Oral Mucosal Lesions Associated with the Wearing of Removable Dentures

Journal of Oral Pathology 1981: 10: 65-80

Review Article

Oral mucosal lesions associated with the wearing ofremovable denturesEJVIND BUDTZ-J0RGENSEN

Department of Prosthetic Dentistry, Royal Dental College, Arhus , Denmark.

Abstract. Lesions of the oral mucosa associated with wearing of removable denturesmay represent acute or chronic reactions to microbial denture plaque, a reaction toconstituents of the denture base material, or a mechanical denture injury. Thelesions constitute a heterogeneous group with regard to pathogenensis. They in-clude denture stomatitis, angular cheilitis, traumatic ulcers, denture irritationhyperplasia, flabby ridges, and oral carcinomas. Denture stomatitis is the mostcommon condition which affects the palatal mucosa in about 50% of wearers ofcomplete or partial removable dentures. Most of the lesions are caused by chronicinfection (Candida albicans) or mechanical injury whereas allergic reactions to thedenture base materials are uncommon. Angular cheilitis (lesions of the angles of themouth) is characterized by maceration, erythema and crust formation. The preva-lence is about 15% among wearers of complete dentures. The lesions have aninfectious origin but several local, including prosthetic, or systemic predisposingconditions are usually present. Traumatic ulcers caused by dentures withoverextended or unbalanced occlusion are seen in about 5% of denture wearers.Denture irritation hyperplasia, which is caused by chronic injury of the tissue incontact with the denture border, is present in about 12% of denture wearers.Flabby ridge, which is replacement of alveolar bone by fibrous tissue, is present in10-20%. Finally, there is evidence that chronic injury of the oral mucosa by de-ntures in rare instances may predispose to development of carcinomas. Most typesof lesions are benign and quite symptomless. However, diagnosis may be difficultand the more severe and dramatic tissue reactions to dentures may indicate under-lying systemic diseases. In order to prevent or minimize the extent of the lesions,denture wearers should be recalled regularly for an examination of the oral cavityand the dentures. It is important that the examination is carried out by a person whohas adequate medical knowledge.

Accepted for publication 6 October 1980

Lesions of the oral mucosa associated with the denture base material or a mechanical denturewearing of removable dentures may represent injury. Among the acute reactions are trau-acute or chronic reactions to microbial den- matic ulcers, allergic reactions to dentureture plaque, a reaction to constituents of the materials, or acute infections. Among the

0300-9777/81/020065-16 $02.50/0 1981 Munksgaard, Copenhagen5 Oral Pathology

66 BUDTZ-J0RGENSEN

chronic reactions are denture stomatitiscaused by chronic infection or trauma, angularcheilitis, denture irritation hyperplasia, flabbyridges, and oral carcinomas. Chronic reactionsare the most frequent. Angular cheilitis mayhave a multicausal etiology and is not neces-sarily related to the presence of dentures.Only a minor part of oral carcinomatous le-sions have a possible association with thewearing of dentures.

Dentures may be the direct cause of theseconditions, due to changing of the environ-mental conditions of the oral cavity and load-ing of the oral mucosa. However, systemicconditions and general diseases may influencethe oral environment and alter tissue re-sponses and resistance. Oral lesions in denturewearers thus constitute a heterogenous groupof tissue changes both with regard topathogenesis, clinical and histopathologicalappearance and possible complications. Inorder to make a proper diagnosis and to in-stitute a relevant therapy and prophylaxis, it is

necessary that the therapeutist has adequatemedical knowledge and that appropriate clini-cal and laboratory examinations are per-formed. It is the purpose of the present surveyto review the literature on clinical featuresand histopathology, and to evaluate etiologi-cal and diagnostic aspects of these pathologi-cal conditions.

Denture stomatitis

Denture stomatitis (denture sore mouth) is aterm used to describe inflammatory changesin the oral mucosa of denture-bearing tissues.These changes are characterized by erythemaand are found under complete or partial den-tures in both jaws, but more frequently in themaxilla. Denture stomatitis can be gradedclinically into three types (Newton 1962);type I shows localized inflammation or pin-point hyperemia; type II shows more diffuseerythema, and type III is a "non-neoplastic"

Table 1. Frequencies of denture stomatitis.

Year

:952l>19642>1967^'1967^'1970^'1972^'1973^'

19748'

19755>

1975^'1976^^'

Country

SwedenSwedenUK

UK

SwedenDenmarkUK

Finland

DenmarkUK

Sweden

No.examined

1,09090

171

522

168

303

206

106

463

7002,277

Age

>20

>29

>65

>20

>60

>20

>65

>20

>65>20

65-74

Per cent

affected

27

47

40

43546717

63 (upper jaw)29 (lower jaw)6514 (type III)36

Descriptionof subjects

Non-randomizedNon-randomizedRandomizedNon-randomizedNon-randomizedNon-randomizedNon-randomized

Non-randomized

RandomizedNon-randomizedRandomized; subjectswith natural teeth ordentures

1. Nyquist; 2. Bergman et al.; 3. Swallow & Adams; 4. Love et al.; 5. Marken & Hedegard; 6.Budtz-J0rgensen; 7. Ritchie; 8. Makila; 9. Budtz-Jorgensen et al.; 10. Ettinger; 11. Axell.*For details: see text.

ORAL LESIONS IN DENTURE WEARERS 67

papillary hyperplasia with inflammation to avarying degree. The papillary hyperplasia isusually localized to the central part of the hardpalate and may be either nodular or mossy inappearance (Ettinger 1975). Type III is seenoften in association with type I or type IL

In selected populations of denture wearersthe prevalence of denture stomatitis has beenshown to vary from 15 to 65% (Table 1). In astudy of 463 randomly selected geriatric den-ture wearers the prevalence of denturestomatitis was found to be as high as 65%(Budtz-j0rgensen et al. 1975). In a study of alarge, randomized group aged 65-^ 74 theprevalence was 36% (Axell 1976); however,this group consisted of denture wearers as wellas subjects with natural teeth and not wearingdentures. The lesions are seen more fre-quently among women than men (Love et al.1967, Bergman et al. 1971, Ettinger 1975).Denture stomatitis may be associated with an-gular cheilitis and glossitis, but subjectivesymptoms are rare (Makila 1969, Davenport1970, Budtz-j0rgensen 1972, Ettinger 1975).

1. PathologyHistopathological changes associated withdenture stomatitis are non-specific and varywith the severity of the lesion. The epithelialchanges include parakeratosis or no keratini-zation, epithelial atrophy, epithelial hyper-plasia and acanthosis; in the lamina propriathere is a chronic inflammation (Ostlund1958, Budtz-Jorgensen 1970, Anneroth &Wictorin 1975, van Mens et al. 1975, Wicto-rin et al. 1975). Electron microscopic studiesof type II and type III lesions have shown ab-sence of keratohyaline granules in the superfi-cial epithelial layers, increase of the intracel-lular spaces of the spinous layer, and infiltra-tion by mononuclear cells in the epithelium(Wictorin et al. 1975). Histochemicaltechniques have demonstrated intracellulardeposits of glycogen in the spinous layer.

which may indicate metabolic disturbances(Budtz-J0rgensen 1970, Flanagan & Porter1971). Invasion of the epithelium by yeastcells or bacteria is seen only incidentally(Cawson 1966, Budtz-Jorgensen 1970).There is no evidence from histological andhistochemical studies of epithelial dysplasia orneoplasia in type III lesions (Bhaskar et al.1970, Flanagan & Porter 1971).

The exfoliative-cytological picture in den-ture stomatitis is characterized by nucleatedepithelial cells with or without cytoplasmaticglycogen and polymorphonuclear leukocytesin varying numbers (Ritchie et al. 1969,Budtz-Jorgensen 1970, Kaaber & Bertram1971).

The permeability of the palatal mucosa towater and salts is increased in patients witheven slight inflammatory changes (Riber &Kaaber 1976, 1978). It is likely, therefore,that the inflamed palatal mucosa will bepermeable to microbial toxins, antigens andantibodies, as are the inflamed gingivae.

2. Etiology

The etiology of denture stomatitis is mul-ticausal. A wide range of both local and sys-temic predisposing conditions may be in-volved in the pathogenesis. The significantdirect causes of denture stomatitis are infec-tion and mechanical irritation and less fre-quently primary toxic or allergic reactionsprovoked by constituents of the denture basematerial (Neill 1965).

2.1. Tissue response to infections. The first torelate the presence of Candida with denturestomatitis was probably Cahn (1936). Thecausal relationship has subsequently beensupported by mycological and immunologiealstudies (Lehner 1965, Cawson 1966,Budtz-j0rgensen & Bertram 1970a, b, Budtz-J0rgensen 1972). The infection is primarilydue to a contamination of the fitting surface of

68 BUDTZ-J0RGENSEN

the dentures by yeasts (Davenport 1970,Budtz-Jorgensen 1972, Olsen 1974, Budtz-Jorgensen et al. 1975, Bergendal et al. 1979,Renner et al. 1979). Actual tissue invasion byyeasts is seen only incidentally (Cawson1966). A few studies have tried to demon-strate a causal relationship between bacterialinfection and denture stomatitis, but no defi-nite proofs have been obtained (Nyquist1953, Van Reenen 1973). The microflora indenture wearers without inflammation seemsto be mainly bacterial (Budtz-Jorgensen et al.1980, Theilade et al. 1980).

2.2. Tissue response to trauma. Several studieshave provided evidence that denturestomatitis is present more frequently in pa-tients with poor-fitting dentures with a non-balanced occlusion (Nyquist 1952, Bergmanet al. 1964, Budtz-Jorgensen & Bertram1970a, Bastiaan 1976). It is assumed thatpin-point hyperemia in the palate (type I) isdue to occlusion of the salivary ducts by aclose-fitting denture (Newton 1962). Healingof denture stomatitis has been reported sub-sequent to prosthetic treatment (Nyquist1952, Bastiaan 1976); however, oral hygienewas not controlled. Other workers believedthat trauma was of minor importance, sincethe lesions healed following meticulous oralhygiene without correction of the dentures(Andrup et al. 1977). In another study, it wasshown that type I lesions responded to cor-rective prosthetic treatment and it was con-cluded that these lesions had a traumaticorigin (Budtz-Jergensen & Bertram 1970b).It has been proposed that type III lesions ofdenture stomatitis are caused by a local nega-tive pressure beneath the denture, which willinitiate a papillary outgrowth (Lambson1966).

2.3. Tissue response to denture base materials.Denture acrylics may cause tissue damage dueto a chemical/toxic irritation or by triggering

an allergic reaction. It seems that epicutane-ous testing with high concentrations of an al-lergen will provoke a toxic reaction whereasdilute solutions of the allergen will ratherelicit an allergic reaction in a sensitized indi-vidual (Greither 1954, Nielsen & Klaschka1971). On the other hand, relatively high con-centrations of an allergen are necessary toelicit an allergic reaction in the oral mucosa. Itis, therefore, difficult to prove whether amucosal reaction has a primary toxic or aller-gic nature. A chemical/toxic irritation due to arelease of acrylic monomer is not likely tooccur in denture wearers. Thus, denturescontaining as much as 35 % free acrylicmonomer did pot cause any mucosal inflam-matory response (Axelsson & Nyquist 1962).Furthermore, a significant release of acrylicmonomer will take place in new denturesonly, and will be quite temporary (Smith &Bains 1956). Contact allergic, i.e. im-munologic, responses to components of thedenture acrylic resin seem to be no more thanan incidental complication to the wearing ofcomplete dentures. According to some casereports, an allergic reaction may occur due tosensitization to acrylic monomer, hydrochi-non, and formalin (Langer 1956, Crissey1965, Stungis & Fink 1969, Rossbach 1975,Giunta & Zablotsky 1976). It is a characteris-tic feature that the tissue response is acute,showing edema and erythema with burningand itching pain. In a gas chromatographicstudy it was shown that acrylic monomerleached from dentures, which had been in usefor several weeks, in sufficient concentrationto give rise to an allergic reaction (McCabe &Basker 1976). Furthermore, it is possible tosensitize various animal species and man ex-perimentally to acrylic monomer (Nyquist1952, Magnusson & Kligman 1969). Thusdenture stomatitis may be the clinicalmanifestation of an allergic reaction to sub-stances released from the denture base; how-ever, the diagnosis is difficult to establish(Kaaber et al. 1979).


2.4. Thermal irritation. Slightly elevatedtemperatures on the palatal mucosa have beendemonstrated in denture wearers sufferingfrom itching and burning pain (Ernst &Wagner 1974). It is not likely, however, thatthe rise of temperature produces a thermalirritation. It is possible that a sHght elevationof the temperature beneath the denture maystimulate multiplication of micro-organismson the mucosa and the tissue surface of thedenture.

3. Predisposing conditions

3.1. Oral hygiene. Subsequent to total toothextraction, a reduction in the concentration ofmicro-organisms in the oral cavity has beenobserved, but following insertion of denturestheir numbers increased again, in particularthe lactobacilli and yeasts (Lilienthal 1950,Bartels 1965). Dentures, therefore, seem toprovide environmental conditions for thepropagation of micro-organisms. Further-more, it was found necessary to cover the mu-cosa by a plate in order to produce an experi-mental infection with C. albicans in the palateof monkeys (Budtz-Jergensen 1971).

Denture plaque accumulations tend to de-crease pH on the palatal mucosa (Zgraggen &Graf 1975), and consumption of carbohy-drates produces a further drop in pH as-sociated with a more severe inflammation anda heavy outgrowth of yeasts on the denture(Olsen & Birkeland 1976, 1977). It is likelythat the acid and relatively anaerobic milieubeneath the dentures is conducive to yeastproliferation and a Candida-'xnducQd denturestomatitis. By means of disclosing solutionslarger accumulations of denture plaque havebeen revealed in patients with denture sto-matitis (Budtz-J0rgensen & Bertram 1970a,Bastiaan 1976). This plaque has the samebasic structure as dental plaque (Theilade &Budtz-j0rgensen 1980). It has been shownthat denture stomatitis will tend to resolve

following institution of plaque control bymechanical or chemical means (Budtz-Jorgensen & Loe 1972, Lindquist et al. 1975,Andrup et al. 1977). Together, these findingsindicate that poor oral and denture hygiene isa major predisposing condition for Candida-induced denture stomatitis.

3.2. Denture base. Micropits and micro-porosities in the denture base may predisposeto denture plaque accumulation. A therapeu-tic effect of lining the denture base withgold-foil has been reported (Nyquist 1952,Spreng 1963). In these studies it was assumedthat gold-foil might have a therapeutic effect,either by reducing trauma or by disrupting thecontact between the allergen (the denturebase) and the palatal mucosa. It is, perhaps,more likely that gold-foil may have therapeu-tical significance by disrupting any contactbetween the contaminated denture base andthe palatal mucosa.

3.3. Denture usage. There is conflicting evi-dence whether the wearing of dentures atnight will increase the susceptibility for den-ture stomatitis (Nyquist 1952, Love et al.1967, Budtz-J0rgensen & Bertram 1970a,Bergman et al. 1971, Ettinger 1975). Sinceleaving out the dentures for 2 weeks will causea spontaneous healing of the mucosa (Turrell1966) it is likely that wearing the dentureconstantly will predispose both for infectionand mechanical irritation of the palate.

3.4. Systemic factors. A number of systemicdiseases and treatments with various drugsmay increase the susceptibility to oral can-didosis and the harmful effect of mechanicalirritation. The systemic factors include endo-crine disturbances (diabetes mellitus, hypo-thyraidism), nutritional deficiencies (iron-deficiency, high carbohydrate intake), malig-nant diseases (leukemia), agranulocytosis and

B UDTZ-J0RGENSEN

drugs such as sedatives, antibiotics, and ste-roids (Winner 1969, Budtz-Jorgensen 1974).One of the adverse effects of therapy withsedatives is xerostomia, which in turn will re-duce the resistance of the oral mucosa totrauma and infection. In these patients symp-toms in association with denture stomatitis areusually pronounced. Nutritional deficienciessuch as deficiency in amino acids, iron andcertain vitamins of the B complex are reputedto lower the resistance of the oral mucosa. Ithas been shown that dietary supplements ofproteins and minerals will increase toleranceto the dentures and cause the inflammation toresolve (Kim et al. 1962, Deely 1965).

4. Diagnosis

It is the purpose of the clinical examination toreveal the direct causes of denture stomatitis(infection, trauma or allergy) as well as possi-ble predisposing conditions in order to insti-tute a corrective therapy and achieve a per-manent cure.

4.1. Infection. The diagnosis of Candida-in-duced denture stomatitis is established bymaking a quantitative estimate of the out-growth of yeasts on the mucosa and the fittingsurface of the denture either by culture or bydirect microscopy of oral smears (Davenport1970, Budtz-J0rgensen 1974, Arendorf &Walker 1979, Renner et al. 1979). Materialfor microscopy or culture is collected byscraping the palatal mucosa or the denture.There is evidence of Candida infection if thedenture and the mucosa are densely colonizedby yeasts. A quantitative estimate of the out-growth of yeasts by culture may be obtainedby means of a miniaturized culture test system(Microstix-Candida, Ames Co., Div. MilesLab., Elkhart, Ind. U.S.A.). This test seems tobe an alternative to the conventional smear asa low-cost screening method for establishing

the diagnosis of candidosis (Budtz-Jorgensen1976).

4.2. Allergy. Immunological testing for allergyin denture stomatitis is only relevant if infec-tion or traumatic factors have been excluded,and if the clinical history and the appearanceof the lesion point to an allergic reaction, i.e.burning sensation and diffuse erythema withedema of the tissues in contact with the den-ture. However, the diagnosis is difficult toconfirm. Thus, a positive delayed hypersensi-tive cutaneous reaction after testing with basematerial from the denture in question mayrepresent mechanical irritation (Nyquist1952, Fisher 1956) or contaminating micro-organisms (Kotilainen 1972). In order to es-tablish a reliable diagnosis it is necessary toscreen the individual components of the den-ture acrylic resin (Kaaber et al. 1978). Thepatient should be referred to a dermatologistfor skin testing.

4.3. Predisposing conditions. If there is noresponse to local treatment, the diagnosisshould be reconsidered and the patient shouldbe referred for a medical examination. A per-sistent denture stomatitis may be a sign of anunderlying systemic disease.

Angular cheilitis

Angular cheilitis (perleche, angular stomati-tis) is the clinical diagnosis of lesions whichaffect the angles of the mouth. The lesions areinfectious in origin but several predisposingfactors may interact. Dentures are one of thepredisposing conditions which is the reasonfor including angular cheilitis among lesions ofthe oral mucosa associated with the wearing ofremovable dentures. Both the skin and themucosa of the commissure may be affectedand the lesion is characterized by maceration,erythema and crust formation. The commis-


Table 2. Frequencies of angular cheilitis in denture wearers.

Year

1962^)1969^'

1972^'

1973^)

1974^'

1976^'

Country

Sv;eden

Finland

Denmark

UK

Denmark

Sweden

Nq examined

1^ 093

339204

206

463

2_,277

Age

>20>20>20

>65

>65

65-74

Per cent

affected

30188

10

19

10

Description of subjects .

Non-randomized

Non-randomized

Non-randomized; with

denture stomatitis

Non-randomized

Randomized

Randomized; subjects withnatural teeth or dentures

1. Nyquist; 2. Makila; 3. Budtz-Jorgensen; 4. Ritchie; 5. Grabowski; 6. Axell.

sures appear wrinkled and with time deepfissures may develop with a tendency tobleeding.

The prevalence of angular cheilitis amongwearers of complete dentures has been shownto vary between 8-30% (Table 2). The lesionsseem to occur more frequently in non-insti-tutionalized subjects than in institutionalizedsubjects within the same age distribution(Nyquist 1962, Chrigstrom et al. 1970,Ritchie 1973, Grabowski 1974, Manderson &Ettinger 1975, Axell 1976). This may possiblyreflect the fact that institutionalized elderlypeople receive a more adequate diet and havebetter oral hygiene. Angular cheilitis is seenmore frequently in women than in men andthe condition seems to be associated with thewearing of removable dentures, but not withan edentulous statQperse (Rose 1968, Turrell1968, Makila 1969, Axell 1976).

7. Etiology

Angular cheilitis apparently has a variedetiology. There is good reason to believe thatthe direct etiological factor is infection byyeasts, staphylococci, or streptococci (Mac-Farlane & Helnarska 1976). It seems, how-

ever, that the infection is secondary to a localor systemic predisposing factor. Thus, topicalchemotherapy of the lesions will not producea permanent cure if the predisposing condi-tions are not removed (Lyon & Chick 1957,Cawson 1963, 1966, Budtz-Jorgensen &Bertram 1970b).

2. Predisposing conditions2.1. Vertical dimension of occlusion andlip-support. It is assumed that overclosure ofthe jaws will produce folds at the angles of themouth in which saliva tends to collect. Theskin subsequently becomes macerated, fis-sured and secondarily infected. Epidemiologi-cal studies have shown an association betweena decreased vertical dimension of occlusionand angular cheilitis (Marcussen 1944, Makila1969, Glantz & Bjorlin 1970, Ritchie &Fletcher 1973). Healing of the lesions hasbeen reported subsequent to prosthetic treat-ment including increasing the vertical dimen-sion of occlusion and building out the buccaldenture flanges to provide proper lip-support(Poyton 1955). Other studies have not showna systemic relationship between overclosureof the jaws and angular cheilitis, and healingof the lesions was reported after the dentures

72 BUDTZ-J0RGENSEN

had not been used for 2 weeks (Neill 1963,Turrell 1968). However, it seems justified toconclude that overclosure may be a predis-posing condition in some cases.

2.2. Denture stomatitis. Several studies haveshown that angular cheilitis occurs more fre-quently in patients with denture stomatitisthan in denture wearers with clinically normaloral mucosa (Lyon & Chick 1957, Cawson1963, Makila 1969, Budtz-j0rgensen 1972,Ritchie & Fletcher 1973). Healing of the an-gular lesions has been reported afterchemotherapy of denture stomatitis or whenthe patients left their dentures out of themouth (Cawson 1966, Turrell 1966, 1968,Budtz-j0rgensen & Bertram 1970b, Budtz-Jorgensen & Loe 1972, Olsen 1975a, b). It isbelieved, therefore, that the infection maystart beneath the maxillary denture and fromthat area spread to the angles of the mouth(Cawson 1966, Budtz-Jorgensen 1974). Fi-nally, the infection may spread from thecommissure to involve the retroangular mu-cosa (Crenea et al. 1965).

2.3. Carbohydrate consumption. A direct as-sociation between angular cheilitis and a largeintake of carbohydrates has been shown and itwas assumed that a high salivary concentra-tion of glucose predisposed to infection, inparticular by yeasts, in the angles of the mouth(Shuttleworth & Gibbs 1960, Neill 1963,Makila 1969, Ritchie & Fletcher 1973).

2.4. Avitaminoses. Avitaminoses may sup-press host resistance, thereby being the un-derlying predisposing condition for infectionof the angles of the mouth. The lesions willusually be bilateral and often be associatedwith glossitis, denture stomatitis, conjunc-tivitis and dermatitis (Shafer et al. 1974). De-ficiencies of B vitamins seem to be particularlyimportant predisposing conditions. Thus, adecreased plasma concentration of thiamine

and riboflavin was demonstrated in a group ofdenture wearers with angular cheilitis (Makila1969). In another study a decreased concen-tration of folic acid was demonstrated in agroup of denture wearers with angular cheili-tis (Rose 1971). Angular cheilitis has beenproduced experimentally by giving individualsa pyridoxine-deficient diet, and healing of thelesions was seen after administration of ribo-flavin, folic acid or pyridoxine (Smith & Mar-tin 1940, Sebrell & Harris 1954, Rose 1971).Other studies provided no evidence for anassociation between vitamin B deficiency andthe occurrence of angular cheilitis (Ellenberg& Pollack, 1942, Machella 1942).

2.5. Anemia. A simple iron deficiency anemiaseems to predispose to angular cheilitis. Thus,a significantly decreased concentration ofplasma iron was demonstrated in a group ofdenture wearers with angular cheilitis and thelesions healed when the diet was supple-mented with iron (Rose 1968). In anotherstudy a decreased plasma concentration ofiron was not present in a group of denturewearers with angular cheilitis although thepatients' diet seemed to be deficient in iron(Makila 1969). A chronic iron deficiencyanemia may give rise to the Plummer-Vinsonsyndrome which is characterized by angularcheilitis, glossitis, denture stomatitis, dys-phagia and spoon-shaped, brittle fingernails(Shafer et al. 1974). This condition is a pre-disposition for the development of carcinomain the upper alimentary tract.

3. DiagnosisThe reason for including angular cheilitisamong denture-induced lesions is the fact thatcomplete dentures may have both a direct andindirect etiologieal significance. Directly,overclosure, poor lip-support and denturestomatitis will predispose for an infection of


the angles of the mouth. Indireetly, poor-funetioning dentures may divert the patient'sehoiee of food to a defieient diet whieh mayresult in a state of nutritional defieieney. Aeorreet diagnosis, therefore, may be diffieultto establish beeause both loeal and systemiepredisposing eonditions may oeeur simul-taneously.

By inspeetion of the dentures it is importantto evaluate the vertieal dimension of oeelusioneorreetly and not uneritieally to assume it tobe lowered when the patient presents an an-gular eheilitis. The lesions should be eheekedfor a myeologieal infeetion. If the eliniealexamination indieates an underlying nutri-tional defieieney or if the lesions do not healfollowing prosthetie treatment or ehemo-therapy, the patient should be referred for athorough medieal examination. In partieular,it is important to make sure that the patientdoes not suffer from a Plummer Vinson syn-drome sinee this eondition may predispose toeareinomas of the oral eavity, hypopharynxand upper part of the esophagus.

Treatment and prevention of denturestomatitis and angular cheilitis

Denture stomatitis and angular eheilitis areeommonly present together. If the etiology ofthe lesions is the same, the lesions will oftenelear up together when the relevant therapy isinstituted. Prosthodonties, ehemotherapy, andremoval of dentures have been employed fortreating patients with denture stomatitis andangular eheilitis.

1. Prosthetic treatment

There is no doubt that providing the patientswith well-fitted, non-traumatizing dentures isan important measure in order to prevent ex-eessive bone resorption of the alveolar ridge

and leakage of saliva in the angles of themouth. There is, however, no evidenee thatsueh treatment will eure a Candida infeetionof the denture bearing tissues (Budtz-J0rgensen 1974).

2. Antimycotic therapy

Speeifie antimyeotie drugs, sueh as Nystatin,Amphoteriein B, or Natamyein have been ef-feetive when used topieally for treatment ofdenture stomatitis, angular eheilitis and glos-sitis (Ritehie et al. 1969, Budtz-Jergensen1974, Olsen 1975a, b). In type III lesions theinflammation will usually resolve, but thehyperplasia will persist. Mouth rinsing with a0.2% solution of Chlorhexidine glueonate ordisinfeetion of the dentures using Chlor-hexidine in a 2 % solution has redueed in-flammation and the number of yeasts har-bored on the mueosa and the dentures(Budtz-j0rgensen & Loe 1972, Olsen 1975a,b). However, reeurrenees have been frequentregardless of whether antimyeoties orChlorhexidine was used. To reduee the risk ofrelapse the following preeautions should betaken: treatment with antimyeotie antibiotiesshould eontinue for 2 to 4 weeks, and the pa-tient should be instrueted in metieulous oraland denture hygiene and to keep the denturesin a disinfeetant solution during the night.

3. Preventive measures

Candida-induced denture stomatitis as-soeiated with angular eheilitis is a frequentand reeurring eomplieation to the wearing ofdentures. Although denture stomatitis is aminor disorder, it should be prevented. It isnot known if the fit of the maxillary dentureeontributes to the infeetion. It ereates a rela-tively aeid and anaerobie milieu that providesoptimal environmental eonditions for yeastgrowth (Budtz-J0rgensen 1974). Further-more, it has been shown that polishing the

74 BUDTZ-J0RGENSEN

fitting surface of the denture provides an im-proved denture cleanliness with subsequenthealing of denture stomatitis (Andrup et al.1977).

Theoretically, the infection is prevented bymeticulous oral and denture hygiene. How-ever, it seems to be difficult to improve thehygienic care in denture wearers (Budtz-J0rgensen 1979). A wide range of denturecleansers are available, but the efficiency ofthese commercial products in removing mi-erobial plaque deposits on the dentures is notfully supported by experimental evidence(Budtz-j0rgensen 1979).

Simple, anti-microbial substances such asChlorhexidine or hypochlorites are effectivebut may cause staining or bleaching of thedentures, and it is not known whether they arebiologically acceptable when used for routinedenture cleansing.

Currently, the preventive measures to rec-ommend are: brush dentures carefully, in-cluding the fitting surface; discontinue wear-ing the dentures at night, and have theocclusion controlled regularly.

4. Conclusions

Denture stomatitis associated with angularcheilitis may have a multicausal etiology, butthere is evidence to suggest that most casesare associated with infection by yeasts, in par-ticular C. albicans. This infection usually doesnot reflect any deep-seated systemic abnor-mality. Most cases are relatively easilytreated, but recurrences are frequent and theinfection tends to spread to other parts of theoral mucosa. Therefore, preventive measuresshould be taken against colonization by Can-dida of the palatal mucosa and the dentures. Itshould be recognized that an oral Candidainfection may disseminate and be fatal in seri-ously ill patients, especially in those subjectedto prolonged treatment with antibiotics, cor-ticosteroids, or immunodepressive drugs.

Furthermore, a denture stomatitis or angularcheilitis refractory to chemotherapy may indi-cate severe underlying nutritional deficienciesor a systemic disease.

Flabby ridge

Flabby ridge (alveolar fibrosis), i.e. remova-ble and extremely resilient alveolar ridge, isdue to a replacement of bone by fibrous tis-sue. The condition is seen in a generalized anda localized form, the latter being confinedmost commonly to the anterior part of themaxilla. In non-randomized groups of denturewearers the prevalence has been reported tobe about 20% (Table 3). The condition isfound more often in women than in men andis usually located in the anterior region of themaxilla (J0lst 1963, Makila 1974). In patientsusing a full upper denture against a lowernatural dentition it appears forward from firstpremolars or canines. If the mucosa coveringthe alveolar ridge is inflamed, it may contrib-ute to the resorption of the alveolar ridge.Histological and histochemical studies offlabby ridges have shown marked fibrosis withinflammatory cell infiltrate and a striking vas-cular reaction (Wallenius & Heyden 1972).The underlying bone revealed resorption.Flabby ridges in denture wearers should beremoved surgically in order to minimizeprogressive reduction of residua! ridges.Flabby ridges may complicate impressiontaking and provide a poor support forremovable dentures. In patients with extremeatrophy of the maxillary alveolar ridge, flabbyridges should not be totally removed since theresilient ridge may create some retention forthe denture.

Denture irritation hyperplasia

A common tissue reaction to ill-fitting den-


Table 3. Frequencies of denture irritation hyperplasia and flabby ridge in denture wearers.

Year

1973I)

19742)

1974^)

1975^'

1976^)

1952^'

1974-^'

J 11976

Country

UK

Denmark

Finland

UK

Sweden

Sweden

Finland

Sweden

No,examined Age Per cent

affected

DENTURE IRRITATION HYPERPLASIA

206

463

133

442

2^277

FLABBY RIDGE

1^090

133

20,333

>65

>65

>20

>65

65-74

>20

>20

>15

3

26

8 (upper7 (lower6

11.5

719 (upper13 (lower8.7

jaw)jaw)

jaw)]aw)

Description of subjects

Non-randomized

Randomized

Non-randomized

Non-randomized


Non-randomizedNon-randomized


1. Ritchie; 2. Grabowski; 3. Makila; 4. Manderson & Ettinger; 5. Axell; 6. Nyquist.

tures is the occurrence of tissue hyperplasiaof the tnucosa in contact with the dentureborder (inflammatory hyperplasia, epulis fis-suratum, redundant tissue). In non-ran-domized groups of denture wearers dentureirritation hyperplasia was found in 5-10%(Table 3). In a large investigation on theprevalence of oral mucosal lesions in differentage groups denture irritation hyperplasia wasfound in 6.3% among subjects aged 55-64and in 11.5% among the subjects above theage of 65 (Axell 1976). The condition is seenmore frequently in women than in men and isusually located in the mucobuccal or mucola-bial folds (Joist 1963, Cooper 1964, Norden-ram & Landt 1969, Ralph & Stenhouse 1972,Cutright 1974, Axell 1976). The lesions arethe result of chronic injury by unstable den-tures or by thin, overextended dentureflanges. The proliferation of tissue may takeplace relatively quickly after prosthetic treat-

ment (Makila 1974). The lesions may besingle or quite numerous and are composed offlaps of hyperplastie connective tissue coveredby stratified squamous epithelium which usu-ally shows slight acanthosis (Cutright 1974,Shafer et al. 1974). Inflammation is variable;however, in the bottom of deep fissures severeinflammation and ulceration may occur.

After replacement or adjustment of thedentures the inflammation and edema maysubside and produce some clinical improve-ment of the condition. After surgical excisionof the tissue and replacement of the denture,the lesions are not likely to recur.

When pressure ulcerations develop and ir-ritation from microbial products is severe thepatient may experience marked discomfort.When such secondary infection of the in-volved tissues and associated lymphaden-opathy are present, the denture irritationhyperplasia may simulate a neoplastie process.

76 BUDTZ-J0RGENSEN

Traumatic ulcers

Traumatic ulcers (sore spots) most commonlydevelop within 1-2 days after insertion of newdentures. The ulcers are small and painful le-sions, covered by a grey, necrotic membraneand surrounded by an inflammatory halo withfirm, elevated borders. Traumatic ulcers havebeen found in 2-3% among institutionalizeddenture wearers (Chrigstrom et al. 1970,Ritchie 1973). In a randomized study of apopulation aged 65-74 years traumatic ulcerswere observed in 5.5% (Axell 1976). The di-rect cause of sore spots is overextended den-ture flanges, or unbalanced occlusion. Condi-tions which suppress resistance of the mucosato mechanical irritation are predisposing, e.g.nutritional deficiencies, diabetes mellitus orxerostomia. In the non-compromised hostsore spots will heal a few days after correctionof the denture. When no treatment is insti-tuted the patient will often adapt to the pain-ful situation. In these cases tissue proliferationaround the periphery of the lesion may giverise to a denture irritation hyperplasia.

Denture-induced carcinoma

In current textbooks on oral pathology it isusually claimed that the possibility of malig-nant transformation of denture induced le-sions should be considered. In extensive his-tological studies of type III lesions of denturestomatitis (papillary hyperplasia) there was,however, no evidence of epithelial dysplasiaor neoplasia (Bhasker et al. 1970, Flanagan &Porter 1971). In a retrospective study of 560patients with intraoral epidermoid car-cinomas, of whom 204 wore dentures, a directconnection between irritation by the pros-theses and development of carcinoma wasclaimed in 86 of the cases (Hobaek 1949).The carcinomas were localized to the palate.

the alveolar ridges and the mucobuccal andlingual folds. 70% of the tumors were foundin women, although oral carcinomas as awhole occur more frequently in men. An as-sociation between oral carcinoma and chronicirritation by dentures was supported by thefact that the prevalence of poor-fitting den-tures was higher in a group of denture wearerswith oral carcinoma than in a group of denturewearers with carcinomas in other parts of thebody (Wynder et al. 1957, Vogler et al. 1962).Case reports have detailed the developmentof oral carcinomas in patients wearing ill-fitt-ing dentures or dentures with a sucking disk(Persson & Wallenius 1961, Beyer & Pape1977). None of these studies seem to providedefinite evidence that oral carcinomas maydevelop due to chronic mechanical orchemical irritation by dentures; however, thestudies underline the necessity of strict andregular controls of all subjects wearingremovable dentures. The opinion is still validthat if a sore spot does not heal followingcorrection malignancy should be suspected(Pindborg 1973). Such cases and clinicallyaberrant manifestations of denture irritationhyperplasia should be immediately referred toan oral pathologist. It should be recognizedthat the prognosis is poor for oral carcinomas,especially for those in the floor of the mouth.

Acknowledgment

The present review is based on a report thatwas prepared in collaboration with and wasapproved by the Educational Committee ofScandinavian Society for Prosthetic Dentistry.The author is grateful to Prof. H. P. Philipsen,Royal Dental College, for valuable help inpreparing this manuscript.


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Address:Dr. Ejvind Budtz-JorgensenDepartment of Prosthetic DentistryRoyal Dental CollegeDK-8000 Arhus, Denmark

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Oral Mucosal Lesions Associated with the Wearing of Removable Dentures