**2. Effect of T1DM on Bone**

### **2.1. Types of Bone formation in craniofacial complex**

Bone forms in two ways, resulting in two types of mature bone – intramembranous and car‐ tilage. Cartilage bone forms in a replacement process within the cartilage models of the em‐ bryo and infant. Intramembranous bone forms through the activation of the osteoblast cell or specialized bone forming cells in one of the layers of fetal connective tissue. The bones of the cranial vault, the face, and the clavicle are intramembranous in origin. All other bones of the body form from cartilage. Intramembranous bone include the mandible, the maxilla, the premaxilla, the frontal bone, the palatine bone, the squamous part of temporal bone, the zy‐ gomatic bone, the medial plate of the pterygoid process, the vomer, the tympanic part of the temporal bone, the nasal bone, the lacrimal bone, and the parietal bone. The original pattern of intramembranous bone changes with progressive maturative growth when these bones begin to adapt to environmental influences. This accounts for deformities due to malfunc‐ tion, disease and other environmental factors [4].

#### **2.2. Causes of growth problems**

Growth disturbances can be associated with specific anatomic or functional defects. They may be of endocrine or non endocrine origin and may result from genetic, nutritional or en‐ vironmental factors. Disturbances in somatic growth show themselves in retardation or ac‐ celeration of the skeletal system, including the facial and cranial bones. Causes for growth problems usually fall into the following categories [5]:

#### **• Familial short stature**

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]. 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‐

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‐

Bone forms in two ways, resulting in two types of mature bone – intramembranous and car‐ tilage. Cartilage bone forms in a replacement process within the cartilage models of the em‐ bryo and infant. Intramembranous bone forms through the activation of the osteoblast cell or specialized bone forming cells in one of the layers of fetal connective tissue. The bones of the cranial vault, the face, and the clavicle are intramembranous in origin. All other bones of the body form from cartilage. Intramembranous bone include the mandible, the maxilla, the premaxilla, the frontal bone, the palatine bone, the squamous part of temporal bone, the zy‐ gomatic bone, the medial plate of the pterygoid process, the vomer, the tympanic part of the temporal bone, the nasal bone, the lacrimal bone, and the parietal bone. The original pattern of intramembranous bone changes with progressive maturative growth when these bones begin to adapt to environmental influences. This accounts for deformities due to malfunc‐

Growth disturbances can be associated with specific anatomic or functional defects. They may be of endocrine or non endocrine origin and may result from genetic, nutritional or en‐ vironmental factors. Disturbances in somatic growth show themselves in retardation or ac‐ celeration of the skeletal system, including the facial and cranial bones. Causes for growth

tes mellitus [3].

402 Type 1 Diabetes

served in the dento-craniofacial complex.

**2.1. Types of Bone formation in craniofacial complex**

tion, disease and other environmental factors [4].

problems usually fall into the following categories [5]:

**2.2. Causes of growth problems**

**2. Effect of T1DM on Bone**

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

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

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‐ imately the same height as their parents.

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

Constant malnutrition, digestive tract diseases, kidney disease, heart disease, lung dis‐ ease, hepatic disease, diabetes, and severe stress can cause growth problems.

#### **• Endocrine (hormone) diseases**

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‐ al hormones, including growth hormone.

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

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 proportion to his/her short stature.

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

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 age, sex, duration of diabetes, or glycosylated hemoglobin levels. These results suggested that in children with uncomplicated T1DM, decreased vertebral bone density is a minor ab‐ normality that affects only cortical bone [6].

**2.6. Diabetic model**

formation [15].

**2.8. Inducing diabetic condition**

Experimental diabetic models include the streptozotocin-induced diabetic rat and the spon‐ taneously diabetic BioBreeding [12] rat. The occurrence of different abnormalities indicating altered bone formation after inducing DM with streptozotocin (STZ) is well documented [3, 13, 14]. Streptozotocin-induced diabetes mellitus (STZ-DM), caused by the destruction of pancreatic β-cells and is similar to T1DM in human, is characterized by mild to moderate hyperglycemia, glucosuria, polyphagia, hypoinsulinemia, hyperlipidemia, and weight loss. STZ-DM also exhibits many of the complications observed in human DM including en‐ hanced susceptibility to infection and cardiovascular disease, retinopathy, alterations in an‐ giogenesis, delayed wound healing, diminished growth factor expression, and reduced bone

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In the usual clinical situation, although T1DM patient is treated with insulin, patient may still suffer from an overall poor diabetic metabolic state with an uncontrollable blood glu‐

All the experimental protocols followed had been approved by the Institutional Animal Care and Use Committee of Tokyo Medical and Dental University, and the experiments were carried out under the control of the University's Guidelines for Animal Experimenta‐ tion. In our investigation we explored the various effects of DM using the streptozotocin DM model. Twelve 3-week old male Wistar rats were used for this study. They were ran‐ domly divided into two groups, the control group and the diabetes group (DM group), each group consists of 6 rats. The rats in the control group were injected intra-peritoneal with a single dose of 0.1M sodium citrate buffer (pH 4.5), while the rats in the DM group were in‐ jected intra-peritoneal with a single dose of citrate buffer containing 60mg/kg body weight of streptozotocin (Sigma Chemical Co., St. Louis, MO, USA). [13, 16 - 18] All animals were fed on standard Rodent diet (Rodent Diet CE-2; Japan Clea Inc., Shizuoka, Japan) with free access to water. Body weights, the presence of glucose in urine and blood glucose levels

Diabetes condition was determined by the presence of glucose in urine and blood. The urine of the rats was tested using reagent strips (Uriace Ga; TERUMO). [20, 21] Blood samples of the rats were obtained via vein puncture of a tail vein, and blood glucose levels were deter‐ mined using a glucometer (Ascensia Brio. Bayer Medical). Positive urine test and a blood

Fig. 1. shows the weights of the rats (mean±SD) in both groups. DM group showed a signifi‐ cant decrease in weight. After STZ injection by 48 hours the urine test showed that the entire DM group had a high glucose level and this was confirmed by the high blood glucose meas‐ urements as shown in Fig. 2. A Student's t-test was used to compare the mean of weights

**2.7. Importance of testing the uncontrolled diabetic condition**

were recorded on day 0,2,7,14,21 and 28 after STZ injection.

glucose level greater than 200 mg/dl was considered DM. [3]

and blood glucose levels in both groups.

cose level and a high and sometimes changing insulin requirement [16].

#### **2.4. Outline of studying the effect of diabetes mellitus on craniofacial growth**

Approximately 60% of adult bone mass including craniofacial bone is gained during the peak of the growth period which coincides with the onset of T1DM condition affecting the bone formation process [8]. It is worth mentioning here that although T1DM condition exact etiological factors are totally unknown however; understanding the course of T1DM condi‐ tion and its impact on craniofacial development may lead to improving the oral health for a large sector of the population worldwide.

Numerous experimental and clinical studies on the complications of DM have demonstrated extensive alterations in bone and mineral metabolism, linear growth, and body composition. Investigators in the fields of bone biology including orthodontics have long been interested in the general causes that affect the normal growth of the craniofacial region. T1DM has been shown to affect the general growth of patients with earlier onset of the disease, espe‐ cially onset before or around the circumpubertal growth spurts [9].

In general, growth of the craniofacial complex is controlled by genetic and environmental factors [3, 10]. Regulatory mechanisms responsible for normal morphogenesis of the face and head involve hormones, nutrients, mechanical forces, and various local growth factors. The poor growth and alterations in bone metabolism have been associated with T1DM in both humans and experimental animals [3]. It is of prime importance investigating the changes in craniofacial bone structure and dynamic bone formation in DM condition to explore the impact of the diabetic condition on various mandibular growth elements and bone quality.

#### **The following parts of this chapter are going to focus on these points:**


#### **2.5. Animal and Experimental diabetic Model**

The animal studies using diabetic model presents various advantages when compared to studies carried out on human diabetic cases. Human studies can be limited by small sample sizes, cross-sectional designs, uncontrolled variables, and often retrospective nature, animal models have been used to yield more rigorous analyses [11].

### **2.6. Diabetic model**

age, sex, duration of diabetes, or glycosylated hemoglobin levels. These results suggested that in children with uncomplicated T1DM, decreased vertebral bone density is a minor ab‐

Approximately 60% of adult bone mass including craniofacial bone is gained during the peak of the growth period which coincides with the onset of T1DM condition affecting the bone formation process [8]. It is worth mentioning here that although T1DM condition exact etiological factors are totally unknown however; understanding the course of T1DM condi‐ tion and its impact on craniofacial development may lead to improving the oral health for a

Numerous experimental and clinical studies on the complications of DM have demonstrated extensive alterations in bone and mineral metabolism, linear growth, and body composition. Investigators in the fields of bone biology including orthodontics have long been interested in the general causes that affect the normal growth of the craniofacial region. T1DM has been shown to affect the general growth of patients with earlier onset of the disease, espe‐

In general, growth of the craniofacial complex is controlled by genetic and environmental factors [3, 10]. Regulatory mechanisms responsible for normal morphogenesis of the face and head involve hormones, nutrients, mechanical forces, and various local growth factors. The poor growth and alterations in bone metabolism have been associated with T1DM in both humans and experimental animals [3]. It is of prime importance investigating the changes in craniofacial bone structure and dynamic bone formation in DM condition to explore the impact

**•** Investigating the effects of juvenile diabetes on general craniofacial growth and skeletal

**•** Analyzing the pattern of association between craniofacial morphology and skeletal matu‐

**•** Determination of the changes in bone morphology in diabetic rat mandible using micro-

**•** Determination of the mineral apposition rate and the bone formation rate in diabetic rat

The animal studies using diabetic model presents various advantages when compared to studies carried out on human diabetic cases. Human studies can be limited by small sample sizes, cross-sectional designs, uncontrolled variables, and often retrospective nature, animal

of the diabetic condition on various mandibular growth elements and bone quality.

**The following parts of this chapter are going to focus on these points:**

mandible using histomorphometric analysis.

models have been used to yield more rigorous analyses [11].

**2.5. Animal and Experimental diabetic Model**

**2.4. Outline of studying the effect of diabetes mellitus on craniofacial growth**

cially onset before or around the circumpubertal growth spurts [9].

normality that affects only cortical bone [6].

404 Type 1 Diabetes

large sector of the population worldwide.

maturation.

ration.

C.T.

Experimental diabetic models include the streptozotocin-induced diabetic rat and the spon‐ taneously diabetic BioBreeding [12] rat. The occurrence of different abnormalities indicating altered bone formation after inducing DM with streptozotocin (STZ) is well documented [3, 13, 14]. Streptozotocin-induced diabetes mellitus (STZ-DM), caused by the destruction of pancreatic β-cells and is similar to T1DM in human, is characterized by mild to moderate hyperglycemia, glucosuria, polyphagia, hypoinsulinemia, hyperlipidemia, and weight loss. STZ-DM also exhibits many of the complications observed in human DM including en‐ hanced susceptibility to infection and cardiovascular disease, retinopathy, alterations in an‐ giogenesis, delayed wound healing, diminished growth factor expression, and reduced bone formation [15].

#### **2.7. Importance of testing the uncontrolled diabetic condition**

In the usual clinical situation, although T1DM patient is treated with insulin, patient may still suffer from an overall poor diabetic metabolic state with an uncontrollable blood glu‐ cose level and a high and sometimes changing insulin requirement [16].

#### **2.8. Inducing diabetic condition**

All the experimental protocols followed had been approved by the Institutional Animal Care and Use Committee of Tokyo Medical and Dental University, and the experiments were carried out under the control of the University's Guidelines for Animal Experimenta‐ tion. In our investigation we explored the various effects of DM using the streptozotocin DM model. Twelve 3-week old male Wistar rats were used for this study. They were ran‐ domly divided into two groups, the control group and the diabetes group (DM group), each group consists of 6 rats. The rats in the control group were injected intra-peritoneal with a single dose of 0.1M sodium citrate buffer (pH 4.5), while the rats in the DM group were in‐ jected intra-peritoneal with a single dose of citrate buffer containing 60mg/kg body weight of streptozotocin (Sigma Chemical Co., St. Louis, MO, USA). [13, 16 - 18] All animals were fed on standard Rodent diet (Rodent Diet CE-2; Japan Clea Inc., Shizuoka, Japan) with free access to water. Body weights, the presence of glucose in urine and blood glucose levels were recorded on day 0,2,7,14,21 and 28 after STZ injection.

Diabetes condition was determined by the presence of glucose in urine and blood. The urine of the rats was tested using reagent strips (Uriace Ga; TERUMO). [20, 21] Blood samples of the rats were obtained via vein puncture of a tail vein, and blood glucose levels were deter‐ mined using a glucometer (Ascensia Brio. Bayer Medical). Positive urine test and a blood glucose level greater than 200 mg/dl was considered DM. [3]

Fig. 1. shows the weights of the rats (mean±SD) in both groups. DM group showed a signifi‐ cant decrease in weight. After STZ injection by 48 hours the urine test showed that the entire DM group had a high glucose level and this was confirmed by the high blood glucose meas‐ urements as shown in Fig. 2. A Student's t-test was used to compare the mean of weights and blood glucose levels in both groups.

The protocol for examining the cephalometric measurements in DM rats involves the fol‐

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**•** Prior to each radiographic session, the rats are anaesthetized with diethyl ether and intra‐

**•** Each animal is then placed in this specially-designed apparatus (Fig. 3) to maintain stand‐ ardized head posture and contact with the film (SGP-3, Mitsutoy, Tokyo, Japan) where the head of each rat is fixed firmly with a pair of ear rods oriented vertically to the sagittal

**•** The settings of lateral and dorsoventral cephalometric radiographs are 50/55kVp,

**•** A 10 mm steel calibration rod is incorporated into the clear acrylic table on which the ani‐

**•** All the radiographs are developed and scanned at high resolution by the same operator.[11]

The cephalometric landmarks (Table 1; Fig. 4) were derived from previous studies on ro‐ dents.[11, 24-26] Selected linear measurements were then obtained (Table 2). To ensure relia‐ bility and replicability of each measurement, each distance was digitized twice and the two

peritoneal injection of 8% chloral hydrate using 0.5ml/100g of body weight.

plane and the incisors are fixed into a plastic ring.

mals are positioned for the radiographs.

**Figure 3.** Apparatus for roentgenographic cephalometry

values were averaged.

15/10mA, and 20/60-sec impulses respectively.[11, 23]

lowing steps:

**Figure 1.** Comparison between the changes of the rat's weight in the control and DM group. \* The weights of the DM group are significantly decreased as compared to the weights of the control group (*p<0.05*).

**Figure 2.** Line graph represents the blood glucose levels for the control and DM group. The blood glucose level in DM group increased significantly 48h post-STZ injection and during the entire experimental period. Values are mean±SD. Significant differences between the two groups are marked with asterisks (p< 0.05).

### **2.9. Analytic studies conducted to test the effect of diabetic condition on craniofacial growth**

#### **Cephalometric analysis**

Cephalometric measurements are still one of the most widely spread diagnostic aids crucial for the diagnosis of various abnormalities in the craniofacial complex [22].

The protocol for examining the cephalometric measurements in DM rats involves the fol‐ lowing steps:


**Figure 3.** Apparatus for roentgenographic cephalometry

**Figure 1.** Comparison between the changes of the rat's weight in the control and DM group. \* The weights of the DM

**Figure 2.** Line graph represents the blood glucose levels for the control and DM group. The blood glucose level in DM group increased significantly 48h post-STZ injection and during the entire experimental period. Values are mean±SD.

**2.9. Analytic studies conducted to test the effect of diabetic condition on craniofacial**

for the diagnosis of various abnormalities in the craniofacial complex [22].

Cephalometric measurements are still one of the most widely spread diagnostic aids crucial

Significant differences between the two groups are marked with asterisks (p< 0.05).

**growth**

406 Type 1 Diabetes

**Cephalometric analysis**

group are significantly decreased as compared to the weights of the control group (*p<0.05*).

The cephalometric landmarks (Table 1; Fig. 4) were derived from previous studies on ro‐ dents.[11, 24-26] Selected linear measurements were then obtained (Table 2). To ensure relia‐ bility and replicability of each measurement, each distance was digitized twice and the two values were averaged.

**Figure 4.** Location of cephalometric points on radiographs: (A) Sagittal and (B) transverse.

**Table 2.** Measurements of craniofacial skeleton

Chicago, IL, USA).

the control group.

*2.9.1. Changes in the Total Skull*

*2.9.2. Changes in the Neurocranium*

no significant differences.

In our studies, evaluation of the craniofacial growth of diabetic rats at the age of 7 weeks was done using lateral and dorsoventral cephalometric radiographs. All of the data in each experiment were confirmed the normal distribution, so a Student's t-test was used to com‐ pare the mean of each data recorded in the control group and in the DM group. All statisti‐ cal analyses were performed at a 5% significance level using statistic software (v. 10; SPSS,

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The size of total skull, denoted by Po-N, was significantly smaller in the DM group than in

Cranial vault length (Po-E), total cranial base length (Ba-E), anterior cranial base length (So-E), Occipital bone length (Ba-CB1), and posterior cranial base length (Ba-So) showed statisti‐ cally significant decrease in DM group (Table 3, Fig. 5, 6), while other dimensions exhibited

**Table 1.** Definitions of radiographic points

**Table 2.** Measurements of craniofacial skeleton

**Figure 4.** Location of cephalometric points on radiographs: (A) Sagittal and (B) transverse.

**Table 1.** Definitions of radiographic points

408 Type 1 Diabetes

In our studies, evaluation of the craniofacial growth of diabetic rats at the age of 7 weeks was done using lateral and dorsoventral cephalometric radiographs. All of the data in each experiment were confirmed the normal distribution, so a Student's t-test was used to com‐ pare the mean of each data recorded in the control group and in the DM group. All statisti‐ cal analyses were performed at a 5% significance level using statistic software (v. 10; SPSS, Chicago, IL, USA).

#### *2.9.1. Changes in the Total Skull*

The size of total skull, denoted by Po-N, was significantly smaller in the DM group than in the control group.

#### *2.9.2. Changes in the Neurocranium*

Cranial vault length (Po-E), total cranial base length (Ba-E), anterior cranial base length (So-E), Occipital bone length (Ba-CB1), and posterior cranial base length (Ba-So) showed statisti‐ cally significant decrease in DM group (Table 3, Fig. 5, 6), while other dimensions exhibited no significant differences.


*2.9.3. Changes in the Viscerocranium*

**Table 4.** Significant changes in the Viscerocranium

**Figure 7.** Viscerocranium

(*p<*0.05).

significant decrease in DM group (Table 4, Fig. 7,8)

**E-N** Nasal length **Mu2-Iu** Palate length **Cb2-Iu** midface length

All measurements of the viscerocranium, including the nasal length (E-N), palatal length (Mu2-Iu), midface length (CB2-Iu), and viscerocranial height (E-Mu1) showed a statistically

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**Table 4 : Significant changes in the Viscerocranium**

**Figure 8.** Changes in the viscerocranial measurements of the control and DM group. All the viscerocranial measure‐ ments are significant. Values are mean±S.D. Significant differences between the two groups are marked with asterisks

**E-Mu1** Posterior viscerocranial height

**Table 3.** Significant changes in the Total skull and Neurocranium

**Figure 5.** Neurocranium

**Figure 6.** Changes in the neurocranial measurements of the control and DM group. All the significant measurements are shown in this figure. Values are mean±S.D. Significant differences between the two groups are marked with aster‐ isks (p<0.05).

### *2.9.3. Changes in the Viscerocranium*

**Table 3: Significant changes in the Total skull and Neurocranium**

**Figure 6.** Changes in the neurocranial measurements of the control and DM group. All the significant measurements are shown in this figure. Values are mean±S.D. Significant differences between the two groups are marked with aster‐

**Po-N** total skull length **Po-E** cranial vault length **Ba-E** total cranial base length **So-E** anterior cranial base length

**Ba-CB1** occipital bone length

**Table 3.** Significant changes in the Total skull and Neurocranium

**Figure 5.** Neurocranium

410 Type 1 Diabetes

isks (p<0.05).

**Ba-So** posterior cranial base length

All measurements of the viscerocranium, including the nasal length (E-N), palatal length (Mu2-Iu), midface length (CB2-Iu), and viscerocranial height (E-Mu1) showed a statistically significant decrease in DM group (Table 4, Fig. 7,8)


**Table 4.** Significant changes in the Viscerocranium

**Figure 7.** Viscerocranium

**Figure 8.** Changes in the viscerocranial measurements of the control and DM group. All the viscerocranial measure‐ ments are significant. Values are mean±S.D. Significant differences between the two groups are marked with asterisks (*p<*0.05).

#### *2.9.4. Changes in the Mandible*

In the DM group, the posterior corpus length (Go-Mn), total mandibular length (Co-Il) and the ramus height (Co-Gn) were significantly shorter than in the control group (Table 5, Fig. 9, 10), whereas no remarkable differences were found in the remaining dimensions.

*2.9.5. Changes in the Transverse X-ray*

**Table 6.** Significant changes in the transverse X-ray

**Figure 11.** Transverse X-ray measurements

with asterisks (p<0.05)

In transverse X-ray only the maximum cranial width (C1-C2) and the bizygomatic width

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**Table 6: Significant changes in the transverse X-ray**

**Figure 12.** Changes in the transverse X-ray measurements of the control and DM group. Two measurements in the transverse X-ray were significant. Values are mean±S.D. Significant differences between the two groups are marked

All other linear measurements showed no significant differences between both groups

(Z1-Z2) were statistically decreased in DM group (Table 6, Fig. 11, 12).

**C1-C2** Maximum cranial width **Z1-Z2** Bizygomatic width


**Table 5.** Significant changes in the Mandible

**Figure 9.** Mandible

**Figure 10.** Changes in the mandible measurements of the control and DM group. Values are mean ± S.D.Significant differences between the two groups are marked with asterisks (*p<*0.05).

#### *2.9.5. Changes in the Transverse X-ray*

*2.9.4. Changes in the Mandible*

412 Type 1 Diabetes

**Table 5.** Significant changes in the Mandible

**Figure 9.** Mandible

In the DM group, the posterior corpus length (Go-Mn), total mandibular length (Co-Il) and the ramus height (Co-Gn) were significantly shorter than in the control group (Table 5, Fig.

**Table 5: Significant changes in the Mandible**

**Figure 10.** Changes in the mandible measurements of the control and DM group. Values are mean ± S.D.Significant

differences between the two groups are marked with asterisks (*p<*0.05).

9, 10), whereas no remarkable differences were found in the remaining dimensions.

**Go-Mn** Posterior corpus length **Co-Il** Total mandibular length

**Co-Gn** Ramus height

In transverse X-ray only the maximum cranial width (C1-C2) and the bizygomatic width (Z1-Z2) were statistically decreased in DM group (Table 6, Fig. 11, 12).

All other linear measurements showed no significant differences between both groups


**Table 6.** Significant changes in the transverse X-ray

**Figure 11.** Transverse X-ray measurements

**Figure 12.** Changes in the transverse X-ray measurements of the control and DM group. Two measurements in the transverse X-ray were significant. Values are mean±S.D. Significant differences between the two groups are marked with asterisks (p<0.05)
