|DENTAL SCIENCE - ORIGINAL ARTICLE
|Year : 2014 | Volume
| Issue : 5 | Page : 122-126
Morphological alterations in the dentition of type I diabetes mellitus patients
Andamuthu Yamunadevi1, Praveen S Basandi2, GS Madhushankari2, Mandana Donoghue3, Alur Manjunath4, Manickam Selvamani2, HK Puneeth5
1 Department of Oral and Maxillofacial Pathology, Vivekanandha Dental College for Women, Tiruchengode, Namakkal, Tamil Nadu, India
2 Department of Oral and Maxillofacial Pathology and Microbiology, College of Dental Sciences and Hospital, Davangere, Karnataka, India
3 Independent researcher and consultant pathologist, Belgaum, Karnataka, India
4 Department of General Medicine, J.J.M Medical College, Davangere, Karnataka, India
5 Department of Oral and Maxillofacial Pathology, St. Joseph Dental College, Eluru, Andhra Pradesh, India
|Date of Web Publication||25-Jul-2014|
Dr. Andamuthu Yamunadevi
Department of Oral and Maxillofacial Pathology, Vivekanandha Dental College for Women, Tiruchengode, Namakkal, Tamil Nadu
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Introduction: Type 1 diabetes mellitus (DM) is an endocrine disorder that occurs commonly in an age group, where the development of primary and permanent dentition takes place. As altered endocrine functions may affect the shape and size of teeth leading to dental anomalies, this study was conducted to look for the occurrence of any dental anomalies in type I DM patients. Materials and Methods: A diabetic camp was conducted at Alur Chandrashekharappa Memorial Hospital, Davangere, where 30 diabetic patients were examined and the impressions of their maxillary and mandibular arches were recorded. Age and sex matched controls were selected randomly, and similar recordings were done. Results: Type I diabetic patients showed statistically significant (P < 0.001) morphological alterations of total number of cusps, including presence of 6 th cusp in mandibular molars and extra cusps in mandibular premolars. Other alterations such as microdontia, flower shaped mandibular molars, prominent cusp of carabelli, and oblique ridge in maxillary molars were also noted. Severe attrition was found in 11 (36.6%) of the diabetic patients, whereas the control group showed attrition only in 2 (6.8%) patients. Conclusion: Remarkable morphological alterations do occur in the dentition of type I DM patients.
Keywords: alterations, odontogenesis, oral manifestations, tuberculum intermedium, tuberculum sextum, type I diabetes mellitus
|How to cite this article:|
Yamunadevi A, Basandi PS, Madhushankari G S, Donoghue M, Manjunath A, Selvamani M, Puneeth H K. Morphological alterations in the dentition of type I diabetes mellitus patients. J Pharm Bioall Sci 2014;6, Suppl S1:122-6
|How to cite this URL:|
Yamunadevi A, Basandi PS, Madhushankari G S, Donoghue M, Manjunath A, Selvamani M, Puneeth H K. Morphological alterations in the dentition of type I diabetes mellitus patients. J Pharm Bioall Sci [serial online] 2014 [cited 2020 Dec 5];6, Suppl S1:122-6. Available from: https://www.jpbsonline.org/text.asp?2014/6/5/122/137415
Oral cavity can be considered as the mirror of the body as manifestations of many systemic diseases reflect in it. Diabetes mellitus (DM), the most common systemic disease of the millennium has broad spectrum of oral manifestations. Advanced periodontal disease and dental caries, sialosis, xerostomia, dysgeusia, prolonged or recurrent fungal and bacterial infections and burning mouth syndrome are well established oral manifestations of this widely prevalent systemic disorder. ,
Among the two types of DM, type I DM is a disease, which commonly occurs in an age group where the development of primary and permanent dentition takes place. It develops as a result of synergetic effects of genetic, environmental, and immunological factors, which lead to a progressive destruction of pancreatic beta cells, thereby causing decreased insulin production.  As a result, through the direct effect of insulin deficiency and ensuing hyperglycemia or via the more long-term effects of vascular disease, bone metabolism, and mineral homeostasis are hampered. ,
Hampering mineral homeostasis will have direct effect on the hard tissues of the body namely, the bone and the teeth. These juvenile DM patients have been found to have decreased vertical height of the alveolar bone  and decreased cephalometric measurements.  Furthermore, in odontogenesis, mineralization defects are proved  and ameloblast's function is hampered due to the absence of secretory proteins,  resulting in enamel and dentin defects. As such metabolic disturbances can cause dental anomalies, this study is aimed at identifying if any morphological alterations occur in the dentition of type I DM patients.
| Materials and Methods|| |
Oral screening camp for type I DM patients was conducted by the Department of Oral and Maxillofacial Pathology, College of Dental Sciences, Davangere in association with Alur Chandrashekharappa Memorial Hospital, where 30 type I DM patients were examined. Case histories, hematological investigations including hemoglobin estimation, fasting blood glucose level, impressions and photographs of the maxillary and mandibular arches were taken after obtaining informed consent from the patients. Following this, age and sex matched healthy controls, were selected randomly from the patients visiting the various Departments of College of Dental Sciences and the impressions of their maxillary and mandibular arches were recorded.
The dental casts and photographs were analyzed for the following variations between the two groups,
1. Morphological alterations: Size - microdontia/macrodontia shape - cuspal morphology, pits and fissures, grooves.
2. Age changes: Attrition.
Third molars were excluded from the study due to their common anomalous nature. Standard dental morphology as described by Woelfel,  Wheeler  was taken for reference and statistical analysis was done using unpaired t-test.
| Results|| |
The dentition of the healthy control group did not show any morphological alterations, while the following morphological alterations were observed in dentition of test group (type I DM group).
- Presence of 6 th cusp in mandibular first molars - 7 cases
- Presence of extra cusps in mandibular second molar - 5 cusps (1 case), 6 cusps (1 case)
- Y pattern in mandibular first premolar - 1 case
- 4 cusps in mandibular second premolar - 1 case
- Flower shaped mandibular molar - 1 case
- Prominent cusp of carabelli and oblique ridge in maxillary molar - 1 case
- Presence of 4 cusps in mandibular first molar - 2 cases (being normal variation,  not included as anomaly).
- Attrition - 11 cases in type I DM group
- Attrition - 2 cases in control group.
The results are tabulated in [Table 1] and are statistically highly significant with P < 0.001.
| Discussion|| |
Type I DM (insulin dependent diabetes mellitus [IDDM]) is due to autoimmune destruction of the beta cells (the so called "type I process"). A similar clinical picture of insulin dependence can be caused by other forms of severe pancreatic damage.  Several years of progressive autoimmune damage usually precede the clinical onset of this type of diabetes. This long prediabetic phase is usually asymptomatic and rarely detected. Early diagnosis in the prediabetic phase can provide an opportunity to prevent subjects with active insulitis from developing clinical disease. Provision of immunosuppressive and immunomodulatory treatments at this prediabetic phase are currently undergoing clinical trials to prevent development of clinical disease. 
Hence, diagnosis at the prediabetic stage becomes the need of the hour and it is here, where as a dentist, our careful observations can aid in early diagnosis. Though various soft tissue pathologies occurring in oral cavity of these patients are well-established, , identifying through morphological alterations in dentition can help to diagnose still earlier as these morphological alterations occur quite early.
Type I diabetes is considerably rarer than type II, accounting for between 5% and 15% of all diabetes. It appears predominantly in childhood, with a peak age at presentation of about 11 years in girls and 14 years in boys - hence the old description of "juvenile - onset."  In this study, the mean age of presentation was 12.4 years in boys and 11.1 years in girls [Table 2].
From the study results, no significant correlation was found between the age at diagnosis of diabetes and the occurrence of morphological alterations. Morphological alterations of the dentition are only be brought about by changes during the odontogenesis stage. The established protracted prediabetic phase in the disease can be assumed to explain the changes without any correlation with the age at diagnosis. Similarly duration of diabetes, fasting blood sugar level, and hemoglobin percentage on the day of examination had no correlation with the presence or absence of morphological alterations.
Regarding the morphological alterations, the results of the study showed more marked alterations in cuspal number and position, in particular mandibular first molar. The occurrence of 6 th cusp in mandibular molars has two forms namely, "tuberculum intermedium" and "tuberculum sextum."  A third lingual cusp developing on mandibular molars on the lingual surface is called a tuberculum intermedium.  If this extra cusp is located on the distal marginal ridge, it is called as tuberculum sextum.  In this study, seven cases showed 6 th cusp in mandibular molars, among them five showed tuberculum intermedium [Figure 1] and two showed tuberculum sextum [Figure 2]. None of the controls showed this anomaly and similarity in the occurrence of this anomaly in notable number of IDDM patients suggests that this finding cannot be incidental.
Other observations included 4 cusps in mandibular second premolar [Figure 3], 'Y' shaped occlusal pattern in mandibular first premolar [Figure 4], mandibular second molar with 5 cusps [Figure 5] and 6 cusps [Figure 4], mandibular first molar with 4 cusps [Figure 6], flower shaped mandibular molar [Figure 7], prominent cusp of carabelli and oblique ridge in maxillary molar [Figure 8]. Furthermore, 4 cases showed localized microdontia in second premolar (1 case) and second molars (3 cases). Few cases showed multiple anomalies [Figure 4] and [Figure 5].
|Figure 3: Four cusps in right mandibular second premolar (lingually 3 cusps)|
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|Figure 4: Y type occlusal pattern in mandibular first premolar along with tuberculum intermedium in first and second molars|
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|Figure 5: Left mandibular first molar with 6 cusps and second molar with 5 cusps|
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|Figure 8: Prominent cusp of carabelli and oblique ridge in left maxillary first molar|
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Thus, totally out of 30 patients, 14 (46.5%) showed developmental variations in size and shape. In contrast, the control group showed no anomalies. This statistically significant (P < 0.001) morphological alteration provides a link between the altered endocrine function and morphodifferentiation stage of odontogenesis. It may be hypothesized that hyperproductivity of the inner enamel epithelium or an altered genetic pathway controlling the enamel knot function cause occurrence of 6 th /supernumerary cusp anomaly in these patients.
The study found regressive alteration in the form of, marked attrition in 11 of the type I DM patients (36.6%) which was more severe than in the two patients (6.8%) of control group. Studies at ultrastructural level on the teeth of diabetic rodents have shown that the DM directly causes enamel hypoplasia, which inturn may contribute to this increased attrition.  The occurrence of enamel hypoplasia in DM is well-explained by the following hypotheses. 
- Due to the secondary effects of DM such as microangiopathy, less calcium is integrated in both the enamel and the bone of diabetic animals
- Second, secondary effectors such as proteins, which control the exact arrangement of the prisms, are absent. In such case, the function of the ameloblasts would also be remarkably decreased
- Also, increased blood glucose concentration would be directly responsible for the irregular prism structure in enamel by influencing the secretory ameloblasts.
Elevated glucose concentration also significantly inhibits osteoblastic calcium deposition and bone maturation. 
No other studies in the literature have focused on the morphological alterations in these patients. Findings similar to our study are also seen in Berardinelli Seip syndrome  and Alstrom's syndrome,  where DM is one of the features. Here enamel hypoplasia and occurrence of talon's cusp are reported, with etiology probably due to this endocrine disturbance, DM.  The proposed hypothesis for the formation of Talon's cusp in this study are "hyperproductivity of the anterior ends of dental lamina, disturbances during morphodifferentiation, such as altered endocrine function, which may affect the shape and size of a tooth without impairing the functions of ameloblasts or odontoblasts, and malinteraction between ectoderm and mesoderm at the time of complex odontogenesis process on the epithelial buddings of the premaxillary region." 
Thus, the results of this study suggest that though all the dental anomalies occurring in different individuals cannot be due to DM, the presence of such anomalies should arouse the suspicion of DM and further signs and symptoms should be elicited and the physician can be consulted for intense blood glucose examination. Genetically induced diabetes like juvenile type I diabetes may lead to much more destruction in the quality and quantity of life than type II diabetes. As our keen observation can interrupt the progress of the disease at the prediabetic phase itself, the value of such reflectors of systemic conditions should not be overlooked or neglected. Further studies on larger sample population and advanced research on odontogenesis can lead this affected young generation toward disease free future.
| Conclusion|| |
The encouraging results of our study strongly suggest that remarkable morphological alterations do occur in the dentition of type I DM patients. The exact mechanism whereby diabetes affects the hard tissue development is as yet to be studied with advanced research on odontogenesis.
| References|| |
|1.||Guggenheimer J, Moore PA, Rossie K, Myers D, Mongelluzzo MB, Block HM, et al. Insulin-dependent diabetes mellitus and oral soft tissue pathologies. I. Prevalence and characteristics of non-candidal lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:563-9. |
|2.||Guggenheimer J, Moore PA, Rossie K, Myers D, Mongelluzzo MB, Block HM, et al. Insulin-dependent diabetes mellitus and oral soft tissue pathologies: II. Prevalence and characteristics of Candida and Candidal lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:570-6. |
|3.||Hakonarson H, Grant SF, Bradfield JP, Marchand L, Kim CE, Glessner JT, et al. A genome-wide association study identifies KIAA0350 as a type 1 diabetes gene. Nature 2007;448:591-4. |
|4.||Abbassy MA, Watari I, Soma K. Effect of experimental diabetes on craniofacial growth in rats. Arch Oral Biol 2008;53:819-25. |
|5.||Shyng YC, Devlin H, Sloan P. The effect of streptozotocin-induced experimental diabetes mellitus on calvarial defect healing and bone turnover in the rat. Int J Oral Maxillofac Surg 2001;30:70-4. |
|6.||Giglio MJ, Lama MA. Effect of experimental diabetes on mandible growth in rats. Eur J Oral Sci 2001;109:193-7. |
|7.||Bensch L, Braem M, Van Acker K, Willems G. Orthodontic treatment considerations in patients with diabetes mellitus. Am J Orthod Dentofacial Orthop 2003;123:74-8. |
|8.||Atar M, Atar-Zwillenberg DR, Verry P, Spornitz UM. Defective enamel ultrastructure in diabetic rodents. Int J Paediatr Dent 2004;14:301-7. |
|9.||Schied RC, Weiss G. Woelfel's Dental Anatomy. 8 th ed. Philadelphia: Library of Congress Cataloging in Publication Data; 2010. p. 331. |
|10.||Ash M. Wheeler's Dental Anatomy, Physiology and Occlusion. 7 th ed. Philadelphia: WB Saunder's Company; 1993. |
|11.||Frier BM, Fisher M. Diabetes mellitus. In: Colledge NR, Brian RW, editors. Davidson's Principles and Practice of Medicine. 21 st ed. Oxford, UK: Churchill Livingstone Elsevier; 2010. p. 800-1. |
|12.||Neville BW, Damm DD, Allen C, Bouquot JE. Oral and Maxillofacial Pathology. 2 nd ed. Philadelphia; WB Saunders Company; 2002. p. 61-2. |
|13.||Solanki M, Patil SS, Baweja DK, Noorani H, Pk S. Talon cusps, macrodontia, and aberrant tooth morphology in Berardinelli-Seip syndrome. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:e41-7. |
|14.||Atar M, Körperich EJ. Systemic disorders and their influence on the development of dental hard tissues: A literature review. J Dent 2010;38:296-306. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2]