Journal of Oral Pathology 1981: 10: 65-80

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 include 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 prevalence 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 dentures 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 underlying 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

wearing of removable dentures may represent
acute or chronic reactions to microbial denture plaque, a reaction to constituents of the
0300-9777/81/020065-16 $02.50/0
5 Oral Pathology

denture base material or a mechanical denture

injury. Among the acute reactions are traumatic ulcers, allergic reactions to denture
materials, or acute infections. Among the
1981 Munksgaard, Copenhagen

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 necessarily related to the presence of dentures.
Only a minor part of oral carcinomatous lesions have a possible association with the
wearing of dentures.
Dentures may be the direct cause of these
conditions, due to changing of the environmental conditions of the oral cavity and loading of the oral mucosa. However, systemic
conditions and general diseases may influence
the oral environment and alter tissue responses 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 institute a relevant therapy and prophylaxis, it is

necessary that the therapeutist has adequate

medical knowledge and that appropriate clinical and laboratory examinations are performed. It is the purpose of the present survey
to review the literature on clinical features
and histopathology, and to evaluate etiological and diagnostic aspects of these pathological 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 dentures 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 pinpoint hyperemia; type II shows more diffuse
erythema, and type III is a "non-neoplastic"

Table 1. Frequencies of denture stomatitis.

Year

Country

No.examined

Age

Per cent
affected

Description
of subjects

:952l>
19642>

Sweden
Sweden

1,090

1967^'
1967^'
1970^'
1972^'
1973^'

Non-randomized
Non-randomized
Randomized
Non-randomized
Non-randomized
Non-randomized
Non-randomized

>20

27

90

>29

47

UK

171

>65

40

UK

522

>20

Sweden
Denmark

168

>60

303

>20

43
54
67

UK

206

>65

17

19748'

Finland

106

>20

63 (upper jaw)
29 (lower jaw)

Non-randomized

19755>

Denmark

463

>65

65

1975^'
1976^^'

UK

700

>20

14 (type III)

Randomized
Non-randomized
Randomized; subjects
with natural teeth or

Sweden

2,277

65-74

36

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.
*For details: see text.

ORAL LESIONS IN DENTURE WEARERS

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 denture wearers the prevalence of denture
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 frequently among women than men (Love et al.
1967, Bergman et al. 1971, Ettinger 1975).
Denture stomatitis may be associated with angular cheilitis and glossitis, but subjective
symptoms are rare (Makila 1969, Davenport
1970, Budtz-j0rgensen 1972, Ettinger 1975).

67

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 denture 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

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 keratinization, epithelial atrophy, epithelial hyperplasia and acanthosis; in the lamina propria
there is a chronic inflammation (Ostlund
1958, Budtz-Jorgensen 1970, Anneroth &
Wictorin 1975, van Mens et al. 1975, Wictorin et al. 1975). Electron microscopic studies
of type II and type III lesions have shown absence of keratohyaline granules in the superficial epithelial layers, increase of the intracellular spaces of the spinous layer, and infiltration by mononuclear cells in the epithelium
(Wictorin et al. 1975). Histochemical
techniques have demonstrated intracellular
deposits of glycogen in the spinous layer.

The etiology of denture stomatitis is multicausal. A wide range of both local and systemic predisposing conditions may be involved in the pathogenesis. The significant
direct causes of denture stomatitis are infection and mechanical irritation and less frequently 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,
Budtz-j0rgensen & Bertram 1970a, b, BudtzJ0rgensen 1972). The infection is primarily
due to a contamination of the fitting surface of

68

BUDTZ-J0RGENSEN

the dentures by yeasts (Davenport 1970,

Budtz-Jorgensen 1972, Olsen 1974, BudtzJorgensen 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 demonstrate a causal relationship between bacterial
infection and denture stomatitis, but no definite 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 patients with poor-fitting dentures with a nonbalanced 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 subsequent 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 corrective prosthetic treatment and it was concluded 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 negative 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 epicutaneous testing with high concentrations of an allergen will provoke a toxic reaction whereas
dilute solutions of the allergen will rather
elicit an allergic reaction in a sensitized individual (Greither 1954, Nielsen & Klaschka
1971). On the other hand, relatively high concentrations 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 allergic 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 35 % free acrylic
monomer did pot cause any mucosal inflammatory 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. immunologic, 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, hydrochinon, and formalin (Langer 1956, Crissey
1965, Stungis & Fink 1969, Rossbach 1975,
Giunta & Zablotsky 1976). It is a characteristic 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 experimentally to acrylic monomer (Nyquist
1952, Magnusson & Kligman 1969). Thus
denture stomatitis may be the clinical
manifestation of an allergic reaction to substances released from the denture base; however, the diagnosis is difficult to establish
(Kaaber et al. 1979).

ORAL LESIONS IN DENTURE WEARERS

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. Furthermore, it was found necessary to cover the mucosa by a plate in order to produce an experimental infection with C. albicans in the palate
of monkeys (Budtz-Jergensen 1971).
Denture plaque accumulations tend to decrease pH on the palatal mucosa (Zgraggen &
Graf 1975), and consumption of carbohydrates produces a further drop in pH associated 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 stomatitis (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

69

following institution of plaque control by

mechanical or chemical means (BudtzJorgensen & 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 Candidainduced denture stomatitis.

3.2. Denture base. Micropits and microporosities in the denture base may predispose
to denture plaque accumulation. A therapeutic 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 therapeutical significance by disrupting any contact
between the contaminated denture base and
the palatal mucosa.
3.3. Denture usage. There is conflicting evidence whether the wearing of dentures at
night will increase the susceptibility for denture 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 candidosis and the harmful effect of mechanical
irritation. The systemic factors include endocrine disturbances (diabetes mellitus, hypothyraidism), nutritional deficiencies (irondeficiency, high carbohydrate intake), malignant diseases (leukemia), agranulocytosis and

B UDTZ-J0RGENSEN

drugs such as sedatives, antibiotics, and steroids (Winner 1969, Budtz-Jorgensen 1974).
One of the adverse effects of therapy with
sedatives is xerostomia, which in turn will reduce the resistance of the oral mucosa to
trauma and infection. In these patients symptoms 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 possible predisposing conditions in order to institute a corrective therapy and achieve a permanent cure.
4.1. Infection. The diagnosis of Candida-induced denture stomatitis is established by
making a quantitative estimate of the outgrowth 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 outgrowth 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 infection 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 denture. However, the diagnosis is difficult to
confirm. Thus, a positive delayed hypersensitive cutaneous reaction after testing with base
material from the denture in question may
represent mechanical irritation (Nyquist
1952, Fisher 1956) or contaminating microorganisms (Kotilainen 1972). In order to establish a reliable diagnosis it is necessary to
screen the individual components of the denture 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 persistent denture stomatitis may be a sign of an
underlying systemic disease.

Angular cheilitis
Angular cheilitis (perleche, angular stomatitis) 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 commis-

71

ORAL LESIONS IN DENTURE WEARERS

Table 2. Frequencies of angular cheilitis in denture wearers.

Year

Country

Nq examined

Age

Per cent

Description of subjects .

affected

1962^)

Sv;eden

1969^'

Finland

1972^'

Denmark

1^093

339
204

>20
>20
>20

30
18
8

Non-randomized
Non-randomized
Non-randomized; with
denture stomatitis

1973^)

UK

206

>65

10

Non-randomized

1974^'

Denmark

463

>65

19

Randomized

1976^'

Sweden

65-74

10

2_,277

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-institutionalized subjects than in institutionalized
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 (MacFarlane & 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 conditions 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, fissured and secondarily infected. Epidemiological 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 treatment including increasing the vertical dimension of occlusion 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

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 predisposing condition in some cases.
2.2. Denture stomatitis. Several studies have
shown that angular cheilitis occurs more frequently 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 angular 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,
Budtz-j0rgensen & Bertram 1970b, BudtzJorgensen & 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). Finally, the infection may spread from the
commissure to involve the retroangular mucosa (Crenea et al. 1965).
2.3. Carbohydrate consumption. A direct association between angular cheilitis and a large
intake of carbohydrates has been shown and it
was assumed that a high salivary concentration of glucose predisposed to infection, 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 suppress host resistance, thereby being the underlying predisposing condition for infection
of the angles of the mouth. The lesions will
usually be bilateral and often be associated
with glossitis, denture stomatitis, conjunctivitis and dermatitis (Shafer et al. 1974). Deficiencies 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 concentration of folic acid was demonstrated in a
group of denture wearers with angular cheilitis (Rose 1971). Angular cheilitis has been
produced experimentally by giving individuals
a pyridoxine-deficient diet, and healing of the
lesions was seen after administration of riboflavin, folic acid or pyridoxine (Smith & Martin 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 supplemented 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, dysphagia and spoon-shaped, brittle fingernails
(Shafer et al. 1974). This condition is a predisposition 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

ORAL LESIONS IN DENTURE WEARERS

the angles of the mouth. Indireetly, poorfunetioning 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 simultaneously.
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 angular eheilitis. The lesions should be eheeked
for a myeologieal infeetion. If the elinieal
examination indieates an underlying nutritional defieieney or if the lesions do not heal
following prosthetie treatment or ehemotherapy, 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 syndrome 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 exeessive bone resorption of the alveolar ridge

73

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 (BudtzJ0rgensen 1974).
2. Antimycotic therapy
Speeifie antimyeotie drugs, sueh as Nystatin,
Amphoteriein B, or Natamyein have been effeetive when used topieally for treatment of
denture stomatitis, angular eheilitis and glossitis (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 Chlorhexidine in a 2 % solution has redueed inflammation and the number of yeasts harbored 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 patient 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 assoeiated 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 relatively aeid and anaerobie milieu that provides
optimal environmental eonditions for yeast
growth (Budtz-J0rgensen 1974). Furthermore, it has been shown that polishing the

74

BUDTZ-J0RGENSEN

fitting surface of the denture provides an improved denture cleanliness with subsequent
healing of denture stomatitis (Andrup et al.
1977).
Theoretically, the infection is prevented by
meticulous oral and denture hygiene. However, it seems to be difficult to improve the
hygienic care in denture wearers (BudtzJ0rgensen 1979). A wide range of denture
cleansers are available, but the efficiency of
these commercial products in removing mierobial 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 recommend are: brush dentures carefully, including the fitting surface; discontinue wearing the dentures at night, and have the
occlusion controlled regularly.
4. Conclusions

Furthermore, a denture stomatitis or angular

cheilitis refractory to chemotherapy may indicate severe underlying nutritional deficiencies
or a systemic disease.

Flabby ridge

Flabby ridge (alveolar fibrosis), i.e. removable and extremely resilient alveolar ridge, is
due to a replacement of bone by fibrous tissue. 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 contribute 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 vascular 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 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 particular C. albicans. This infection usually does
not reflect any deep-seated systemic abnormality. 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 Candida of the palatal mucosa and the dentures. It
should be recognized that an oral Candida
infection may disseminate and be fatal in seriously ill patients, especially in those subjected
to prolonged treatment with antibiotics, cor- Denture irritation hyperplasia
ticosteroids, or immunodepressive drugs. A common tissue reaction to ill-fitting den-

75

ORAL LESIONS IN DENTURE WEARERS

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

Country

No,examined

Age

Per cent

Description of subjects

affected
DENTURE IRRITATION HYPERPLASIA
1973I)

UK

206

>65

19742)

Denmark

463

>65

26

1974^)

Finland

133

>20

1975^'

UK

442

>65

1976^)

Sweden

8 (upper jaw)

Non-randomized

Randomized

Non-randomized

7 (lower jaw)
2^277

65-74

6
11.5

Non-randomized
Randomized; subjects with
natural teeth or dentures

FLABBY RIDGE
1952^'

Sweden

1974-^'

Finland

J1

Sweden

Non-randomized

>20

19 (upper jaw)

Non-randomized

>15

13 (lower ]aw)
8.7

Randomized; subjects with

1^090

>20

133
20,333

1976
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 fissuratum, redundant tissue). In non-randomized 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 mucolabial folds (Joist 1963, Cooper 1964, Nordenram & Landt 1969, Ralph & Stenhouse 1972,
Cutright 1974, Axell 1976). The lesions are
the result of chronic injury by unstable dentures 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 usually 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 improvement 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 irritation from microbial products is severe the
patient may experience marked discomfort.
When such secondary infection of the involved tissues and associated lymphadenopathy are present, the denture irritation
hyperplasia may simulate a neoplastie process.

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 lesions, 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 direct cause of sore spots is overextended denture flanges, or unbalanced occlusion. Conditions 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 instituted the patient will often adapt to the painful 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 malignant transformation of denture induced lesions should be considered. In extensive histological 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 carcinomas, of whom 204 wore dentures, a direct
connection between irritation by the prostheses 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 association between oral carcinoma and chronic
irritation by dentures was supported by the
fact that the prevalence of poor-fitting dentures 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-fitting dentures or dentures with a sucking 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.

ORAL LESIONS IN DENTURE WEARERS

References
Andrup, B., Andersson, B. & Hedegard, B. (1977)
Proteshygien III. Racker rengoring av helprotesen for stomatitutlakning. Tandldkartidningen
69, 394-398.
Anneroth, G. & Wictorin, L. (1975) Denture
stomatitis. A histological and mieroradiographie
study of the alveolar mucosa. Odontologisk Revy
26, 135-144.
Arendorf, T. M. & Walker, D. M. (1979) Oral candidal populations in health and disease. British
Dental Journal 147, 267-272.
Axell, T. (1976) A prevalence study of oral mucosal
lesions in an adult Swedish population.
Odontologisk Revy 27 (suppl. 36), 1-103.
Axelsson, B. & Nyquist, G. (1962) The leaching
and biological effects of the residual monomer of
methylmethacrylate. Odontologisk Revy 13,
370-379.
Bartels, H. A. (1965) Local and systemic factors in
oral moniliasis. New York Journal of Dentistry
35, 283-285.
Bastiaan, R. J. (1976) Denture sore mouth.
Aetiological aspects and treatment. Australian
Dental Journal 21, 375-382.
Bergendal, T. Holmberg, K. & Nord, C.-E. (1979)
Yeast colonization in the oral cavity and feces in
patients
with
denture
stomatitis. Aeta
odontologica Seandinavica 37, 3 7 ^ 5 .
Bergman, B., Carlsson, G. E. & Ericsson, S. (1971)
Effect of differences in habitual use of complete
dentures on underlying tissues. Scandinavian
Journal of Dental Research 79, 449-460.
Bergman, B., Carlsson, G. E. & Hedegard, B.
(1964) A longitudinal two-year study of a
number of full denture cases. Aeta odontologiea
Seandinavica 22, 3-26.
Beyer, J. D. & Pape, H.-D. (1977) Zur Entstehung
eines Mundschleimhautkarzinoms durch exogene
Dauerreize. Deutsehe Zahndrtzliche Zeitschrift
32, 611-613.
Bhaskar, S. N., Beasley, J. D. & Cutright, D. E.
(1970) Inflammatory papillary hyperplasia of the
oral mucosa: report of 341 cases. Journal of the
American Dental Association 81, 949-952.
Budtz-J0rgensen, E. (1970) Denture stomatitis. III.
Histopathology of trauma- and candida-induced
inflammatory lesions of the palatal mucosa. Aeta
odontologica Seandinavica 28, 551-579.
Budtz-Jorgensen, E. (1971) Denture stomatitis. IV.
An experimental model in monkeys. Aeta
odontologica Seandinavica 29, 513-526.
Budtz-Jorgensen, E. (1972) Denture stomatitis. V.
Candida agglutinins in human sera. Aeta
odontologica Seandinavica 30, 313-325.

77

Budtz-Jorgensen, E. (1974) The significance of

Candida albieans in denture stomatitis. Thesis.
Scandinavian Journal of Dental Research 82,
151-190.
Budtz-Jorgensen, E. (1976) Evaluation of a dehydrated test strip, Microstix'^-Candida for detection of Candida induced denture stomatitis.
Scandinavian Journal of Dental Research 84,
229-233.
Budtz-Jorgensen, E. (1979) Materials and methods
for cleaning dentures. Journal of Prosthetic Denistry 42, 619-623.
Budtz-J0rgensen, E. & Bertram, U. (1970a) Denture stomatitis I. The etiology in relation to
trauma and infection. Aeta odontologica Seandinavica 28, 71-92.
Budtz-j0rgensen, E. & Bertram, U. (1970b) Denture stomatitis II. The effect of antifungal and
prosthetic treatment. Aeta odontologiea Seandinavica 28, 283-304.
Budtz-J0rgensen, E. & Loe, H. (1972)
Chlorhexidine as a denture disinfectant in the
treatment of denture stomatitis. Scandinavian
Journal of Dental Research 80, 457-464.
Budtz-Jorgensen, E., Stenderup, A. & Grabowski,
M. (1975) An epidemiologic study of yeasts in
elderly denture wearers. Community Dentistry
and Oral Epidemiology 3, 115-119.
Budtz-J0rgensen, E., Theilade, E., Theilade, J. &
Zander, H. A. (1980) A method for studying
plaque development on dentures. Scandinavian
Journal of Dental Research, in press.
Cahn, L. R. (1936) The denture sore mouth. Annals
of Dentistry 3, 33-36.
Cawson, R. A. (1963) Denture sore mouth and angular cheilitis. British Dental Journal 115,
441^49.
Cawson, R. A. (1966) Chronic oral eandidosis,
denture stomatitis, and chronic hyperplastie eandidosis. In Symposium on Candida Infections,
eds. Winner, H. & Hurley, R., pp. 138-152.
Edinburgh and London: E. & S. Livingstone.
Cernea, P., Crepy, C , Kuffer, R., Mascaro, J. M.,
Badillet, G. & Marie, J.-L. (1965) Aspects peu
connus de candidoses buccale. Les candidoses a
foyers multiples de la cavite buccale. Revue
Stomatolgie {Paris) 16, 103-138.
Chrigstrom, K., Hedegard, B. & Marken, K.-E.
(1970) Gerodontologiska studier: IV. Oralstatus
och vardbehov vid en vSrdhems - och pensioner
institution i Stockholm. Swedish Dental Journal
63, 981-995.
Cooper, E. H. (1964) Hyperplasia of the oral tissues caused by ill-fitting dentures. British Dental
Journal 116, 111-114.

78

BUDTZ-J0RGENSEN

Crissey, J. T. (1965) Stomatitis, dermatitis and

denture materials. Archives of Dermatology 92,
45-49.
Cutright, D. E. (1974) The histopathologic findings
in 583 cases of epulis fissuratum. Oral Surgery,
Oral Medicine, Oral Pathology 37, 401-411.
Davenport, J. C. (1970) The oral distribution of
Candida in denture stomatitis. British Dental
Journal 116, 111-114.
Deeley, R. A. (1965) The effect of protein versus
placebo supplementation upon denture tolerance. Journal of Prosthetic Dentistry 15, 65-72.
Ellenberg, M. & Pollack, H. (1942) Pseudo ariboflavinosis. Journal of the American Medical Association 119, 790-792.
Ernst, F. D. & Wagner, I.-V. (1974) Intraorale
Temperaturmessung - eine Moglichkeit zur
Objektivisierung des Syndroms "brennender
Mund". Zahn-, Mund- und Kieferheilkunde 62,
647-660.
Ettinger, R. L. (1975) The etiology of inflammatory
papillary hyperplasia. Journal of Prosthetic Dentistry 34, 254-261.
Fisher, A. A. (1956) Allergic sensitization of the
skin and oral mucosa to acrylic resin denture
materials. Journal of Prosthetic Dentistry 6,
593-602.
Flanagan, V. D. & Porter, K. (1971) Histochemical
studies of papillary hyperplasia of the palate: enzyme histochemistry of papillary hyperplasia and
normal palatal mucosa. Journal of Dental Research 50, 1346-1351.
Giunta, J. & Zablotsky, N. (1976) Allergic
stomatitis caused by self-polymerizing resin. Oral
Surgery, Oral Medicine, Oral Pathology 41,
631-637.
Glantz, P.-O. & Bjorlin, G. (1970) Angular
cheilosis. Swedish Dental Journal 63, 545-549.
Grabowski, M. (1974) Den Aildre Befolknings
Oralstatus og Odontologiske Behandlingsbehov i
Vestsjcellands Amt. Thesis. Arhus: Royal Dental
College, Denmark.
Greither, A. (1954) Die toxisehe Schwelle der
Schleimhaut im Prothesen-Test verglichen mit
den Lappchentest an der Haut. Dermatologische
Wochenschrift 129, 388-392.
Hobaek, A. (1949) Dental prostheses and intraoral
epidermoid carcinoma. Acta Radiologica 32,
259-273.
Joist, O. (1963) Konsforskel i forekomsten af protesebetingede irritationshyperplasier. Tandlcegebladet 67, 545-554.
Kaaber, S. & Bertram, U. (1971) Cytology of the
inflammatory exudate in denture stomatitis.
Scandinavian Journal of Dental Research 79,
81-91.

Kaaber, S., Thulin, H. & Nielsen, E. (1979) Skin

sensitivity to denture base materials in the burning mouth syndrome. Contact Dermatitis 5,
90-96.
Kim, M. S., Ringsdorf, W. M. & Cheraskin, E.
(1962) Factors in denture tolerance. Practical
Dental Monographs, pp. 364.
Kotilainen, R. (1972) Stomatitis prothetica and allergy. Proceedings of the Finnish Dental Society
68, 1-6.
Lambson, G. O. (1966) Papillary hyperplasia of the
palate. Journal of Prosthetic Dentistry 16,
636-645.
Langer, H. (1956) Das Schleimhautbrennen beim
Tragen von Akrylatplatten. Deutsche Zahndrtzliche Zeitschrift 11, 1321-1327.
Lehner, T. (1965) Symposium denture sore mouth.
III. Immunofluorescent investigation of Candida.
Dental Practitioner and Dental Record 16,
142-146.
Lilienthal, B. (1950) Studies of the flora of the
mouth. II: Yeast-like organisms: some
observations on their incidence in the mouth.
Australian Journal of Experimental Biology and
Medical Science 28, 279-286.
Lindquist, L., Andrup, B. & HedegSrd, B. (1975)
Proteshygien 11. Klinisk vardering av ett hygienprogram for patienter med protesstomatit.
Tandldkartidningen 67, 872-879.
Love, W., Goska, F. & Mixon, R. (1967) The
etiology of mueosal inflammation associated with
dentures. Journal of Prosthetic Dentistry 17,
515-527.
Lyon, D. G. & Chick, A. O. (1957) Denture sore
mouth and angular cheilitis. Dental Practitioner
and Dental Record 7, 403-406.
MacFarlane, T. W. & Helnarska, S. J. (1976) The
microbiology of angular cheilitis. British Dental
Journal 140, 403-406.
Maehella, T. E. (1942) Studies on the B vitamins in
the human subject. 111. The response of cheilosis
to vitamin therapy. American Journal of Medical
Science 203, 114-119.
Magnusson, B. & Kligman, A. M. (1969) The identification of contact allergens by animal assay.
The guinea pig maximation test. Journal of Investigative Dermatology 52, 268276.
Makila, E. (1969) Prevalence of angular stomatitis.
Correlation with composition of food and
metabolism of vitamins and iron. Acta
odontologica Scandinavica 27, 655680.
Makila, E. (1974) Primary oral status and adaptation to complete dentures. A clinical follow-up
study in groups over and under 65 years. Annales
Academiae Scientiarum Fennicae 164, 129.

ORAL LESIONS IN DENTURE WEARERS

Manderson, R. D. & Ettinger, R. L. (1975) Dental

status of the institutionalized elderly population
of Edinburgh. Community Dentistry and Oral
Epidermiology 3, 100-107.
Macussen, P. V. (1944) Inflammation of the skin in
the corners of the mouth (perleche) as a
symptom of local and universal diseases. Acta
Dermatologica et Venerologica 24, 83-112.
Marken, K.-E. & Hedegard, B. (1970) Gerodontologiska
studier:
III.
Oralstatus
och
tandvardsbehov hos aldre personer i Stockholms
stad. Swedish Dental Journal 63, 963-980.
McCabe, J. F. & Basker, R. M. (1976) Tissue sensitivity to acrylic resin. A method of measuring
the residual monomer content and its clinical application. British Dental Journal 140, 347-359.
Neill, D. J. (1963) Aetiology and treatment of angular cheilitis - a preliminary report. Dental
Practitioner and Dental Record 13, 247-249.
Neill, D. J. (1965) Symposium on denture sore
mouth. I. An aetiological review. Dental Practitioner and Dental Record 16, 135-138.
Newton, A. V. (1962) Denture sore mouth. British
Dental Journal 112, 357-360.
Nielsen, C. & Klaschka, F. (1971) Teststudien an
der Mundschleimhaut bei Ekzemallergikeren.
Deutsche Zahn- Mund- und Kieferheilkunde 57,
201-218.
Nordenram, A. & Landt, H. (1969) Hyperplasia of
the oral tissues in denture cases. Acta
odontologica Scandinavica 27, 481-491.
Nyquist, G. (1952) A study of denture sore mouth.
An investigation of traumatic, allergic and toxic
lesions of the oral mucosa arising from the use of
full dentures. Acta odontologica Scandinavica 10,
suppl. 9.
Nyquist, G. (1953) The influence of denture
hygiene and the bacterial flora on the condition
of the oral mucosa in full denture cases. Acta
odontologica Scandinavica 11, 2460.
Nyquist, G. (1962) Om betthojdens betydelse for
stomatitis angularis hos helprotesepatienter. In
Goteborgs Tandldkare Sailskaps Arsbok, pp.
45-53,. Goteborg, Sweden.
Olsen, I. (1974) Denture stomatitis. Occurrence
and distribution of fungi. Acta odontologica
Scandinavica 32, 329-333.
Olsen, I. (1975a) Denture stomatitis. Effects of
chlorhexidine and amphotericin B on the mycotic
flora. Acta odontologica Scandinavica 33, 41-46.
Olsen, I. (1975b) Denture stomatitis. The clinical
effects of chlorhexidine and amphotericin B.
Acta odontologica Scandinavica 33, 47-52.
Olsen, I. & Birkeland, J. M. (1976) Initiation and
aggravation of denture stomatitis by sucrose

79

rinses. Scandinavian Journal of Dental Research

84, 94-97.
Olsen, I. & Birkeland, J. M. (1977) Denture
stomatitis - yeast occurrence and the pH of saliva
and denture plaque. Scandinavian Journal of
Dental Research 85, 130-134.
Ostlund, S. G. (1958) The effect of complete dentures on the gum tissues. Acta odontologica
Scandinavica 16, 1 ^ 3 .
Persson, P.-A. & Wallenius, K. (1961) Squamouscell carcinoma of the maxilla in relation to denture-induced gingival hyperplasia. Odontologisk Tidskrift 69, 461-466.
Pindborg, J. J. (1973) Atlas of Diseases of the Oral
Mucosa, 2nd. edn. Copenhagen: Munksgaard.
Poyton, H. G. (1955) A case of angular cheilitis.
British Dental Journal 99, 303-304.
Ralph, J. P. & Stenhouse, D. (1972) Denture-induced hyperplasia of the oral soft tissues. Vestibular lesions, their characteristics and treatment. British Dental Journal 132, 68-70.
Renner, R. P., Lee, M., Andors, L., McNamara, T.
F. & Brook, S. (1979) The role of C. albicans in
denture stomatitis. Oral Surgery Oral Medicine,
Oral Pathology 47, 323-328.
Riber, E. & Kaaber, S. (1976) Changes in the water
permeability of palatal mucosa after complete
denture treatment. Scandinavian Journal of
Dental Research 84, 357-361.
Riber, E. & Kaaber, S. (1978) Barrier properties of
inflamed denture loaded mucosa to water. Scandinavian Journal of Dental Research 86,
386-391.
Ritchie, G. M. & Fletcher, A. M. (1973) Angular
inflammation. Oral Surgery, Oral Medicine, Oral
Pathology 36, 358-366.
Ritchie, G. M. & Fletcher, A. M. (1973) Angular
inflammation. Oral Surgery Oral Medicine, Oral
Pathology 36, 358-366.
Ritchie, G. M., Fletcher, A. M., Main, D. M. G. &
Prophet, A. S. (1969) The eitology, exfoliative
cytology, and treatment of denture stomatitis.
Journal of Prosthetic Dentistry 22, 185-200.
Rose, J. A. (1968) Aetiology of angular cheilitis.
Iron metabolism. British Dental Journal 125,
67-72.
Rose, J. A. (1971) Folic-acid deficiency as a cause
of angular cheilosis. Lancet 2, 253-254.
Rossbach, A. (1975) Ein Beitrag zur Atiologie der
Prothesenstomatopatien. Deutsche Zahndrtzliche
Zeitschrift 30, 148-149.
Sebrell, W. H. & Harris, R. S. (1954) The Vitamins.
Chemistry, Physiology, Pathology, Vols. II and
III. New York: Academic Press Inc.
Shafer, W. G., Hine, M. K. & Levy, B. M. (1974)^

80

BUDTZ-J0RGENSEN

Textbook of Oral Pathology, 3rd edn. Philadelphia: W. B. Saunders.

Shuttleworth, C. W. & Gibbs, F. J. (1960) The
aetiological significance of Candida albicans in
chronic angular cheilitis and its treatment with
nystatin. British Dental Journal 108, 354-357.
Smith, D. C. & Bains, M. E. D. (1956) The detection and estimation of residual monomer in
polymethyl methacrylate. Journal of Dental Research 35, 16-24.
Smith, S. G. & Martin, D. W. (1940) Cheilosis successfully treated with synthetic vitamin B6. Proceedings of the Society for Experimental Biology
and Medicine 43, 660663.
Spreng, M. A. (1963) Allergie und Zahnmedizin,
2nd edn. Leipzig: J. A. Barth.
Stungis, T. E. & Fink, J. N. (1969) Hypersensitivity
to acrylic resin. Journal of Prosthetic Dentistry
22, 425^29.
Swallow, N. & Adams, D. (1967) Survey of dental
disease in adults in the Rhondda Fawr. British
Dental Journal 123, 137-144.
Theilade, J. & Budtz-Jorgensen, E. (1980) Electron
microscopic study of denture plaque. Journal de
Biologie Buccale, in press.
Theilade, E. & Budtz-Jorgensen, E. & Theilade, J.
(1980) Predominant cultivable microflora of
denture plaque. Scandinavian Journal of Dental
Research, in press.
Turrell, A. J. W. (1966) Aetiology of inflamed upper denture-bearing tissues. British Dental Journal 118, 542-546.
Turrell, A. J. W. (1968) Vertical dimension as it
relates to the etiology of angular cheilosis. Journal of Prosthetic Dentistry 19, 119-125.

Van Mens, P. R., Pinkse-Veen, M. J. & James, J.

(1975) Histologieal features of the palatal mucosa in denture sore mouth. Journal of Oral Rehabilitation 2, 273-280.
Van Reenen, J. F. (1973) Microbiologic studies on
denture stomatitis. Journal of Prosthetic Dentistry 30, 493-505.
Vogler, W. R., Lloyd, J. W. & Milmore, B. K.
(1962) A retrospective study of etiological factors in cancer of the mouth, pharynx, and larynx.
Cancer 15, 246-258.
Wallenius, K. & Heyden, G. (1972) Histochemical
studies of flabby ridges. Odontologisk Revy 23,
169-180.
Wictorin, L. Anneroth, G. & Frithiof, L. (1975)
Denture stomatitis. A cUnical, electron-microscopic, microradiographic, and light microscopic study. Acta odontologica Scandinavica
33, 299-311.
Winner, H. L (1969) The transition from commensalism to parasitism. British Journal of Dermatology. 81, suppl. 1: 62-68.
Wynder, E. L., Bross, L J. & Feldman, R. M.
(1957) A study of the etiological factors in cancer
of the mouth. Cancer 10, 1300-1323.
Zgraggen, U. & Graf, H. (1975) pH-Veranderungen
unter
Oberkiefervollprothesen.
Schweizerische Monatsschrift fiir Zahnheilkunde
85, 797-812.
Address:
Dr. Ejvind Budtz-Jorgensen
Department of Prosthetic Dentistry
Royal Dental College
DK-8000 Arhus, Denmark