Drinking alcoholic beverages is one of the oldest socially acceptable forms of behavior which can lead to the development of alcohol addiction. Long-term alcohol drinking has, together with numerous psychological and somatic complications, harmful consequences for the oral health. Patients suffering from alcoholism generally have poorer oral hygiene, dental care, periodontal status, fewer teeth, more carious lesions, gingival diseases, inter-dental papillae bleeding and deep gingival pockets associated with bone loss, as well as higher rate of oropharyngeal cancer. The changes in the oral microbiome affect the immune system, metabolism of carcinogens and digestion, which also leads to the development of local oral diseases as well as systemic gastrointestinal and cardiovascular illnesses. Harmful impact of alcohol on oral health can be direct, caused by local toxic effects of alcohol and as a consequence of systemic diseases associated with alcohol drinking, causing changes in the entire oral mucosa. Poor dietary habits additionally contribute to a poorer dental status while frequent simultaneous usage of tobacco products additionally increases the risk of developing periodontitis, tooth loss and oral carcinoma. Excessive alcohol drinking can seriously affect the oral cavity where, despite easy access via clinical examination, we still lack clinical data and a clear mechanism of development of the described changes.
SUMMARY -Alcohol addiction is a heterogeneous psychiatric disorder according to both phenotype and etiology. Difference in phenotype characteristics manifests in the manner the addiction arises, history of the alcoholic and history of drinking, comorbid disorders, and the phenomenon of abstinence difficulties. Concerning the etiology of alcoholism, the disease itself is considered to be a consequence of an interactive influence of the environment and genetic factors. Numerous researches conducted in the last decades discovered many aspects of the biochemical, cell and molecular bases of alcohol addiction, leading to a conclusion that alcoholism is, like many other addictions, a brain disease. By recognizing alcoholism as a disease which basically implies changes of the neurobiological mechanisms, as well as a clear genetic basis, it was supposed that the disease, having its basis solely in the symptomatology, is essentially heterogeneous. By trying to solve the problem of a clinically heterogeneous nature of the disease during the last fifty years, various sub-classifications of such patients have been suggested. According to Cloninger, subtypes of alcoholism differ also according to changes in the brain neurotransmission systems, i.e. it is supposed that patients suffering from alcoholism type 1 have a more pronounced dopaminergic transmission deficit, while dopaminergic transmission is not disturbed significantly in patients diagnosed with alcoholism type 2, who, however, have a significant lack of serotonergic transmission. In such a way, Cloninger actually presented the basis of the so-called neurobiological alcoholism model. Since he has connected differences in neurotransmission with differences in personality characteristics, this model is also known as the psychobiological model of alcoholism. The characteristic of alcoholism type 1 is avoiding damage (Harm Avoidance, HA) decreased dopamine transmission and increased serotonin transmission, while the significant characteristic of alcoholism type 2 is seeking for excitement (Novelty Seeking, NS), unchanged dopamine transmission and decreased serotonin transmission. These neurochemical differences among alcoholism subtypes represent the basis for a different therapy approach. Intake of alcohol changes different gene expression in the human brain. The inheritance model of alcoholism is not fully explained, however, it is considered that the disease is connected to a larger gene number included in neurotransmission, cell mechanisms and general metabolic function, with a simultaneous influence of the environment. The contribution of genetic factors is stronger in certain types of alcoholism and thus we have been confronted in the last years of alcoholism research with studies researching the connections of some alcoholism subtypes with the polymorphism phenomenon in the genes coding the synaptic proteins included in the alcoholism etiology. The primary role of monoamine oxidase (MAO) in the brain is catalysis of deamination of the oxidative neurotransmitter a...
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