IOSR Journal of Dental and Medical Sciences (IOSR-JDMS)

e-ISSN: 2279-0853, p-ISSN: 2279-0861. Volume 13, Issue 1 Ver. V. (Jan. 2014), PP 36-39
www.iosrjournals.org

Oral changes in Diabetes a review

Ngairangbam Sanjeeta1
1
(MDS, Assistant Professor, Dental College, Regional Institute of Medical Sciences, Imphal))

Abstract: Diabetes mellitus is a chronic disease affecting all age groups and one of the leading causes of
mortality and morbidity worldwide. Many chronic macrovascular and microvascular complications of diabetes
have been reported in the literature with few reports on diabetes and associated various oral soft tissue
abnormalities. In this review, the known correlations between oral disease and diabetes mellitus are highlighted
with the aims to increase the awareness of oral changes, complications of diabetes mellitus and to emphasize on
need of studies to control these complications. It treats in depth some of the complications such as periodontal
disease, fungal infection and salivary dysfunction.
Keywords: Diabetes Mellitus, Oral, Complications, Taste, Fungal.

I. INTRODUCTION
The countries with the largest number of diabetes are India, China and the US, with India beginning to
be regarded as the diabetic capital of the world. 1 The chronic hyperglycemia and attendant metabolic
dysregulation in diabetes mellitus (DM) may be associated with secondary damage in multiple organ systems,
especially the kidneys, eyes, nerves and blood vessels.2 The association between DM and changes in the oral
cavity have been the subject of reports in both the medical and dental literatures. A number of oral soft tissue
abnormalities have been associated with DM by various reports, with more emphasis being given on its relation
with periodontal diseases.3 There are strong evidence of both type 1 and type 2 diabetic patients having more
severe periodontal disease than do individuals without diabetes.4-7 Other specific conditions that have been
identified include geographic tongue, fissured tongue, median rhomboid glossitis, hyperplastic gingivitis, lichen
planus, parotid gland enlargement, candidiasis, xerostomia, burning sensations of oral mucosa, taste
disturbances, increased incidence and severity of dental caries, traumatic ulcers, etc. 3 Grinspan syndrome is an
interesting condition in which there is coexistence of DM, lichen planus and hypertension in the same
individual.

Pathogenesis
The underlying cause for increased susceptibility to infection, impaired wound healing capabilities and
vascular injury following chronic hyperglycemia in DM can be attributed to various underlying mechanisms.2
The underlying mechanisms2,8 which, in turn, affect infections can be associated with
Sorbitol- myoinositol osmolarity changes
Oxidative- redox stress
Non-enzymatic glycation reactions (advanced glycation end products- AGEs)
Activation of the protein kinase C- diacylglycerol pathway.
The diabetic state impairs the synthesis of collagen and glycosaminoglycans in the gingiva, enhances crevicular
fluid collagenolytic activity and results in the loss of periodontal fibres, supporting alveolar bone, loosening and
exfoliation of the teeth.9
Diabetes- induced changes in immune cell function produces an inflammatory immune-cell phenotype
(upregulation of proinflammatory cytokines from monocytes/ polymorph nuclear leukocytes and
downregulation of growth factors from macrophages), predisposing to chronic inflammation, rogressive tissue
9
breakdown, and diminished tissue repair capacity.

Sialosis
Sialosis which is defined as an asymptomatic, non-inflammatory, non-neoplastic enlargement of the
salivary glands due to metabolic causes has been observed frequently in diabetic patients, with one report
involving 24% of the diabetic subjects. Sialosis is caused by fatty infiltration of the interstitium and enlargement
of the acinar cells and, in diabetics, is characterized by bilateral enlargement of the parotid salivary glands
though the submandibular gland may also be involved. Compensatory hyperplasia of the glandular parenchyma
following a declining plasma insulin concentration, and a compensatory mechanism to combat xerostomia in
diabetics has been interpreted by investigators as the causes of the glandular enlargement. 10

www.iosrjournals.org 36 | Page
 Oral changes in Diabetes a review

Xerostomia
Xerostomia is a subjective sensation of the dryness of the mouth and has been a feature of uncontrolled
diabetes. Xerostomia in diabetes is traced to decreased salivary secretion related to various factors associated
with diabetes. Microvascular disease, autonomic neuropathy, dehydration and loss of urinary electrolytes
resultant to polyuria are considered as causative mechanisms for the decreased salivary secretion in diabetics. 10
Experimental studies in diabetic rats have shown that fatty infiltration and degeneration of the parotid gland
destroy the secretory tissue leading to diminished saliva production.10 However, more than a third of diabetic
patients report xerostomia in the presence of normal production of saliva with some studies reporting
comparable or increase in volumes of salivary secretion. Hence, the pathogenesis of this condition still remains
unclear and may have a psychological component.10

Taste impairment
All the primary taste sensations may be blunted as is demonstrated by chemical gustometry. Taste
threshold may also be altered and is demonstrable by electrogustometry. Impairment of the sweet taste has been
most frequently reported and may be present at diagnosis. Although taste impairment is usually well tolerated, a
blunted sweet sensation may favour sweet tasting food and may exacerbate the hyperglycemia in an
undiagnosed diabetic patient. The role of altered taste sensation in the predilection for food containing refined
sugar and the subsequent poor dietary compliance in some diabetics has not been investigated. Sulphonylureas,
the group of drugs commonly used type 2 diabetes have been shown to be associated with altered taste
sensation10.

Oral lichen planus and lichenoid reaction

Lichen planus is a mucocutaneous disorder of uncertain aetiology. An association between oral lichen
planus (OLP) and impaired glucose tolerance has been reported, but may be coincidental as it has not been
confirmed by various investigators. OLP may either regress spontaneously or may respond to local treatment
unrelated to the glycemic state in DM. The triad of OLP, DM and hypertension in Grinspans syndrome may be
a coincidental association. What is clinically diagnosed as lichen planus could perhaps be a lichenoid reaction
developing as a side-effect of certain oral hypoglycemic or antihypertensive drugs 10-11.

Oral candidosis
Candida species have frequently been reported to be more prevalent and have been isolated in greater numbers
from the oral cavity of diabetics compared to non-diabetic individuals. Enhanced growth of the yeast may be
attributed to low salivary secretion and presence of a high concentration of salivary glucose. Subjects with
diabetes were found to be at least five times more likely than control subjects to have oral soft tissue disease
attributable to candidiasis. Prerequisites for candidal infections like enhanced adhesiveness of candida to oral
epithelium and an impaired immune response due to defective neutrophil function is a feature of diabetes 10.

Dental caries
Saliva and gingival crevicular fluid, in addition to constituents of the diet are the source of fermentable
carbohydrates required for the growth of cariogenic bacteria. Significantly elevated levels of glucose in saliva
and crevicular fluid, along with decreased salivation as they occur in diabetics may promote the increase in the
incidence of dental caries. Although the total oral intake of refined carbohydrates may be reduced in diabetic
patients, ingestion of food still occurs at frequent intervals throughout the day, and causes a repeated reduction
in the pH of the oral cavity which is another factor for the increased susceptibility10.

Mucormycosis
It is a rare but serious systemic fungal infection that may occur in uncontrolled diabetes. Mucormycosis
is an aggressive, frequently fatal invasive fungal infection that can develop in immunocompromised patients.
Mucor is often recognized as a triad of symptoms, such as uncontrolled diabetes mellitus, periorbital infection
and meningoenchephalitis13.

Tongue changes
Various studies report increased incidence of median rhomboid glossitis, benign migratory glossitis,
burning mouth syndrome or fissuring of the dorsum of the tongue.
Median rhomboid glossitis which is a painless, central, depapillated area on the middle third of the dorsum of
the tongue has been reported in 30% of 175 diabetic patients surveyed.10
There has been a four fold increase in incidence of geographic tongue compared to non diabetes according to a
survey10. In non-diabetic patients this lesion responds to systemic zinc therapy.

www.iosrjournals.org 37 | Page
 Oral changes in Diabetes a review

Burning mouth syndrome which particularly affects the tongue and reported in subjects with undiagnosed
diabetes are not related primarily to candidal infection and almost always resolves when glycemic control is
instituted. Acute neuritis, chronic neuropathic lesion and xerostomia seen in diabetics are implicated in the
aetiology, highlighting its multifactorial origin.
Fissured tongue was present in 28.0% in a survey of 175 diabetics 12. Majority of them showed varying degree of
placation with a transverse component to the fissures. Symmetrical, medially placed, double, longitudinal
fissures extending from sulcus terminalis, meeting centrally to demarcate a triangular area of tongue were seen
in some instances.

Traumatic ulcers and irritation fibromas

Higher prevalence for oral ulcers and irritation fibromas are reported in diabetics. Several mechanisms
like slower healing time, microangiopathy or a defective function of the polymorph nuclear leukocytes may be
responsible3.

Periodontium and DM
The relationship between periodontal disease and DM has been extensively studied and has been
definitive enough to consider periodontitis as the sixth complication of DM. 14 In diabetes with poor glycemic
control, gingival and periodontal inflammations are manifested as increase in incidence and severity, with deep
periodontal pockets, rapid bone loss, and frequent periodontal abscess. There has also been a correlation
between the severity of the periodontal destruction, the duration of the diabetes and the presence of diabetic
complications. Defective polymorphonuclear leukocyte function with resultant susceptibility of infection,
increased collagenase activity, decreased synthesis and maturation of collagen and extra cellular matrix are
postulated as causes of poor periodontal health in diabetics. The abnormal state of the collagen is attributed to
excessive formation of advanced glycation end products (AGEs) in hyperglycemic states, which crosslink the
collagen rendering it less soluble and hence less likely to be repaired or replaced.8
Tendency towards enlarged gingiva, sessile or pedunculated gingival polyps, polypoid gingival proliferations,
abscess formation, periodontitis, and loosened teeth are the other varieties of periodontal changes described in
DM.

II. Conclusion
The oral changes in diabetes are less likely to be seen in well controlled diabetics. The changes are not
specific or pathognomonic for diabetes. The association of specific oral diseases and diabetes is not only of
importance in the detection of undiagnosed diabetes, but also in the elucidation of the pathogenesis of various
oro-facial diseases. However, the association of certain oral conditions with DM is not definitive and is still a
matter of debate. In view of the ever increasing sedentary lifestyles and poor eating habits that have contributed
to the escalation of DM worldwide, DM-related oral diseases deserve adequate recognition and further
investigation.

References
[1]. S h a r m a A, T i wa r i A. D i a b e t e s m e l l i t u s a n d D e n t a l D i s e a s e - a r e v i e w . J ID A 2 0 0 2 ; 7 3 : 1 1 6 - 2 1 .
[2]. A l v i n C P o w e r s . D i a b e t e s M e l l i t u s . In : Fa u c i A S , B r a u n wa l d E , Ka s p e r D L , H a u s e r S L, L o n g o D L ,
J a m e s o n J L , L o s c a l z o J , e d i t o r s . H a r r i s o n s P r i n c i p l e s o f In t e r n a l M e d i c i n e . 1 7 t h E d . U n i t e d S t a t e s
o f A m e r i c a : M c Gr a w - H i l l ; 2 0 0 8 : 2 2 7 5 3 0 4 .
[3]. Gu g g e n h e i m e r J , M o o r e P A , R o s s i e K, M y e r s D , M o n g e l l u z z o M B , B l o c k H M . In s u l i n - d e p e n d e n t
d i a b e t e s m e l l i t u s a n d o r a l s o f t t i s s u e p a t h o l o g i e s . I. P r e v a l e n c e a n d c h a r a c t e r i s t i c s o f n o n - c a n d i d a l
lesions. Oral Surg Oral M ed Oral Pathol Oral Radiol Endod 2000; 8 9 (5): 563 69.
[4]. Fin est one AJ, B ouriji. Diabetes m ellitus in peri odontal di seas e. Diabet es1967:10: 336 40.
[5]. C e r d a J . P e r i o d o n t a l d i s e a s e i n N ID D M . T h e e f f e c t o f a g e a n d t i m e s i n c e d i a g n o s i s . J P e r i o d o n t o l
1995; 65: 991 95.
[6]. C a m p u s G, S a l e m A, U z z a u S , B a l d o n i E , T o n o l o G . D i a b e t e s a n d p e r i o d o n t a l d i s e a s e : A c a s e
c o n t r o l s t u d y. J P e r i o d o n t o l 2 0 0 5 ; 7 6 ( 3 ) : 4 1 8 2 5 .
[7]. S h l o s s m a n M , K n o w l e r W C , P e t t i t D J , G e n c o R J . T yp e 2 D M a n d p e r i o d o n t a l d i s e a s e . J A D A 1 9 9 0 ;
121: 532 36.
[8]. K l o k k e v o l d P R , M e a l e y B L , a n d C a r r a n z a F A . In f l u e n c e o f S y s t e m i c D i s e a s e a n d D i s o r d e r s o n t h e
p e r i o d o n t i u m . In : N e w m a n M G, T a k e i H H , C a r r a n z a F A , e d i t o r s . C a r r a n z a s C l i n i c a l
Period ontology. 9 th ed. Philadelphia, Pennsylvania: Saunders; 2003. pp 208 -11.
[9]. Ki r a n M , A r p a k N , U n s a l E , E r d o g a n M F. T h e f f e c t o f i m p r o v e d p e r i o d o n t a l h e a l t h o n m e t a b o l i c
c o n t r o l i n t yp e 2 d i a b e t e s m e l l i t u s . J C l i n P e r i o d o n t o l 2 0 0 5 ; 3 2 ( 3 ) : 2 6 6 7 2 .
[10]. L a m e y P J , D a r wa z e h AM , F r i e r B M . O r a l d i s o r d e r s a s s o c i a t e d wi t h d i a b e t e s m e l l i t u s . D i a b e t M e d
1992; 9 (5): 410 1 6.
[11]. B o r g h e l l i R F , P e t t i n a r i I L , C h u c h u r r u J A, S t i r p a r o M A. O r a l l i c h e n p l a n u s i n p a t i e n t s wi t h
d i a b e t e s : An e p i d e m i o l o g i c s t u d y. O r a l S u r g O r a l M e d O r a l P a t h o l 1 9 9 3 ; 7 5 : 4 9 8 5 0 0 .

www.iosrjournals.org 38 | Page
 Oral changes in Diabetes a review
[12]. V i j a ya b a l a G S , An n i g e r i R G, S u d a r s h a n R . M u c o r m yc o s i s i n a d i a b e t i c Ke t o a c i d o s i s p a t i e n t . A s i a n
Pac J Trop Biomed 2013; 3(10):830 -33.
[13]. F a r m a n A G. At r o p h i c l e s i o n s o f t h e t o n g u e : A p r e v a l e n c e s t u d y a m o n g 1 7 5 d i a b e t i c p a t i e n t s . J O r a l
Pathol 1976; 5: 255 64.
[14]. Loe H. Period ontal disease. Th e sixth complication of diabetes mellitus. Diab et es Care1993;
16:329-34.

www.iosrjournals.org 39 | Page