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Review Article

Oral mucosal lesions associated with the wearing of

removable dentures

EJVIND BUDTZ-J0RGENSEN

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

Abstract. Lesions of the oral mucosa associated with wearing of removable dentures

may represent acute or chronic reactions to microbial denture plaque, a reaction to constituents of the denture base material, or a mechanical denture injury. The lesions constitute a heterogeneous group with regard to pathogenensis. They in-clude denture stomatitis, angular cheilitis, traumatic ulcers, denture irritation hyperplasia, flabby ridges, and oral carcinomas. Denture stomatitis is the most common condition which affects the palatal mucosa in about 50% of wearers of complete or partial removable dentures. Most of the lesions are caused by chronic infection (Candida albicans) or mechanical injury whereas allergic reactions to the denture base materials are uncommon. Angular cheilitis (lesions of the angles of the mouth) is characterized by maceration, erythema and crust formation. The preva-lence is about 15% among wearers of complete dentures. The lesions have an infectious origin but several local, including prosthetic, or systemic predisposing conditions are usually present. Traumatic ulcers caused by dentures with overextended or unbalanced occlusion are seen in about 5% of denture wearers. Denture irritation hyperplasia, which is caused by chronic injury of the tissue in contact 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 in 10-20%. Finally, there is evidence that chronic injury of the oral mucosa by de-ntures in rare instances may predispose to development of carcinomas. Most types of lesions are benign and quite symptomless. However, diagnosis may be difficult and 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 cavity and the dentures. It is important that the examination is carried out by a person who has adequate medical knowledge.

Accepted for publication 6 October 1980

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

0300-9777/81/020065-16 $02.50/0 © 1981 Munksgaard, Copenhagen

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66 BUDTZ-J0RGENSEN

chronic reactions are denture stomatitis caused by chronic infection or trauma, angular cheilitis, denture irritation hyperplasia, flabby ridges, and oral carcinomas. Chronic reactions are the most frequent. Angular cheilitis may have 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 the wearing of dentures.

Dentures may be the direct cause of these conditions, due to changing of the environ-mental conditions of the oral cavity and load-ing of the oral mucosa. However, systemic conditions and general diseases may influence the oral environment and alter tissue re-sponses and resistance. Oral lesions in denture wearers thus constitute a heterogenous group of tissue changes both with regard to pathogenesis, clinical and histopathological appearance and possible complications. In order to make a proper diagnosis and to in-stitute a relevant therapy and prophylaxis, it is

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

Denture stomatitis

Denture stomatitis (denture sore mouth) is a term used to describe inflammatory changes in the oral mucosa of denture-bearing tissues. These changes are characterized by erythema and are found under complete or partial den-tures in both jaws, but more frequently in the maxilla. Denture stomatitis can be graded clinically into three types (Newton 1962); type I shows localized inflammation or pin-point hyperemia; type II shows more diffuse erythema, 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 Sweden Sweden UK UK Sweden Denmark UK Finland Denmark UK Sweden No.examined 1,090 90 171 522 168 303 206 106 463 700 2,277 Age >20 >29 >65 >20 >60 >20 >65 >20 >65 >20 65-74 Per cent affected 27 47 40 43 54 67 17 63 (upper jaw) 29 (lower jaw) 65 14 (type III) 36 Description of subjects Non-randomized Non-randomized Randomized Non-randomized Non-randomized Non-randomized Non-randomized Non-randomized Randomized Non-randomized Randomized; subjects with natural teeth or dentures

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.

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papillary hyperplasia with inflammation to a varying degree. The papillary hyperplasia is usually localized to the central part of the hard palate and may be either nodular or mossy in appearance (Ettinger 1975). Type III is seen often in association with type I or type IL

In selected populations of denture wearers the prevalence of denture stomatitis has been shown to vary from 15 to 65% (Table 1). In a study of 463 randomly selected geriatric den-ture wearers the prevalence of denden-ture stomatitis was found to be as high as 65% (Budtz-j0rgensen et al. 1975). In a study of a large, randomized group aged 65-^74 the prevalence was 36% (Axell 1976); however, this group consisted of denture wearers as well as subjects with natural teeth and not wearing dentures. 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 subjective symptoms are rare (Makila 1969, Davenport 1970, Budtz-j0rgensen 1972, Ettinger 1975).

1. Pathology

Histopathological changes associated with denture stomatitis are non-specific and vary with the severity of the lesion. The epithelial changes include parakeratosis or no keratini-zation, epithelial atrophy, epithelial hyper-plasia and acanthosis; in the lamina propria there is a chronic inflammation (Ostlund 1958, Budtz-Jorgensen 1970, Anneroth & Wictorin 1975, van Mens et al. 1975, Wicto-rin et al. 1975). Electron microscopic studies of 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). Histochemical techniques have demonstrated intracellular deposits of glycogen in the spinous layer.

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

1970, Flanagan & Porter 1971).

The exfoliative-cytological picture in den-ture stomatitis is characterized by nucleated epithelial cells with or without cytoplasmatic glycogen and polymorphonuclear leukocytes in varying numbers (Ritchie et al. 1969, Budtz-Jorgensen 1970, Kaaber & Bertram

1971).

The permeability of the palatal mucosa to water and salts is increased in patients with even slight inflammatory changes (Riber «& Kaaber 1976, 1978). It is likely, therefore, that the inflamed palatal mucosa will be permeable to microbial toxins, antigens and antibodies, 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 significant direct causes of denture stomatitis are infec-tion and mechanical irritainfec-tion and less fre-quently primary toxic or allergic reactions provoked by constituents of the denture base material (Neill 1965).

2.1. Tissue response to infections. The first to

relate the presence of Candida with denture stomatitis was probably Cahn (1936). The causal relationship has subsequently been supported by mycological and immunologieal studies (Lehner 1965, Cawson 1966, j0rgensen & Bertram 1970a, b, Budtz-J0rgensen 1972). The infection is primarily due to a contamination of the fitting surface of

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68 BUDTZ-J0RGENSEN

the dentures by yeasts (Davenport 1970, Jorgensen 1972, Olsen 1974, Budtz-Jorgensen et al. 1975, Bergendal et al. 1979, Renner et al. 1979). Actual tissue invasion by yeasts is seen only incidentally (Cawson 1966). A few studies have tried to demon-strate a causal relationship between bacterial infection and denture stomatitis, but no defi-nite proofs have been obtained (Nyquist 1953, Van Reenen 1973). The microflora in denture wearers without inflammation seems to be mainly bacterial (Budtz-Jorgensen et al. 1980, Theilade et al. 1980).

2.2. Tissue response to trauma. Several studies

have provided evidence that denture stomatitis is present more frequently in pa-tients with poor-fitting dentures with a non-balanced occlusion (Nyquist 1952, Bergman et al. 1964, Budtz-Jorgensen & Bertram 1970a, Bastiaan 1976). It is assumed that pin-point hyperemia in the palate (type I) is due to occlusion of the salivary ducts by a close-fitting denture (Newton 1962). Healing of denture stomatitis has been reported sub-sequent to prosthetic treatment (Nyquist 1952, Bastiaan 1976); however, oral hygiene was not controlled. Other workers believed that trauma was of minor importance, since the lesions healed following meticulous oral hygiene without correction of the dentures (Andrup et al. 1977). In another study, it was shown that type I lesions responded to cor-rective prosthetic treatment and it was con-cluded that these lesions had a traumatic origin (Budtz-Jergensen & Bertram 1970b). It has been proposed that type III lesions of denture stomatitis are caused by a local nega-tive pressure beneath the denture, which will initiate a papillary outgrowth (Lambson

1966).

2.3. Tissue response to denture base materials.

Denture acrylics may cause tissue damage due to 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 whereas dilute solutions of the allergen will rather elicit an allergic reaction in a sensitized indi-vidual (Greither 1954, Nielsen & Klaschka 1971). On the other hand, relatively high con-centrations of an allergen are necessary to elicit an allergic reaction in the oral mucosa. It is, therefore, difficult to prove whether a mucosal reaction has a primary toxic or aller-gic nature. A chemical/toxic irritation due to a release of acrylic monomer is not likely to occur in denture wearers. Thus, dentures containing as much as 3—5 % free acrylic monomer did pot cause any mucosal inflam-matory response (Axelsson & Nyquist 1962). Furthermore, a significant release of acrylic monomer will take place in new dentures only, and will be quite temporary (Smith & Bains 1956). Contact allergic, i.e. im-munologic, responses to components of the denture acrylic resin seem to be no more than an incidental complication to the wearing of complete dentures. According to some case reports, an allergic reaction may occur due to sensitization to acrylic monomer, hydrochi-non, and formalin (Langer 1956, Crissey 1965, 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 burning and itching pain. In a gas chromatographic study it was shown that acrylic monomer leached from dentures, which had been in use for several weeks, in sufficient concentration to give rise to an allergic reaction (McCabe & Basker 1976). Furthermore, it is possible to sensitize various animal species and man ex-perimentally to acrylic monomer (Nyquist 1952, Magnusson & Kligman 1969). Thus denture stomatitis may be the clinical manifestation of an allergic reaction to sub-stances released from the denture base; how-ever, the diagnosis is difficult to establish (Kaaber et al. 1979).

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2.4. Thermal irritation. Slightly elevated

temperatures on the palatal mucosa have been demonstrated in denture wearers suffering from itching and burning pain (Ernst & Wagner 1974). It is not likely, however, that the rise of temperature produces a thermal irritation. It is possible that a sHght elevation of the temperature beneath the denture may stimulate multiplication of micro-organisms on the mucosa and the tissue surface of the denture.

3. Predisposing conditions

3.1. Oral hygiene. Subsequent to total tooth

extraction, a reduction in the concentration of micro-organisms in the oral cavity has been observed, but following insertion of dentures their numbers increased again, in particular the lactobacilli and yeasts (Lilienthal 1950, Bartels 1965). Dentures, therefore, seem to provide environmental conditions for the propagation 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 palate of 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 and a heavy outgrowth of yeasts on the denture (Olsen & Birkeland 1976, 1977). It is likely that the acid and relatively anaerobic milieu beneath the dentures is conducive to yeast proliferation and a Candida-'xnducQd denture stomatitis. By means of disclosing solutions larger accumulations of denture plaque have been revealed in patients with denture sto-matitis (Budtz-J0rgensen & Bertram 1970a, Bastiaan 1976). This plaque has the same basic structure as dental plaque (Theilade & Budtz-j0rgensen 1980). It has been shown that denture stomatitis will tend to resolve

following institution of plaque control by mechanical or chemical means (Budtz-Jorgensen & Loe 1972, Lindquist et al. 1975, Andrup et al. 1977). Together, these findings indicate that poor oral and denture hygiene is a major predisposing condition for

Candida-induced denture stomatitis.

3.2. Denture base. Micropits and

micro-porosities in the denture base may predispose to denture plaque accumulation. A therapeu-tic effect of lining the denture base with gold-foil has been reported (Nyquist 1952, Spreng 1963). In these studies it was assumed that gold-foil might have a therapeutic effect, either by reducing trauma or by disrupting the contact between the allergen (the denture base) and the palatal mucosa. It is, perhaps, more likely that gold-foil may have therapeu-tical significance by disrupting any contact between the contaminated denture base and the palatal mucosa.

3.3. Denture usage. There is conflicting

evi-dence whether the wearing of dentures at night will increase the susceptibility for den-ture stomatitis (Nyquist 1952, Love et al. 1967, Budtz-J0rgensen & Bertram 1970a, Bergman et al. 1971, Ettinger 1975). Since leaving out the dentures for 2 weeks will cause a spontaneous healing of the mucosa (Turrell 1966) it is likely that wearing the denture constantly will predispose both for infection and mechanical irritation of the palate.

3.4. Systemic factors. A number of systemic

diseases and treatments with various drugs may increase the susceptibility to oral can-didosis and the harmful effect of mechanical irritation. The systemic factors include endo-crine disturbances (diabetes mellitus, hypo-thyraidism), nutritional deficiencies (iron-deficiency, high carbohydrate intake), malig-nant diseases (leukemia), agranulocytosis and

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B UDTZ-J0RGENSEN

drugs such as sedatives, antibiotics, and ste-roids (Winner 1969, Budtz-Jorgensen 1974). One of the adverse effects of therapy with sedatives is xerostomia, which in turn will re-duce the resistance of the oral mucosa to trauma and infection. In these patients symp-toms in association with denture stomatitis are usually pronounced. Nutritional deficiencies such as deficiency in amino acids, iron and certain vitamins of the B complex are reputed to lower the resistance of the oral mucosa. It has been shown that dietary supplements of proteins and minerals will increase tolerance to the dentures and cause the inflammation to resolve (Kim et al. 1962, Deely 1965).

4. Diagnosis

It is the purpose of the clinical examination to reveal 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 by

making a quantitative estimate of the out-growth of yeasts on the mucosa and the fitting surface of the denture either by culture or by direct microscopy of oral smears (Davenport 1970, Budtz-J0rgensen 1974, Arendorf & Walker 1979, Renner et al. 1979). Material for microscopy or culture is collected by scraping the palatal mucosa or the denture. There is evidence of Candida infection if the denture and the mucosa are densely colonized by yeasts. A quantitative estimate of the out-growth of yeasts by culture may be obtained by means of a miniaturized culture test system (Microstix-Candida, Ames Co., Div. Miles Lab., Elkhart, Ind. U.S.A.). This test seems to be an alternative to the conventional smear as a low-cost screening method for establishing

the diagnosis of candidosis (Budtz-Jorgensen 1976).

4.2. Allergy. Immunological testing for allergy

in denture stomatitis is only relevant if infec-tion or traumatic factors have been excluded, and if the clinical history and the appearance of the lesion point to an allergic reaction, i.e. burning sensation and diffuse erythema with edema of the tissues in contact with the den-ture. However, the diagnosis is difficult to confirm. Thus, a positive delayed hypersensi-tive cutaneous reaction after testing with base material from the denture in question may represent mechanical irritation (Nyquist 1952, Fisher 1956) or contaminating micro-organisms (Kotilainen 1972). In order to es-tablish a reliable diagnosis it is necessary to screen the individual components of the den-ture acrylic resin (Kaaber et al. 1978). The patient should be referred to a dermatologist for skin testing.

4.3. Predisposing conditions. If there is no

response to local treatment, the diagnosis should be reconsidered and the patient should be referred for a medical examination. A per-sistent denture stomatitis may be a sign of an underlying systemic disease.

Angular cheilitis

Angular cheilitis (perleche, angular stomati-tis) is the clinical diagnosis of lesions which affect the angles of the mouth. The lesions are infectious in origin but several predisposing factors may interact. Dentures are one of the predisposing conditions which is the reason for including angular cheilitis among lesions of the oral mucosa associated with the wearing of removable dentures. Both the skin and the mucosa of the commissure may be affected and the lesion is characterized by maceration, erythema and crust formation. The

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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 N q examined 1^093 339 204 206 463 2_,277 Age >20 >20 >20 >65 >65 65-74 Per cent affected 30 18 8 10 19 10 Description of subjects . Non-randomized Non-randomized Non-randomized; with denture stomatitis Non-randomized Randomized

Randomized; subjects with natural teeth or dentures

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

sures appear wrinkled and with time deep fissures may develop with a tendency to bleeding.

The prevalence of angular cheilitis among wearers of complete dentures has been shown to vary between 8-30% (Table 2). The lesions seem to occur more frequently in non-insti-tutionalized subjects than in instinon-insti-tutionalized subjects within the same age distribution (Nyquist 1962, Chrigstrom et al. 1970, Ritchie 1973, Grabowski 1974, Manderson & Ettinger 1975, Axell 1976). This may possibly reflect the fact that institutionalized elderly people receive a more adequate diet and have better oral hygiene. Angular cheilitis is seen more frequently in women than in men and the condition seems to be associated with the wearing of removable dentures, but not with an edentulous statQperse (Rose 1968, Turrell 1968, Makila 1969, Axell 1976).

7. Etiology

Angular cheilitis apparently has a varied etiology. There is good reason to believe that the direct etiological factor is infection by yeasts, staphylococci, or streptococci (Mac-Farlane & Helnarska 1976). It seems,

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

2. Predisposing conditions

2.1. Vertical dimension of occlusion and lip-support. It is assumed that overclosure of

the jaws will produce folds at the angles of the mouth in which saliva tends to collect. The skin subsequently becomes macerated, fis-sured and secondarily infected. Epidemiologi-cal studies have shown an association between a decreased vertical dimension of occlusion and angular cheilitis (Marcussen 1944, Makila 1969, Glantz & Bjorlin 1970, Ritchie & Fletcher 1973). Healing of the lesions has been reported subsequent to prosthetic treat-ment including increasing the vertical dimen-sion of occludimen-sion and building out the buccal denture flanges to provide proper lip-support (Poyton 1955). Other studies have not shown a systemic relationship between overclosure of the jaws and angular cheilitis, and healing of the lesions was reported after the dentures

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72 BUDTZ-J0RGENSEN

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

2.2. Denture stomatitis. Several studies have

shown that angular cheilitis occurs more fre-quently in patients with denture stomatitis than in denture wearers with clinically normal oral mucosa (Lyon & Chick 1957, Cawson 1963, Makila 1969, Budtz-j0rgensen 1972, Ritchie & Fletcher 1973). Healing of the an-gular lesions has been reported after chemotherapy of denture stomatitis or when the patients left their dentures out of the mouth (Cawson 1966, Turrell 1966, 1968, j0rgensen & Bertram 1970b, Budtz-Jorgensen & Loe 1972, Olsen 1975a, b). It is believed, therefore, that the infection may start beneath the maxillary denture and from that area spread to the angles of the mouth (Cawson 1966, Budtz-Jorgensen 1974). Fi-nally, the infection may spread from the commissure to involve the retroangular mu-cosa (Crenea et al. 1965).

2.3. Carbohydrate consumption. A direct

as-sociation between angular cheilitis and a large intake of carbohydrates has been shown and it was assumed that a high salivary concentra-tion of glucose predisposed to infecconcentra-tion, in particular 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 infection of the angles of the mouth. The lesions will usually be bilateral and often be associated with glossitis, denture stomatitis, conjunc-tivitis and dermatitis (Shafer et al. 1974). De-ficiencies of B vitamins seem to be particularly important predisposing conditions. Thus, a decreased plasma concentration of thiamine

and riboflavin was demonstrated in a group of denture wearers with angular cheilitis (Makila 1969). In another study a decreased concen-tration of folic acid was demonstrated in a group of denture wearers with angular cheili-tis (Rose 1971). Angular cheilicheili-tis has been produced experimentally by giving individuals a pyridoxine-deficient diet, and healing of the lesions 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 an association between vitamin B deficiency and the occurrence of angular cheilitis (Ellenberg & Pollack, 1942, Machella 1942).

2.5. Anemia. A simple iron deficiency anemia

seems to predispose to angular cheilitis. Thus, a significantly decreased concentration of plasma iron was demonstrated in a group of denture wearers with angular cheilitis and the lesions healed when the diet was supple-mented with iron (Rose 1968). In another study a decreased plasma concentration of iron was not present in a group of denture wearers with angular cheilitis although the patients' diet seemed to be deficient in iron (Makila 1969). A chronic iron deficiency anemia may give rise to the Plummer-Vinson syndrome which is characterized by angular cheilitis, glossitis, denture stomatitis, dys-phagia and spoon-shaped, brittle fingernails (Shafer et al. 1974). This condition is a pre-disposition for the development of carcinoma in the upper alimentary tract.

3. Diagnosis

The reason for including angular cheilitis among denture-induced lesions is the fact that complete dentures may have both a direct and indirect etiologieal significance. Directly, overclosure, poor lip-support and denture stomatitis will predispose for an infection of

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the angles of the mouth. Indireetly, poor-funetioning dentures may divert the patient's ehoiee of food to a defieient diet whieh may result in a state of nutritional defieieney. A eorreet diagnosis, therefore, may be diffieult to establish beeause both loeal and systemie predisposing eonditions may oeeur simul-taneously.

By inspeetion of the dentures it is important to evaluate the vertieal dimension of oeelusion eorreetly and not uneritieally to assume it to be lowered when the patient presents an an-gular eheilitis. The lesions should be eheeked for a myeologieal infeetion. If the elinieal examination indieates an underlying nutri-tional defieieney or if the lesions do not heal following prosthetie treatment or ehemo-therapy, the patient should be referred for a thorough medieal examination. In partieular, it is important to make sure that the patient does not suffer from a Plummer Vinson syn-drome sinee this eondition may predispose to eareinomas of the oral eavity, hypopharynx and upper part of the esophagus.

Treatment and prevention of denture stomatitis and angular cheilitis

Denture stomatitis and angular eheilitis are eommonly present together. If the etiology of the lesions is the same, the lesions will often elear up together when the relevant therapy is instituted. Prosthodonties, ehemotherapy, and removal of dentures have been employed for treating patients with denture stomatitis and angular eheilitis.

1. Prosthetic treatment

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

and leakage of saliva in the angles of the mouth. There is, however, no evidenee that sueh treatment will eure a Candida infeetion of 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 of denture stomatitis, angular eheilitis and glos-sitis (Ritehie et al. 1969, Budtz-Jergensen 1974, Olsen 1975a, b). In type III lesions the inflammation will usually resolve, but the hyperplasia will persist. Mouth rinsing with a 0.2% solution of Chlorhexidine glueonate or disinfeetion 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 frequent regardless of whether antimyeoties or Chlorhexidine was used. To reduee the risk of relapse the following preeautions should be taken: treatment with antimyeotie antibioties should eontinue for 2 to 4 weeks, and the pa-tient should be instrueted in metieulous oral and denture hygiene and to keep the dentures in a disinfeetant solution during the night.

3. Preventive measures

Candida-induced denture stomatitis

as-soeiated with angular eheilitis is a frequent and reeurring eomplieation to the wearing of dentures. Although denture stomatitis is a minor disorder, it should be prevented. It is not known if the fit of the maxillary denture eontributes to the infeetion. It ereates a rela-tively aeid and anaerobie milieu that provides optimal environmental eonditions for yeast growth (Budtz-J0rgensen 1974). Further-more, it has been shown that polishing the

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74 BUDTZ-J0RGENSEN

fitting surface of the denture provides an im-proved denture cleanliness with subsequent healing of denture stomatitis (Andrup et al.

1977).

Theoretically, the infection is prevented by meticulous oral and denture hygiene. How-ever, it seems to be difficult to improve the hygienic care in denture wearers (Budtz-J0rgensen 1979). A wide range of denture cleansers are available, but the efficiency of these commercial products in removing mi-erobial plaque deposits on the dentures is not fully supported by experimental evidence (Budtz-j0rgensen 1979).

Simple, anti-microbial substances such as Chlorhexidine or hypochlorites are effective but may cause staining or bleaching of the dentures, and it is not known whether they are biologically acceptable when used for routine denture 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 the occlusion controlled regularly.

4. Conclusions

Denture stomatitis associated with angular cheilitis may have a multicausal etiology, but there is evidence to suggest that most cases are associated with infection by yeasts, in par-ticular C. albicans. This infection usually does not reflect any deep-seated systemic abnor-mality. Most cases are relatively easily treated, but recurrences are frequent and the infection tends to spread to other parts of the oral mucosa. Therefore, preventive measures should be taken against colonization by

Can-dida of the palatal mucosa and the dentures. It

should be recognized that an oral Candida infection may disseminate and be fatal in seri-ously ill patients, especially in those subjected to prolonged treatment with antibiotics, cor-ticosteroids, or immunodepressive drugs.

Furthermore, a denture stomatitis or angular cheilitis refractory to chemotherapy may indi-cate severe underlying nutritional deficiencies or a systemic disease.

Flabby ridge

Flabby ridge (alveolar fibrosis), i.e. remova-ble and extremely resilient alveolar ridge, is due to a replacement of bone by fibrous tis-sue. The condition is seen in a generalized and a localized form, the latter being confined most commonly to the anterior part of the maxilla. In non-randomized groups of denture wearers the prevalence has been reported to be about 20% (Table 3). The condition is found more often in women than in men and is usually located in the anterior region of the maxilla (J0lst 1963, Makila 1974). In patients using a full upper denture against a lower natural dentition it appears forward from first premolars or canines. If the mucosa covering the alveolar ridge is inflamed, it may contrib-ute to the resorption of the alveolar ridge. Histological and histochemical studies of flabby ridges have shown marked fibrosis with inflammatory cell infiltrate and a striking vas-cular reaction (Wallenius & Heyden 1972). The underlying bone revealed resorption. Flabby ridges in denture wearers should be removed surgically in order to minimize progressive reduction of residua! ridges. Flabby ridges may complicate impression taking and provide a poor support for removable dentures. In patients with extreme atrophy of the maxillary alveolar ridge, flabby ridges should not be totally removed since the resilient ridge may create some retention for the denture.

Denture irritation hyperplasia

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den-Table 3. Frequencies of denture irritation hyperplasia and flabby ridge in denture wearers. Year 1973I) 19742) 1974^) 1975^' 1976^) 1952^' 1974-^' J 1 1976 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 (upper 7 (lower 6 11.5 7 19 (upper 13 (lower 8.7 jaw) jaw) jaw) ]aw) Description of subjects Non-randomized Randomized Non-randomized Non-randomized

Randomized; subjects with natural teeth or dentures

Non-randomized Non-randomized

Randomized; subjects with natural teeth or dentures

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

tures is the occurrence of tissue hyperplasia of the tnucosa in contact with the denture border (inflammatory hyperplasia, epulis fis-suratum, redundant tissue). In non-ran-domized groups of denture wearers denture irritation hyperplasia was found in 5-10% (Table 3). In a large investigation on the prevalence of oral mucosal lesions in different age groups denture irritation hyperplasia was found in 6.3% among subjects aged 55-64 and in 11.5% among the subjects above the age of 65 (Axell 1976). The condition is seen more frequently in women than in men and is usually 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 are the result of chronic injury by unstable den-tures or by thin, overextended denture flanges. The proliferation of tissue may take place relatively quickly after prosthetic

treat-ment (Makila 1974). The lesions may be single or quite numerous and are composed of flaps of hyperplastie connective tissue covered by 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 severe inflammation and ulceration may occur.

After replacement or adjustment of the dentures the inflammation and edema may subside and produce some clinical improve-ment of the condition. After surgical excision of 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 the patient may experience marked discomfort. When such secondary infection of the in-volved tissues and associated lymphaden-opathy are present, the denture irritation hyperplasia may simulate a neoplastie process.

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76 BUDTZ-J0RGENSEN

Traumatic ulcers

Traumatic ulcers (sore spots) most commonly develop within 1-2 days after insertion of new dentures. The ulcers are small and painful le-sions, covered by a grey, necrotic membrane and surrounded by an inflammatory halo with firm, elevated borders. Traumatic ulcers have been found in 2-3% among institutionalized denture wearers (Chrigstrom et al. 1970, Ritchie 1973). In a randomized study of a population aged 65-74 years traumatic ulcers were 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 mucosa to mechanical irritation are predisposing, e.g. nutritional deficiencies, diabetes mellitus or xerostomia. In the non-compromised host sore spots will heal a few days after correction of the denture. When no treatment is insti-tuted the patient will often adapt to the pain-ful situation. In these cases tissue proliferation around the periphery of the lesion may give rise to a denture irritation hyperplasia.

Denture-induced carcinoma

In current textbooks on oral pathology it is usually 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 denture stomatitis (papillary hyperplasia) there was, however, no evidence of epithelial dysplasia or neoplasia (Bhasker et al. 1970, Flanagan & Porter 1971). In a retrospective study of 560 patients with intraoral epidermoid car-cinomas, of whom 204 wore dentures, a direct connection between irritation by the pros-theses and development of carcinoma was claimed in 86 of the cases (Hobaek 1949). The carcinomas were localized to the palate.

the alveolar ridges and the mucobuccal and lingual folds. 70% of the tumors were found in women, although oral carcinomas as a whole occur more frequently in men. An as-sociation between oral carcinoma and chronic irritation by dentures was supported by the fact that the prevalence of poor-fitting den-tures was higher in a group of denture wearers with oral carcinoma than in a group of denture wearers with carcinomas in other parts of the body (Wynder et al. 1957, Vogler et al. 1962). Case reports have detailed the development of oral carcinomas in patients wearing ill-fitt-ing dentures or dentures with a suckill-fitt-ing disk (Persson & Wallenius 1961, Beyer & Pape 1977). None of these studies seem to provide definite evidence that oral carcinomas may develop due to chronic mechanical or chemical irritation by dentures; however, the studies underline the necessity of strict and regular controls of all subjects wearing removable dentures. The opinion is still valid that if a sore spot does not heal following correction malignancy should be suspected (Pindborg 1973). Such cases and clinically aberrant manifestations of denture irritation hyperplasia should be immediately referred to an oral pathologist. It should be recognized that 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 that was prepared in collaboration with and was approved by the Educational Committee of Scandinavian Society for Prosthetic Dentistry. The author is grateful to Prof. H. P. Philipsen, Royal Dental College, for valuable help in preparing this manuscript.

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Address:

Dr. Ejvind Budtz-Jorgensen

Department of Prosthetic Dentistry Royal Dental College

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