**4. Conclusions**

and thus can easily eliminate many variables that can affect the outcome of the results of

In vitro studies on animal models affected by the streptozotocin induced diabetic condition showed that there is a low concentration of calcium and fluoride in the growing rats` inci‐ sors after inducing the diabetic condition by the streptozotocin injection [54]. Moreover, there was a concomitant increase in the concentration of calcium in blood serum and a decrease in fluoride concentration in blood serum. It was suggested that the decrease of calcium concen‐ tration in the teeth structure in this study was due to decrease of the cellular activity of ameloblasts during the enamel development [54]. This suggestion may be backed by the results obtained from a similar streptozotocin induced diabetic rat model which showed that the diabetic condition is associated with a decrease in the calcium deposition in bone due to a generalized metabolic activity decrease [12, 28]. The recorded increase in calcium in blood serum was attributed to the absence of insulin which aids in the transfer of calcium from the blood serum to the body tissues. The low concentration of fluoride observed in the tooth structure and in the blood serum may be attributed to the incorporation of the fluoride in bone matrix which is induced by the high concentration of the estrogen observed in the blood serum [54]. Moreover, the increase in fluoride elimination in urine may have caused this decrease in

The saliva contents and rate of flow are among the critical factors that predict the caries inci‐ dence in the oral cavity. Type 1 DM is among the endocrine disease that elevates the glucose

The mechanism by which the glucose level may increase in saliva may be explained by previous research showed that the increase of blood glucose level in T1DM cases is associated with a concomitant increase of glucose level in saliva. Moreover, it was previously suggested that T1DM causes an increase in the permeability of the basement membrane of the parotid gland that favors the transfer of glucose from the parotid gland to the saliva in the oral cavity [3]. The mechanism by which T1DM decreases the salivary flow may be attributed to the detri‐ mental effects induced by the T1DM condition on the salivary gland tissues itself causing a

The factors of increased glucose level and decrease in salivary flow cause the improper clearance of glucose from the oral cavity and impairs the buffering capacity of saliva rendering it more acidic, these aforementioned effects consequently increase the metabolic activities of the bacterial biofilm in the oral cavity and render teeth more susceptible to dental caries [3].

Previous research work [3] showed that the dietary habits conducted by the diabetic pa‐ tients do not have a significant effect on the prevalence of caries in these patients when com‐ pared to normal individuals and thus it may be concluded that the increase in caries prevalence in diabetic patients is likely associated with factors affecting the development of teeth or due to some detrimental effects induced by the oral environment that increases the

any experiments conducted on humans.

424 Type 1 Diabetes

fluoride concentration in the diabetic rats.

**3.3. Effects of Type 1 Diabetes on salivary status**

generalized decrease in the saliva in the oral cavities.

risk of caries occurrence in oral cavities of T1DM patients.

level concentration in saliva and decreases the salivary rate of flow.

It is obvious that the T1DM condition significantly affects craniofacial growth, bone forma‐ tion mechanism and the quality of the bone formed which may alter many aspects of plan‐ ning and treatment of orthodontic patients affected by this globally increasing hormonal disturbance. Moreover, T1DM condition impairs the proper tooth development and alters the oral environment rendering teeth more susceptible to dental caries.

There should be a new strategy for treating orthodontic patients suffering from metabolic disorders specially those disorders having direct and indirect effects on bone growth as the diabetic condition. The orthodontic craniofacial linear measurements were significantly de‐ creased in the T1DM cases when compared to normal cases. Moreover, greater risks of de‐ veloping dental caries and possible tooth loss are associated with patients suffering from T1DM; these risks may complicate the outcome of orthodontic treatment which is associated with less ability of orthodontic patients to implement proper oral hygiene measures due to increased areas of bacterial biofilm formation around orthodontic brackets

These comprehensive studies done on bone and craniofacial growth suggest that planning the treatment in craniofacial region for patients affected with hormonal disorders is a more complex procedure when compared to the treatment of normal patients, moreover it is sug‐ gested that it is of prime importance to keep close attention to the general systemic condi‐ tion of these patients and administer the proper hormonal therapy for these patients when needed to avoid any detrimental effects on bone resulting from any hormonal imbalance. Moreover, it is highly recommended to closely monitor the salivary and the dental condi‐ tions of these patients to allow early intervention for treating any developing dental caries.

Within the limitations of this *in vitro* study, it was concluded that:


**6.** Good control of diabetes mellitus should be considered before orthodontic treatment by a long time inorder to obtain the best outcome.

[5] Kumar, P., & Clark, M. (2009). *Kumar and Clark's Clinical Medicine* (7th edition), Elsev‐

The Effect of Type 1 Diabetes Mellitus on the Dento-Craniofacial Complex

http://dx.doi.org/10.5772/52973

427

[6] El -Bialy, T., Aboul-Azm, S. F., & El -Sakhawy, M. (2000). Study of craniofacial mor‐ phology and skeletal maturation in juvenile diabetics (Type I). *American Journal of Or‐*

[7] Roe, T. F., Mora, S., Costen, G., Kaufman, F., Carlson, M., & Gilsanz, V. (1991). Verte‐ bral bone density in insulin-dependent diabetic children. *Metabolism*, 40(9), 967-971. [8] Eastell, R., & Lambert, H. (2002). Diet and healthy bones. *Calcified Tissue International*,

[9] Chew, F. S. (1991). Radiologic manifestations in the musculoskeletal system of mis‐ cellaneous endocrine disorders. *Radiologic Clinics of North America*, 29(1), 135-147. [10] Yonemitsu, I., Muramoto, T., & Soma, K. (2007). The influence of masseter activity on

[11] Singleton, D. A., Buschang, P. H., Behrents, R. G., & Hinton, R. J. (2006). Craniofacial growth in growth hormone-deficient rats after growth hormone supplementation.

[12] Abbassy, M. A., Watari, I., & Soma, K. (2008). Effect of experimental diabetes on cra‐

[13] Hough, S., Avioli, L. V., Bergfeld, M. A., Fallon, M. D., Slatopolsky, E., & Teitelbaum, S. L. (1981). Correction of abnormal bone and mineral metabolism in chronic strepto‐ zotocin-induced diabetes mellitus in the rat by insulin therapy. *Endocrinology*, 108(6),

[14] Tein, MS, Breen, S. A., Loveday, B. E., Devlin, H., Balment, R. J., Boyd, R. D., et al. (1998). Bone mineral density and composition in rat pregnancy: effects of streptozo‐ tocin-induced diabetes mellitus and insulin replacement. *Experimental Physiology*,

[15] Thrailkill, K. M., Liu, L., Wahl, E. C., Bunn, R. C., Perrien, D. S., Cockrell, G. E., et al. (2005). Bone formation is impaired in a model of type 1 diabetes. *Diabetes*, 54(10),

[16] Follak, N., Kloting, I., Wolf, E., & Merk, H. (2004). Histomorphometric evaluation of the influence of the diabetic metabolic state on bone defect healing depending on the

[17] Alkan, A., Erdem, E., Gunhan, O., & Karasu, C. (2002). Histomorphometric evalua‐ tion of the effect of doxycycline on the healing of bone defects in experimental diabe‐ tes mellitus: a pilot study. *Journal of Oral and Maxillofacial Surgery*, 60(8), 898-904. [18] Mc Cracken-Wesson, MS, Aponte., R., Chavali, R., & Lemons, J. E. (2006). Bone asso‐ ciated with implants in diabetic and insulin-treated rats. *Clinical Oral Implants Re‐*

defect size in spontaneously diabetic BB/OK rats. *Bone*, 35(1), 144-152.

*American Journal of Orthodontics and Dentofacial Orthopedics*, 130(1), 69-82.

*thodontics and Dentofacial Orthopedics*, 118(2), 189-195.

rat mandibular growth. *Archives of Oral Biology,*, 52(5), 487-493.

niofacial growth in rats. *Archives of Oral Biology*, 53(9), 819-825.

ier.

70(5), 400-404.

2228-2234.

83(2), 165-174.

2875-2881.

*search*, 17(5), 495-500.
