**1. Introduction**

Diabetes mellitus (DM) is one of the systemic diseases affecting a considerable number of patients worldwide [1]. Numerous experimental and clinical studies on the complications of DM have demonstrated extensive alterations in bone and mineral metabolism, linear growth, and body composition [2]. Depletion of insulin in Type 1 Diabetes Mellitus (T1DM) causes a reduction of bone mineral density and decreases skeletal mass, thus altering linear growth, body composition and delaying fracture healing. A considerable sector of literature was dedicated to studying the effects of T1DM on long bones; however, fewer studies dis‐ cussed the effects of T1DM type on the craniofacial complex which is regulated by hor‐ mones, nutrients, mechanical forces, and various local growth factors.

Bone metabolism in the craniofacial complex involves a mosaic growth sites that grow at different rates and mature at different times, its growth and by analogy, the response to growth disruption is much more complex than that of the appendicular skeleton. Previous studies showed that T1DM may significantly affect the bone remodeling process which is observed during conducting treatments involving the application of mechanical or function‐ al forces to the craniofacial complex and the teeth as those applied during orthodontic movement. Moreover, it is expected that the T1DM may alter the general growth of patients due to insulin deficiency and consequently leads to delayed skeletal maturation.

Type 1 diabetes mellitus (T1DM) is an endocrine–metabolic syndrome of childhood and adolescence, characterized by hyperglycemia as a cardinal biochemical feature, with impor‐ tant consequences for physical and emotional development. Several mechanisms have been reported to explain the altered bone remodeling in diabetes, one of which is diminished

© 2013 Abbassy et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

bone formation as a result of decreased osteoblastic activity or enhanced apoptosis of osteo‐ blastic cells. Another contributing factor may be increased bone resorptive activity. Howev‐ er, it is still controversial whether osteoclastic recruitment and function are altered in diabetes, because no change or decrease in the activity of osteoclasts has been reported [1].

**• Familial short stature**

imately the same height as their parents.

al hormones, including growth hormone.

proportion to his/her short stature.

**2.3. Effect of DM on Bone and Growth**

**• Endocrine (hormone) diseases**

Familial short stature is a tendency to follow the family's inherited short stature (shortness).

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

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

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A child who tends to be shorter than average and who enters puberty later than average, but is growing at a normal rate. Most of these children tend to eventually grow to approx‐

Constant malnutrition, digestive tract diseases, kidney disease, heart disease, lung dis‐

Adequate production of the thyroid hormone is necessary for normal bone growth. Cush‐ ing's syndrome can be caused by a myriad of abnormalities that are the result of hyperse‐ cretion of corticosteroids by the adrenal gland. Growth hormone deficiency involves a problem with the pituitary gland (small gland at the base of the brain) that secretes sever‐

A condition called intrauterine growth restriction (IUGR), slow growth within the uterus occurs during a pregnancy. The baby is born smaller in weight and length than normal, in

Hand-wrist radiographs have been studied in juvenile diabetics [6]. There is delayed ap‐ pearance or delayed development of a center of ossification, usually of a carpal bone. These defects occur twice as frequently in boys than in girls, and the total incidence of juvenile dia‐ betics with anomalies and developmental defects is 24.3%. There is also retardation of bone growth in 60% of diabetic males and 51% of diabetic females. The longer the duration of dia‐ betes, the greater the tendency to bone growth retardation. The decreased bone mass in dia‐ betics has been explained by decreased proliferative capacity of the diabetic fibroblasts, and early senescence of all cells has been suggested as basic to the diabetic problem. This degen‐ eration would lead to early osteopenia in bone [6]. The yearly bone loss was reported to be 1.35% in patients with T1DM [7]. In addition, the rate of bone mineral loss is significantly greater among patients with a deterioration of the metabolic state, despite increasing insulin dosage, when compared with patients with unchanged or improved insulin secretion. This may indicate that the exogenous insulin administration does not fully compensate for the decrease in endogenous insulin secretion. These studies also showed increased bone resorp‐ tion in T1DM patients with no signs of vitamin D deficiency associated with the disease. Vertebral bone density has been studied in T1DM children [7]. It was found that diabetic children exhibited cortical bone density that was slightly, but significantly, lower than the controls. The decrease in cortical bone density in the diabetic group did not correlate with

**• Constitutional growth delay with delayed adolescence or delayed maturation**

ease, hepatic disease, diabetes, and severe stress can cause growth problems.

**• Congenital (present at birth) problems in the tissues where growth occurs**

**• Illnesses that affect the whole body (Also called systemic diseases.)**

Among researchers, there is lack of consensus about the impact of this disease on dental health. It has been suggested that hyperglycemia is associated with decreased salivary se‐ cretion and high salivary glucose levels, particularly in cases of severe insulin deficiency. Consequently, an increased cariogenic challenge in such individuals can be expected. How‐ ever, no clear evidence has been found for an association between dental caries and diabe‐ tes mellitus [3].

The main aim of this chapter is to discuss the complexity of the dento-craniofacial system and how it is affected by T1DM condition. Moreover, the various detrimental effects of T1DM on the dento-craniofacial complex will be explored using the dynamic histomorpho‐ metric analysis and a histological study that will demonstrate that T1DM condition induced various detrimental effects on the quality of bone and on the bone turnover process ob‐ served in the dento-craniofacial complex.
