Advanced Glycation End-products (AGEs) result when proteins and lipids are attached to sugars. These AGEs are held accountable for the progression of many diseases, including Diabetes Mellitus (DM), which is known to result in chronic periodontitis. Diabetes, which expresses itself in Type 1 and 2, has been seen to have differing impacts on periodontitis depending on its expression. This study thus seeks to analyze the clinical factors that affect the accumulation of AGEs in Type 1 DM and its actual accumulation in such patients. Thus gum tissue samples were collected from 16 diabetes-free people, 16 with type 1 DM, 16 with type 2 DM, all with severe periodontitis, and 16 without either disease. These samples were studied through immunohistochemistry to identify the AGE expression, and the results reflected a higher amount in type 1 DM compared to those with type 2 in the epithelium, vessels, and fibroblasts. Factors such as age, body mass index (BMI), lipid concentration, and glycated hemoglobin have no direct relation to the gingival expression of AGEs. The main clinical factor established to affect is the length of time one had been affected by type 1 DM, which has a direct relation to the dominant expression of AGEs in the tested tissues. This has led to the conclusion that the more a person is exposed to type 1 DM, the higher they produce AGEs, and the more chronic the periodontitis reported among such patients.
Diabetes mellitus, as stated, is expressed as either type 1 DM (T1DM) or type 2 DM (T2DM), which occur due to different processes in the body. T1DM is brought about by the destruction of the beta cells that produce insulin while T2DM occurs when the body develops a resistance to insulin or its production reduces significantly. Both conditions result in hyperglycemia, which is excess glucose in the bloodstream than what the body needs at a particular time (Zizzi, Tirabassi, Aspriello, Piemontese, Rubini & Lucarini, 2013).
Elevated levels of blood sugar relate directly to the number of AGEs produced by the body, which 'are derived from the intracellular auto-oxidation of glucose to glyoxal, decomposition of the Amadori product (glucose-derived 1-amino-1-deoxyfrutose lysine adducts) and fragmentation of glyceraldehyde-3-phosphate and dihydroxyacetone phosphate to methylglyoxal'. These dicarbonyls react with the amino acids of proteins to form AGEs, thus altering the functions of these proteins and their cell receptors, allowing for receptors for AGE (RAGE), which are known to increase inflammation. Hyperglycemia is also known to fire the pro-inflammatory transcription factor significantly, thus promoting inflammation (Zizzi et al., 2013).
Periodontitis is a gum infection caused by bacterial build-up, which affects the soft tissues surrounding the teeth resulting in the formation of pockets around it if left to fester; it ends up eating the alveolar bone support that holds the teeth leading to them falling out. Although bacteria play a significant role in the propagation of periodontitis, other risk factors weigh in such as the genetic background of an individual and other environmental stressors like diabetes. AGEs are in the gingiva of diabetes mellitus patients with periodontitis pointing to their role in the destruction that happens periodontal.
This study was thus motivated by various issues; first, most studies were conducted to explore the effects of RAGE and pay little attention to those of AGE as a single unit affecting periodontitis (Detzen, Cheng, Chen, Papapanou & Lalla, 2019). Second, few pieces of research have considered these effects as expressed by patients affected by T1DM which have proved to be different from those who have T2DM. Finally, clinical factors that affect the prevalence of AGE in gum tissue are unexplored (Zizzi et al., 2013).
The subjects, as earlier mentioned, were chosen in folds of 16 while paying attention to specific criteria. The first 16, who were to act as the control, were healthy individuals with neither periodontitis nor diabetes. The other 16 were individuals with diagnosed, severe, chronic periodontitis but without diabetes. The next 32(16-16) were diagnosed with a similar case of periodontitis with T1DM and T2DM, respectively. They were all older than thirty-five years, were not active smokers, had no other known disease apart from diabetes, and had not received any treatment for periodontitis.
Evaluation ensued both clinically and radiographically while paying attention to certain periodontal factors like the gingival index, plaque index, sulcus bleeding index, probing depth measured to the next millimeter, and clinical attachment loss. Radiographs enabled an understanding of the magnitude of bone loss. Next, the subject's blood was measured under biochemical parameters that sought to get a glimpse of the cholesterol levels in the blood and plasma glucose.
Finally, an immunohistochemical study was carried out on samples collected to find out the AGE levels in the gum tissues of all the subjects involved in the study. All the tests done above were carried out by one person to ensure similarity in readings and avoid minor discrepancies.
Various tests were applied including; The Shapiro-Wilk test, the chi-square test, The Kruskal-Wallis test, and the Mann-Whitney U-test to explore the different variables that came up during analysis. Expected differences in that T1DM patients were younger than those of T2DM and glucose levels were higher in diabetic patients than those without it. Further, notice highlighted that among patients with periodontitis, bacteria-causing inflammation was present.
The following images show immunostaining of advanced glycosylation end-products (AGEs) on gingival tissue from periodontitis patients with type 1 diabetes mellitus (T1DM); periodontitis patients with type 2 diabetes mellitus (T2DM); periodontitis patients without diabetes mellitus (PD-S); and systemically and periodontally healthy subjects (CT). The original magnification was *200
The immunohistochemical evaluation observed that AGE cells were more predominant among T1DM patients' epithelial and vessel tissues than any other, while those with neither diabetes nor periodontitis had very weak presences. Patients with T2DM had notable AGE cells, however not as much as those with T1DM, those with periodontitis, but no diabetes ranked third. It is also crucial to note that exposure to T1DM for long played a critical role in determining the prevalence of AGE cells per person. Below is a table showing the result of the distribution of these AGE cells among subjects' epithelium, fibroplast, gingival tissue, and vessels (Zizzi et al., 2013).
The essence of this study was to explore the clinical factors affecting the accumulation of AGEs in T1DM patients and explore the collection itself. Based on the results obtained from this study, it is safe to conclude that AGEs are present among T1DM patients to a greater extent and directly influence the severity of periodontitis in them. By ensuring that all participants in the study, except the control, had severe, chronic periodontitis, the field was leveled to produce reliable results concerning the role played by AGEs in the growth of the disease.
AGEs were present in samples of all subjects with diabetes; however, those who had had the disease for an extended period expressed severe forms of periodontitis compared to those who had it in the short term. Explaining this realization is the fact that prolonged exposure to diabetes mellitus interferes with the glycemic control of the body resulting in heightened production of AGEs over the years. This AGE, in turn, modifies the proteins present in the blood causing them to be 'more resistant to proteolysis, and therefore to turnover, (30, 31), thus causing proteins containing various AGE adducts to accumulate rapidly after the onset of diabetes mellitus (31)' (Zizzi et al., 2013).
To support this theory is the fact that other complications brought about by the influence of AGE in diabetes mellitus, like; retinopathy, neuropathy, and nephropathy, are heavily influenced by the long duration of hyperglycemia in the blood. We can be able to deduce the same for periodontitis caused by similar factors. Other factors, such as age and BMI, showed no relationship with AGE levels but are instead independent factors on their own (Zizzi et al., 2013).
Research have proved that BMI has a direct relation to periodontal health. In the instances where one is obese, the chances are high that they may suffer from periodontitis. However, obesity can bring about the onset of diabetes since it gives room for the deposition of adipose tissue, which alters the proper functioning of the T and B- cells. This ultimately may lead to reduced insulin sensitivity, which affects the healing of wounds and thus plays a role in the soreness of gums. More research is, however, needed to understand the relationship between obesity and periodontitis fully (Zizzi et al., 2013).
Age, on the other hand, influences periodontal diseases as from teen years to forty years, this has to do mostly with the fact that at this age diets tend to change, and people involve themselves with certain "risk factors" such as smoking, which eventually affect oral health. However, it has very little to do with AGE levels in the body, as there is no proof that the two relate in any way. This involvement with other determinants also tends to go hand in hand with sex since, generally, it affects brevity to try new things (Zizzi et al., 2013). This was unexpected to some degree since previous data links age to AGE disposal in various organs of the body.
The research conducted also found no relationship between glycated hemoglobin (hbA1c) and AGE levels affecting periodontitis in all the study groups. Glycated hemoglobin gives the general glucose level in a person's blood; it thus seems ironic that it does not relate directly to the AGE levels. However, explaining this is the fact that it usually reflects readings of years for one's blood sugar to be well established, but in our study, we only focused on three months' worth of data, which can be misguiding.
In conclusion, from the research conducted and the results obtained, it is clear that the prevalence of Advanced Glycation End-products is increased in both type 1 and type 2 diabetes mellitus associated periodontitis. This increase is further propagated by the duration of infection of Diabetes Mellitus per person, with more severe cases seen in patients who have suffered from it for a longer time. Other factors such as age, glycated hemoglobin, and Body Mass Index do not have a direct relation to AGE deposition in the blood (Zizzi et al., 2013).
Hyperglycemia, which is characteristic of diabetes mellitus, is the primary cause for the formation of AGEs as it allows for there to be a build-up of glucose in the blood which breaks down into incomplete molecules that pair with either proteins or lipids, and these are what are referred to as AGEs (Yu, Li, Ma & Fu, 2012).. They gather around the periodontal area and inhibit the fighting off bacteria, which in turn results in the development of periodontitis since bacteria mainly cause the disease. Since the body cannot fight it off quickly, the virus grows to a place where the alveolar bone is affected too, and it begins to waste away.
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