

NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS • 287

ing (Fig. 12-46). Similar affections may involve the

labial, buccal and tongue mucosa and in addition

cheilitis may be seen. The clinical manifestations,

which are characteristic, form the basis of the diagno-

sis, which may be supported by resolving of the le-

sions after cessation of using the allergen-containing

agent (Holmstrup 1999).

Foods

Allergic reactions attributable to food may manifest

both as type I and type IV reactions. Type I reaction

with severe swelling has been described after intake

of food components such as peanuts and pumpkin

seed. Birch pollen allergy is associated with some

types of oral mucosa allergy, and more than 20% of

patients with oral allergy may be hypersensitive to

kiwi, peach, apple, chestnut and salami (Yamamoto et

al. 1995, Antico 1996, Asero et al. 1996, Liccardi et al.

1996, Rossi et al. 1996, Helbling 1997, Wutrich 1997).

Another food allergen resulting in gingivitis or

gingivostomatitis is red pepper (Serio et al. 1991,

Hedin et al. 1994). Unless it has been demonstrated

that the lesions resolve after removal of the allergen,

the diagnosis is difficult to establish.

Other gingival manifestations of systemic

conditions

Gastro-intestinal diseases

Crohn's disease

Crohn's disease is characterized by chronic granu-

lomatous infiltrates of the wall of the last ileal loops,

but any part of the gastro-intestinal tract can be af-

fected.

The oral cavity is part of the gastrointestinal tract.

It is thus not surprising that Crohn's disease can occur

from the rectum to the lips. The number of reports of

lesions involving the periodontium is limited (van

Steenberghe et al. 1976), which is probably related to a

tradition by many clinicians of using the term aphtous

lesions for any ulcerative disease of the oral mucosa.

The oral lesions have striking similarity with those of

the intestinal tract as revealed by rectoscopy, i.e.

irregular long ulcerations with elevated borders with

a cobblestone appearance. Usually, the periodontal

lesions appear after the diagnosis has been establ-

ished on the basis of the intestinal affection, but some-

times the oral lesions are the first findings leading to

the diagnosis (Fig. 12-47). Exacerbations of the oral

lesions appear in parallel with those of the intestine.

An increased risk of periodontal destruction has been

reported associated with a defective neutrophil func-

tion (Lamster et al. 1982).

The term orofacial granulomatosis has been used

as a collective diagnosis of Crohn's disease, Melkers-

son-Rosenthal syndrome and sarcoidosis, because

these diseases show the same histopathologic fea-

tures, i.e. non-caseating, epitheloid cell granulomas in

Fig. 12-47. Crohn's disease often presents oral, includ

ing gingival, lesions with mucosal hyperplasia. This is

a granulomatous gingival hyperplasia of the upper in-

cisor region.

Fig. 12-48. Granulomatous gingival hyperplasia may

be due to sarcoidosis, which is one of the orofacial

granulomatosis, including also Crohn's disease and

Melkersson-Rosenthal syndrome.

the affected tissue; although rarely, all three diseases

may present gingival lesions, characterized by swel-

lings (Pindborg 1992), sarcoidosis sometimes being

fiery red granular gingival overgrowth (Fig. 12-48).

Among 45 cases of oral sarcoidosis, 13% had gingival

lesions (Blinder et al. 1997).

The local treatment consists of corticoid paste ap-

plication daily or twice daily during painful exacerba-

tions and a meticulous oral hygiene to reduce addi-

tional inflammation of the oral cavity.

Hematological disorders

Leukemia

Leukemia is a malignant hematological disorder with

abnormal proliferation and development of leuko-

cytes and their precursors in blood and bone marrow.

It can involve any of the subsets of leukocytes, poly-

morphonuclear leukocytes, lymphocytes or mono-

cytes. The normal hematopoiesis is suppressed and, in

most cases of leukemia, the white blood cells appear in

the circulating blood in immature forms. The

leukemic cell proliferation at the expense of normal

hematopoietic cell lines causes bone marrow failure

and depressed blood cell count. As a consequence of

the inability to produce sufficient functional white

blood cells and platelets, death may result from infec-

288 • CHAPTER 12

Fig. 12-49. Acute myelogenous leukemia with exten

sive swelling of the gingiva.

Fig. 12-50. Acute lymphocytic leukemia with gingival

ulceration in a child.

Fig. 12-51. Acute myelogenous leukemia with petec-

chia and swelling of the gingiva. This patient had sev-

eral episodes of spontaneous bleeding from the

gingiva, which prevented oral hygiene procedures

from being undertaken.

tion or bleeding associated with neutropenia and

thrombocytopenia.

The classification of leukemia is based on its course,

acute or chronic, and origin of cells involved. The basic

forms are: acute lymphocytic leukemia (ALL), acute

myelogenous leukemia (AML), chronic lymphocytic

leukemia (CLL) and chronic myelogenous leukemia (

CML). Acute leukemias have an aggressive course

resulting in death within 6 months if untreated. They

occur rather seldom and patients are usually either

under 20 or over 60 years of age. Chronic leukemias,

of which the lymphocytic form is the most common,

have less pronounced bone marrow failure and a more

indolent course usually lasting several years. They

occur during adulthood and normally after the age of

40. Whereas the peripheral granulocyte count is mark-

edly elevated in chronic leukemia, it may be elevated,

decreased or normal in acute leukemia (McKenna

2000).

Gingival manifestations in leukemia, which in-

clude extensive swelling (Fig. 12-49), ulceration (Fig.

12-50), petecchia (Fig. 12-51), and erythema, are much

more common in acute than in chronic forms. Some-

times the manifestations lead to the diagnosis of leu-

kemia. Thus, 69% of patients with acute leukemia had

oral signs of leukemia on examination and 33% of the

patients had gingival swelling (Pindborg 1992). In

another study gingival swelling was revealed in 21%

of AML patients but in no patients with ALL (Meyer

et al. 2000). The latter group, on the other hand,

showed both gingival erythema and ulcer in 36%. In

leukemic children, only 10-17% appear to possess gin-

gival swelling (Curtis 1971, Michaud et al. 1977). The

pronounced gingival swelling seen in leukemic pa-

tients is mostly due to plaque-induced inflammation,

since a stringent plaque control appears to resolve the

swelling (Barrett 1984), but it may be due to the pres-

ence of leukemic infiltrates, although this has been

NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS •

289

reported to be an uncommon feature of leukemic pa-

tients (Barrett 1984). Due to secondary thrombocy-

topenia, gingival bleeding is a common sign in

leukemic patients. It has been reported as the initial

4.4% of patients with chronic forms (Lynch & Ship

1967).

In general, the periodontal treatment of patients

with leukemia is important, and it aims at reducing

plaque as a source of bacteremia and damage to the

periodontal tissues both during disease and during

periods of chemotherapy. In such periods, potentially

pathogenic bacteria occur in plaque simultaneous

with granulocytopenia in these patients (Peterson et

al. 1990). The reduction of periodontal inflammation

may also prevent episodes of gingival bleeding. As

with many other patients, chemical plaque control in

combination with mechanical debridement appears to

be most effective and is the preferred method of peri-

odontal therapy in leukemic patients (Holmstrup &

Glick 2002). However, the increased tendency to

bleeding in many of these patients may necessitate the

use of methods alternative to toothbrushing. A study

of professional plaque removal preceding mouth-

rinsing with 0.1% chlorhexidine in patients with AML

showed that the additional initial removal of plaque

and calculus was more effective in reducing gingival

inflammation than mouthrinsing with chlorhexidine

alone (Bergman et al. 1992). A one-day antibiotic pro-

phylaxis regimen with a combination of piperacillin

and netilmicin was given prior to and after the me-

chanical debridement.

Periodontal treatment always involves a close co-

operation with the medical department or specialist

responsible for coordination of the patient's treat-

ment.

TRAUMATIC LESIONS

The background of traumatic lesions of the oral tissues

may be factitious, iatrogenic or accidental. Chemical

as well as physical and thermal injuries may affect the

periodontium (Armitage 1999).

Chemical injury

Surface etching by various chemical products with

toxic properties may result in mucosal reactions in-

cluding reactions of the gingiva. Chlorhexidine-in-

duced mucosal desquamation (Flotra et al. 1971,

Almquist & Luthman 1988) (Fig. 12-52), acetylsalicylic

acid burn (Najjar 1977), cocaine burn (Dello Russo &

Temple 1982), and slough due to dentifrice detergents

are examples of such reactions (Muhler 1970). These

lesions are reversible and resolve after quitting the

toxic influence. Another chemical injury to the gingi-

val tissue may be caused by incorrect use of caustics

Fig. 12-52. Chlorhexidine-induced mucosal desquama

tion. This is a reversible type of lesion, which is com

pletely normalized after stopping chlorhexidine use.

by the dentist. Paraformaldehyde used for pulp mum-

mification may give rise to inflammation and necrosis

of the gingival tissue if the cavity sealing is insufficient

(Di Felice & Lombardi 1998). Usually, the diagnosis is

obvious from the clinical findings and the patient

history.

Physical injury

Oral hygiene agents and inexpedient procedures can

be injurious to the gingival tissues. If the physical

traumas are limited, the gingival response is hyper-

keratosis, resulting in a white leukoplakia-like, fric-

tional keratosis (Fig. 12-53). In case of more violent

trauma the damage varies from superficial gingival

laceration to major loss of tissue resulting in gingival

recession (Axell & Koch 1982, Smukler & Landsberg

Fig. 12-53. Frictional keratosis due to violent tooth-

brushing. Note the cervical abrasion of adjacent

teeth.

290 • CHAPTER 12

Fig. 12-54. Gingival wounding due to improper tooth-

brushing. Note the characteristic horizontal extension of

the lesion and the non-inflamed interdental papillae.

Fig. 12-55. Gingival wounding due to improper tooth-

brushing. Note the characteristic horizontal extension of

the lesion, which affects the most prominent part of the

tooth arch.

Fig. 12-56. Self-inflicted gingival recession with ulcer-

ated margin due to 7-year-old child's scratching with

fingernail.

Fig. 12-57. Self-inflicted gingival ulceration with bleed-

ing surface caused by finger scratching.

NON-PLAQUE INDUCED INFLAMMATORY GINGIVAL LESIONS • 291

1984). Abrasivity of dentifrice, great brushing force

and horizontal movement of the toothbrush contrib-

ute to the gingival injury even in young patients.

Characteristic findings in these patients are extremely

good oral hygiene, cervical tooth abrasion, and unaf-

fected tops of the interdental papillae in the site of

injury (Figs. 12-54 and 12-55). The disease has been

termed traumatic ulcerative gingival lesion (Axell &

Koch 1982). Dental flossing may also cause gingival

ulceration and inflammation primarily affecting the

top of the interdental papillae. The prevalence of such

findings is unknown (Gillette & Van House 1980). The

diagnosis of physical injuries is based on the clinical

findings. An important differential diagnosis is ne-

crotizing gingivitis (Blasberg et al. 1981), see Chapter

10. The latter normally reveals itself as a necrotic

gingival margin and interdental papillae, while

brushing trauma leads to ulcerations of a few millime-

ters of the gingival margin.

A type of physical injury to the gingival tissues is

self-inflicted. Sometimes the lesions are termed gingi-

vitis artefacta. The lesions often show ulceration of the

gingival margin often associated with recession (Fig.

12-56). Such lesions are most common in children and

young individuals and two-thirds appear to involve

female patients. Picking at or scratching the gingiva

with a finger or a fingernail usually produces the

lesions, which may be hemorrhagic (Fig. 12-57). Some-

times the lesions are made by instruments (Pattison

1983). The correct diagnosis is often difficult to establ-

ish based on clinical findings, and identification of the

offending agent may be impossible.

Thermal injury

Extensive thermal burns of the oral mucosa are very

rare, but minor burns particularly from hot beverages

are seen occasionally. Their predilection by site is the

palatal and labial mucosa but any part of the oral

mucosa can be involved including the gingiva (Colby

et al. 1961). The area involved is painful and erythe-

matous and may slough a coagulated surface. Vesicles

may also occur (Laskaris 1994) and sometimes the

lesions present as ulceration, petecchia or erosion (Fig.

12-58). Obviously, the history is important for reach-

ing the correct diagnosis. Common causes are hot

coffee, pizza and melted cheese, but dental treatments

involving improper handling of hot hydrocolloid im-

pression material, hot wax or cautery instruments are

other causes (Colby et al. 1961).

Foreign body reactions

Another type of tissue reaction is established through

epithelial ulceration that allows entry of foreign ma-

terial into gingival connective tissue. This can happen

Fig. 12-58. Thermal burn with slight erosion of palatal

gingiva due to hot coffee intake.

Fig. 12-59. Amalgam tattoo of attached gingiva.

via abrasion or cutting (Gordon & Daley 199Th), a

route of tissue injury, which is best exemplified by the

amalgam tattoo (Buchner & Hansen 1980) (Fig. 12-59).

Gingival inflammation associated with foreign bodies

has been termed foreign body gingivitis. A clinical

study of this condition has shown that it often presents

as a red or combined red/white painful chronic lesion

frequently misdiagnosed as lichen planus (Gordon &

Daley 1997a). An X-ray microanalysis of foreign body

gingivitis showed that most of the identified foreign

bodies were of dental material origin, usually abra-

sives (Gordon & Daley 199Th). Another way of intro-

ducing foreign substances into the tissues is self-in-

flicted injury, for instance due to chewing on sticks or

self-induced tattooing (Gazi 1986). It is uncertain

whether the inflammatory reaction in such cases is

due to a toxic or in some instances an allergic reaction.

292 • CHAPTER 12

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