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Diabetes Mellitus being a metabolic disorder of carbohydrate metabolism affects all tissue
of the body. There are a plethora of oral manifestations which occur in diabetes mellitus. Most of the oral pathologies are either exacerbated or triggered by diabetes. Except for Median Rhomboid Glossitis there are no specific pathognomnic manifestations associated with diabetes.
Median Rhomboid Glossitis
Central papillary atrophy of tongue - It was described classically as a congenital
abnormality of the tongue which is presumably due to failure of die tuberculum impar to retract or withdraw before fusion of the lateral halves of the tongue, so that a structure devoid of papillae is interposed between them. Most current evidence strongly suggest an etiologic relationship between MRG and a localized chronic fungal infection specially Candida albicans. Farman found in large series of patients that this condition is particularly common among diabetics. It appears as an ovoid, diamond, or rhomboid shaped reddish patch or plaque on the dorsal surface of the tongue immediately anterior to the circumvallate papillae. A flat or slightly raised area sometimes mamelonated it stands out distinctly from the rest of the tongue because it has no filliform papillae. It is most obvious clinically when the rest of the tongue appears coated or the papillae are heavy and matted. The etiology is unclear but has recently been linked with invasion of Candida species and a significant decrease in number and function of specialized macrophages (Langerhans cells) in the epithelium of the lesion. The incidence is less than 1% approximately 3 cases per thousand population. It is 3 times more common in men than in women. There is no specific treatment. Spontaneous remission is also known. Some cases respond to Nystatin & Amphotercin B.
Microbiologic studies of oral flora in diabetes
Significant differences in distribution and ratios of bacterial morphotypes in gingival
crevices of type I diabetics have been observed. The microflora from IDDM patients contained higher proportions of gram negative rods & total gram negative bacteria than healthy controls. These morphotypes are considered to be periodontaly more pathogenic forms than other types found in gingival crevices.
A statistically significant difference in the incidence of staphylococci in diabetics as
compared with non diabetics and preponderance of staphylococcus saprophyticus in non-diabetics and S. epidermidis in diabetics have been reported.
IDDM patients with periodontitis have a subgingival flora composed mainly of
Capnocytophaga, anaerobic vibrios & Actinomyces species. Certain organisms like Bacteroides gingivalis, B intermedius, & Actinobacillus actinomycetemcomitans which are common in periodontal lesions of non diabetics are present in low numbers in diabetics. Black pigrnented bacteroides species specally B gingivalis and also B intermedius and Wolinella recta are prominent in severe periodontal lesions of patients with NIDDM. Individuals who are 45 years old or older and who are diabetic and smoke have a 20 times higher risk of periodontal diseases then patients who don't have these indicators. If they are also infected subgingivally with B forsythus or Pdrphyromonas gingivalis the risk increases to 30-50 times. Candidal colonization is attributed to increased genetic susceptibility, altered immune response and a change in the oral biochemical environment favoring exuberant growth.
Biochemical changes in oral milieu in diabetics.
The glucose content of gingival fluid and blood is higher in diabetic patients. The gingival
fluid from diabetics contain a reduced level of cyclic adenosine monophosphate (C-AMP) compared with that of non diabetics. Because C-AMP reduces inflammation, this is another possible mechanism that could lead to increased severity of gingival inflammation in diabetics. The salivary blood glucose level 1 hour after meals is higher in diabetics but is not usually of diagnostic significance.
Histologic features : It has been shown that thickening of capillary basement membrane
warrants special attention because this hampers with the transport of nutrition & oxygen to gingiva thereby decreasing its resistance to local irritants. It has been suggested that gingival biopsies may be an important aid in detectionof prediabetic and diabetic states. Electron microscopic studies of gingival biopsies specimen have shown a statistically significant increase in thickness of the BM of capillaries in diabetics.
It is a universal consensus that the basic crux of diabetes management lies in the
stringent maintenance of blood glucose at physiologic levels. Most of the oral conditions get worsened in uncontrolled diabetics moreover a recent study supports the view that gingivitis & other pathologies of mouth cavity occur earlier in type I diabetes compared to non-diabetic controls.
In uncontrolled diabetics following findings can be seen in the oral mucosa.
- Xerostomia — Diabetics mellitus also predisposes to xerostomia. There is diminished salivary secretion. Patient complaints of dryness and burning sensation in the mouth. Oral mucosa is dry atrophic and inflamed. It may manifest as atrophy of the papillae inflammation, fissuring and cracking and in severe cases by areas of denudation, soreness, burning and pain in the mucous membrane and tongue. In chronic cases it predisposes to rampant dental caries and subsequent loss of tooth.
- Chelosis and tendency towards drying and cracking
- Greater predominance of 'Candida albicans', hemolytic streptococci & staphylococci.
- Increase tooth sensibility to percussion.
- Increase incidence of enamel hypoplasia.
- Increased incidence of dental caries. Altered eruption patterns of the teeth.
- Localized osteitis (dry socket) after exodontia - This is due to arteriolar changes viz. wall
thickening, narrowed lumen, medial degeneration and vacuolization, and artherosclerosis
leading to decreased blood supply.
Most striking changes in uncontrolled diabetics are reduction in defense mechanisms and
the increased susceptibility to infections leading to destructive periodontal disease. On the contrary well controlled diabetic show none of the above mentioned changes.
Diabetes and the Periodontium : A variety of periodontal changes have been described
in diabetics. The majority of well controlled studies have shown a higher prevalence and severity of periodontal disease in diabetics than in non diabetics with similar local irritation, including greater loss of attachment, increased bleeding on probing and increased tooth mobility. Diabetes per se does not cause these conditions but there are indications that it alters the response of the periodontal tissues to local irritants and that hastens bone loss in periodental disease and retards post surgical healing of the periodontal tissues.
Periodontitis in IDDM appears to start after age 12. The prevalence of periodontitis has
been reported as being 9.8% in 13 -18 years old increasing to 39% in those 19 years and older. IDDM children tend to have more destruction around the first molars and incisors than else where but it becomes more generalized at older ages. Other studies have shown that rate of periodontal destruction is similar for diabetics and non diabetics up to age of 30 years but thereafter its incidence is greater in diabetic population. Patients showing overt clinically proven diabetes more than 10 years have greater loss of periodontal structures than those with a diabetic history of less than 10 years.
Diabetes manifest as following :
- Tendency towards abscess formation - Frequent periodontal abscess is a salient
characteristic feature of periodontal disease in diabetics.
- Diabetic periodontodasia
- Enlarged gingival
- Sessile or psdunculated gingival polyps
- Polypoid gingival proliferation
- Loosened teeth
- Gingival Angiopathy - Diabetic patients exhibit this condition in the form of PAS positive
diastase resistant thickening of vessel wall, hyalinization and luminal obliteration of
vessel wall. Similar changes are also formed in periodontal ligament vessels of diabetic
patients,
- Severe gingivitis
- Deep periodontal pockets.
Delayed wound healing : Wound in diabetic patients are notoriously slow to heal and
frequently show complications in repair process. Minor dental procedures like dental extractions may show undue delay in would healing. This is probably the direct reflection of disturbances in cellular carbohydrate metabolism.
Management of dental conditions in diabetes mellitus :
It is advisable to use local anaesthetic agents without epinephrine in dental procedures,
because minimal does of epinephrine have been shown to elevate blood glucose concentrations, this is particularly relevant if accidental intravenous injection occurs when giving a mandibular block. Secondly there is increased incidence of dry sockets mainly associated with mandibular extractions, is thought to be related to a reduced blood supply to the mandible caused by atherosclerosis in long standing diabetics. Epinephrine will further reduced the blood supply to the area which may increase the likelihood of dry socket. Following extraction, suturing of sockets to aid hemostasis is recommended.
A physician's advice should always be sought before arranging general anesthetics for
dental treatment. Although some reports suggest antibiotic prophylaxis before dental surgery to prevent subsequent infection, there does not appear to be good evidence to support this treatment. If however, oral infection does occur after treatment, appropriate antibiotic therapy should be initiated at that stage. Complicated oral procedures in dental emergencies should be avoided whenever possible in uncontrolled diabetics until stablization of blood glucose levels can be achieved. All type of general dental treatment may be performed safely in the dental office on controlled diabetic patients.
REFERENCES
1. Farman A.G., Atrophic lesions of the tongue. ApreVaSence study among 175 diabetic
patients. J. Oral. Path. 5 : 255, 1976.
2. Russel B.J., Gingival changes in Diabetic Mellitus. Vascular changes. Acta patho.
Microbio. Scand. 68 : 161, 1966.
3. Carter L.C., MRG - A puzzling entity. Compendia Contin. Educ. Dent., 1990, 11 : 446.
4. Fannin A. Carranza - Endocrinologic influences on the periodontium
5. GKckmans Clinical Period ontology 8th edition 444 - 459.
6. Belting C.M., Hinicker J.J., Dummett C.O. - Incluences of DM on severity of
Periodontal Disease. J. Periodontology 35 : 476,1964.
7. Cianciola L.J., Park B.H., Bruck E., Musovich L., Genco R.J., - Prevalence of
periodontal diseases in IDDM. J. Am. Dent. Ass. 104 : 653,1982.
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