Diabetes mellitus is a serious metabolic disease and an important medical, social and economic problem globally. Long-term untreated hyperglycaemia – the main cause of a carbohydrate, lipid and osmotic imbalance – affects all tissues and organs in the body and leads to development of typical disease manifestations such as polydipsia, polyuria and polyphagia. This metabolic imbalance initiates other tissue and organ complications, some of which are extremely serious vasculopathies, cardiovascular diseases, neuropathies, myopathies, eye complications, renal complications and deteriorated regeneration and healing of wounds (Ceriello, 2005).
The basic etiopathogenetic mechanism in diabetes mellitus is either a real lack of insulin (type 1) or a biological lack of insulin (type 2) arising from its peripherally changed utilization and subsequent insufficiency. Insulin is a polypeptide produced by beta-cells of the pancreas and is necessary for glucose metabolism, keeping the glucose level in the blood within values of 4 – 6 mmol/1 ml. Glucose is metabolized in all tissues and is the main energy source in the organism. Lack of insulin causes hyperglycaemia and unmetabolised glucose is excreted mostly by the kidneys. This state leads to the development of polyuria, requiring increased intake of liquids and food and causing tissues to metabolise other sources of energy (fats, proteins) much more. Insufficient effectiveness of insulin means the energy requirements of the organism are not fulfilled; the organism searches for additional energy sources, mainly for proteins and fats. Increased metabolism of fats leads to excretion of so-called keto-compounds by the kidneys accompanied by a typical smell which can be detected in the patient’s breath and sweat.
Nowadays we divide diabetes mellitus into the insulin-dependent type 1 DM, also called children’s or adolescent DM, which presents an absolute lack of insulin caused by the autoimmune destruction of pancreatic beta-cells; and type 2 DM, which is known as adult diabetes, is a more frequent form of this illness and runs without clinical symptoms for a longer time. The initial stages of the disease are characterized by insulin-tissue resistance connected with inadequate glucose tolerance. Increased insulin resistance of receptors and tissue produces an increased insulin requirement and forces its production in the pancreas. If insulin production in the pancreas drops below 50 per cent, a so-called pre-diabetic condition develops. This is characterized by after-strain hyperglycaemia, also called postprandial hyperglycaemia, which often runs sub-clinically. If it remains undiagnosed, it can develop into a more advanced form with various tissue and organ complications, oral manifestations and complications (Straka, 2011). The most frequent oral complications of diabetes are diabetes gingivitis and periodontitis, which are together considered to be the seventh most common complication of DM. In type 2 diabetes, the incidence of periodontitis is 2.9 – 3.0 times higher than in non-diabetic patients (Nelson et al., 1990; Tsai et al., 2002).
2. Classification of diabetes mellitus
The present classification of diabetes mellitus uses the AAD (American Association of Diabetes) division and distinguishes four types of DM.
Type 1 DM – autoimmune type (older synonym is IDDM – insulin-dependent diabetes mellitus), diabetes of young people;
Type 2 DM – non-autoimmune (an older synonym is NIDDM – non-insulin-dependent diabetes mellitus), diabetes of adults, insulin non-resistant type;
Specific types of DM
3. Etiopathogenesis of DM and diabetic periodontitis
3.1. Type 1 diabetes mellitus (T1DM)
T1DM starts as an autoimmune and destructive reaction against the patient’s own pancreatic beta-cells. The main risk factor is a genetic predisposition to such an autoimmune reaction. Some authors distinguish six stages of T1DM development described as follows: the 1st stage, known as genetic predisposition, passes into the 2nd so-called activating stage, which is characterized by immediate activation of autoimmune reactions. The 3rd stage, for which immune abnormalities are typical, passes into the 4th stage characterized by loss of glucose-stimulating insulin production. Clinically present diabetes in the 5th stage is a reflection of the large destruction of B-cells and leads to their total destruction in the 6th and final stage (Rybka, 1990). In young patients with T1DM, an increased susceptibility to gingivitis and periodontitis has been detected. This state is often accompanied by more extensive damage to periodontal tissue and an early onset of gingivitis after the patients reach the age of 11. Periodontal pockets were detected in 9.8% of a group of young patients aged 13 – 18 years, compared with a 1.7% occurrence in a healthy control group (Straka, 2001; Rybka, 1990).
3.1.1. Etiopathogenic and risk factors
An increased prevalence of gingivitis and periodontitis in adolescents with T1DM is mostly attributed to various etiopathogenetic and risk factors of the primary illness:
3.1.2. Influence of T1DM treatment on the state and course of periodontitis
Several studies report that balanced levels of glycaemia in T1DM patients have a beneficial influence on the degree of periodontal tissue damage during periodontitis as well as on its clinical course. These results associate total systemic changes with destructive changes to the periodontium depending on the therapeutic result of the glycaemia level. The given relationship acts reciprocally. (Straka, 2001; Farkaš et al., 2011; Cianciola et al. 1982, Lyons, 1992) However the results of other present-day clinical studies negate the positive correlation between periodontal therapy and its beneficial influence on the course of the primary illness. Periodontal therapy in T1DM subjects prevented periodontal infection, but did not significantly influence the level of glycated haemoglobin (Tervonen et al., 2009). Statistically insignificant results of periodontological therapy on glycated haemoglobin concentrations have also been confirmed by another independent study (Lambés et al., 2008).
3.2. Type 2 diabetes mellitus (T2DM)
The etiopathogenesis of T2DM and its most frequent oral complication are closely interconnected. Their mutual associations can be observed in various stages of the primary disease. One of the early pathological symptoms of broken homeostasis of glucose is its increased postprandial (after-strain) level in the blood. This type of hyperglycaemia is bound to food and develops several years before it is clinically manifested by T2DM. The pre-diabetic stage of the disease is characterized by the presence of several markers, of which the most important is glycated haemoglobin A1c, which represents the amount of glycated haemoglobin in erythrocytes (given in percentages). The pre-diabetic stage of the disease, measured by means of HB1c, FPG, and 2-hOGTT can be relevant in the development of some angiopathies, mainly retinopathy (Ceriello, 2005; Straka, 2011; Rybka, 1990). In T2DM aetiology as well as in the development of diabetic periodontitis, the following groups of factors and mechanisms play crucial roles:
3.3. Gestational DM (GDM)
Gestational DM is characterized with high blood sugar levels inpregnant women, who were not diagnosed for DM previously. Its prevalencein pregnant women varies from 5 to 7 percent. Usually is concern atransient form, while placental and maternal adipose tissues producehormones which can change metabolism of glucose (Friedlander et al.,2007). Some authors state that in up to 50 per cent of women with GDM,T2DM can develop within 3.5 years. Although there is lack of relevantstudies to this topic and no anonymous conclusion was done, most authorsconfirm the hypothesis that pregnant women with GDM have a high risk todevelop a severe form of an inflammatory diseases of the periodont (Novak et al.,2006; Friedlander et al., 2007; Xiong, et al., 2006). Thisrelationship runs in both directions and presence of inflammatorydiseases unfavorably influences the mother's organism and the healthstate of the foetus (Novak et al., 2006; Straka et al., 2011).
From the given knowledge we can summarise several theoretical and practical conclusions which are important for the diabetological and periodontological management of a patient as well as for management of mutual therapeutical associations and procedures:
Patients with diabetes mellitus have twice or three times a larger incidence of periodontitis. This is in relation to significant deterioration of several periodontal parameters such as gingivitis, higher prevalence of periodontal pockets, deeper periodontal pockets, higher BOP score and loss of attachment.
Our present state of knowledge defines DM periodontitis as one of the systemic complications of diabetes though its main etiopathogenic associations in cell-altered immunity, in glycation of periodontal tissues, vascular damage of the periodontium, increased proteolysis and osteolysis of periodontal structures, which result from increased concentrations of pro-inflammatory cytokines, deficient regeneration of collagen structures and quantitative multiplication of periodontal bacterial pathogens.
The level of inflammatory destruction of the periodontium is different in patients with a good level of control of the primary diabetic disease from patients with insufficient control. Changes in periodontal structures can also be detected during the latent stage of diabetes and are reflected in unspecified laboratory and clinical findings.
Nowadays the mutual relationship between these two diseases is considered to run in two directions. Local inflammation in the periodontium significantly influences the systemic disease due to increased susceptibility of the diabetic patient to infection and increased insulin resistance. Deterioration of periodontal parameters and clinical manifestations lead to worsening of the diabetic disease. Without reduction of inflammation in the periodontium we cannot expect any significant improvement of the primary disease.
In collaboration with a diabetologist, we are trying to diagnose gingivitis and periodontitis in the initial stages of diabetes and in detection of the patient’s genetic predisposition to diabetic disease.
During treatment of resistant and refractory types of periodontitis, it is necessary to test for diabetic disease, to contact a diabetologist and to try to detect individual pre-diabetic states.
Microbial factors were considerably emphasized in the past. Some studies indicated specific subgingival microflora of some strains, namely P. intermedia and strain capnocytophaga (Khoury et al., 2008). Our current knowledge, described in several studies, indicates that there is no difference in the distribution of individual pathogens in non-diabetic and diabetic patients with periodontitis. However patients with DM are afflicted more often by repeated infectious diseases (Khoury, et al., 2008).
In the chapter, Periodontitis and Diabetes mellitus,, authors deal with mutual relation between both diseases which we percept nowadays as a bidirectional, in the meaning of a mutual reciprocal etiopathogenetic association. They briefly present etiopathogenesis and classification of two main types of diabetes mellitus. The main objective of chapter is to outline and present the mutual etiopathogenetic association. In spite there is not known any distinct causal molecular relation between mentioned diseases in present, exists the certain multifactorial interpretation of mutual pathogenetic coherence in larger epidemiologic, genetic, metabolic, immunologic and therapeutic context. These more specifically defined etiological associations help us as well in diagnostic and therapeutic management in the practice of both diseases, what is emphasized in the conclusion section.