# Histological Aspects Regarding Dental Pulp of Diabetic Patients
## 4 Discussion  
The influence of diabetes on dental structures has been previously studied, especially focusing on periodontal disease associated with diabetes [19]. The endodontic pathology associated with the diabetic condition in human subjects is more difficult to prove because dental pulp is not an exposed organ, as periodontal structures. Previous observations [20] suggest that the dental pulp of diabetic patients is in a state of inflammation because of nerve damage and local microcirculation breakdown, leading finally to pulp necrosis. The condition called \"Diabetic odontalgia\" was described in relation with longstanding hyperglycemia. It manifests as dental pain, which is easily confused with pulpitis, so uncontrolled diabetes might affect even the success of endodontic treatment [21], despite the fact that regenerative endodontics research has increased in popularity lately [22; 23]. Figure 9: Radicular dental pulp tissue of a 70 year old female, type 2 diabetes HE staining, \(\times\)200. Contrary to other studies, in our study group, none of the teeth analyzed had clinical symptoms of pulpitis. In the present study we aimed to assess the histological aspects of dental pulp specimens of vital carious teeth of patients with type 2 diabetes. For the histological study, we used the Hematoxylin-Eosin (HE) stain. All pulp specimens had histological aspects of inflammation to a certain degree, with areas of fibrosis and fibro-sclerosis, accompanied with limfoplasmocitar infiltrate. Most of the specimens presented pulp calcifications, fibrosis and vascular changes, consisting of the thickening of the vascular wall by increasing its content in collagen, with most blood vessels presenting microscopic aspects of arteriosclerosis. Those observations suggest the fibrotic transformation of the pulp tissue, together with vascular changes, which could be consequences of hyperglycemia. It was shown previously that diabetic patients develop microangiopathy and arteriosclerosis [9], our study confirms those observations. The fibrotic changes in dental pulp, in some cases accompanied with areas of necrosis, can also be a consequence of ischemia, installed because of arteriosclerosis. Pulpal calcifications were also a characteristic of most of the specimens included in this study. The influence of the carious lesions in pulp stones formation could be linked to dentinal properties [24], in terms of the number and diameter of dentinal tubules on one side, and the rate of carious lesion progression on the other side [25; 26; 27]. The multiple diffuse calcifications can be a result of chronic hypoxia and cell death. Pulps of diabetics are more prone to such calcifications and have been linked to elevated hyperglycemia, duration of diabetes and diabetic vascular changes [13; 14]. Other studies found that diabetic patients have pulp inflammatory lesions and even areas of pulp necrosis [9]. Recent, similar studies [27] showed that in the case of a diabetic patient, morphological changes in dental pulp can occur, depending on the status of the glycemic control of the patient and the time period from the onset of the diabetes. Structural changes observed include inflammation with the presence of calcifications, frequently sickle-shaped [28; 29], or even necrosis. Similar histological aspects were observed among the pulp specimens included in this study, but no correlation could be established between the level of the glycemia or the time period from the diagnosis of diabetes and pulp structural changes, probably because of the relatively small number of pulp specimens analyzed. The presence of pulp calcifications seems to be associated with the duration of diabetes. Other associated systemic conditions could also influence the dental pulp histologic aspects, but patients were selected among those who did not report other known systemic diseases during anamnesis. One limitation to this study is the relative low number of patients included in the study, with a large age group interval (36-70 years old).