-
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
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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.
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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
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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).
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ORAL LESIONS IN DENTURE WEARERS 69
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
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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
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-
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ORAL LESIONS IN DENTURE WEARERS 71
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
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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
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ORAL LESIONS IN DENTURE WEARERS 73
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
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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-
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ORAL LESIONS IN DENTURE WEARERS 75
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
Randomized; subjects withnatural teeth or dentures
Non-randomizedNon-randomized
Randomized; subjects withnatural teeth or dentures
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.
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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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ORAL LESIONS IN DENTURE WEARERS 77
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Address:Dr. Ejvind Budtz-JorgensenDepartment of Prosthetic
DentistryRoyal Dental CollegeDK-8000 Arhus, Denmark