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59MEDICAL SCIENCES
RISK FACTORS FOR PERIODONTAL DISEASES
Boitsaniuk S.,
PhD, Associate Professor Patskan L., PhD, Associate Professor Pogoretska K.
PhD, Associate Professor I. Horbachevsky Ternopil National Medical University,
Ternopil
ABSTRACT
Periodontal disease (PD) encompasses a cluster of diseases that result in inflammatory responses and chronic destruction of the tissues that surround and support the teeth, namely the gingiva, periodontal ligament, cementum and alveolar bone (collectively referred to as the "periodontium"). An understanding of risk factors is essential for clinical practice.
Keywords: Periodontal disease, risk factors, dental plaque, modifiable factors non-modifiable factors.
Introduction. Periodontitis is a chronic disease of the hard and soft tissues supporting the teeth initiated by bacterial plaque, which then causes a host immuno-inflammatory response that, over time, may result in progressive destruction of the periodontal ligament and alveolar bone if not adequately resolved.
Periodontitis is one of the most ubiquitous diseases and is characterized by the destruction of connective tissue and dental bone support following an inflammatory host response secondary to infection by perio-dontal bacteria [1, 2]. It is now generally agreed that almost all forms of periodontal disease occur as a result of mixed microbial infections within which specific groups of pathogenic bacteria coexist [3, 4, 5, 6].
Role of plaque in periodontal disease Dental plaque is the principal etiological factor in the pathogenesis of PD. The presence of plaque is necessary, but is not of itself sufficient, for periodontal disease to occur. Dental plaque is a unique and dynamic biofilm, highly heterogeneous and polymicrobial, usually of a yellowish color, that develops naturally on the teeth's smooth surfaces [7].
The microbes involved with PD are largely gram negative anaerobic bacilli, as mentioned, with some anaerobic cocci and a large quantity of anaerobic spiro-chetes. The main organisms linked with deep destructive periodontal lesions are Porphyromonas gingivalis, Prevotella inter-media, Bacteroides forsythus, Actino-bacillus actinomycetumcomitans, and Treponema denticola. Control of the oral biofilm is a primary objective of periodontal disease prevention. The routine removal of supragingival plaque through personal oral Risk factors for periodontal disease divided
hygiene is the most effective, efficient, and economical means to achieve this goal.
A daily regimen of thorough mechanical oral hygiene procedures, including toothbrushing and interdental cleaning, is key to controlling biofilm accumulation [8, 9, 10, 11, 12].
Although bacterial plaque buildup is the main cause of periodontal disease, several other factors, including other diseases, medications and oral habits, also can contribute. These are factors that can increase your risk of gum disease or make it worse once the infection has set in. Risk is defined as the probability that an individual will get a specific disease in a given period.
Risk factors for periodontal disease
Risk factors may be modifiable or non-modifiable. Modifiable risk factors are usually environmental or behavioral in nature whereas non-modifiable risk factors are usually intrinsic to the individual and therefore not easily changed. Risk indicators are probable or putative risk factors that have been identified in cross-sectional studies but not confirmed through longitudinal studies.
Risk predictors/markers, although associated with increased risk for disease, do not cause the disease. It is important to make the distinction that risk factors are associated with a disease but do not necessarily cause the disease. Risk factors therefore are part of the causal chain for a particular disease or can lead to an exposure of an individual to a disease and therefore the presence of risk factors implies a direct increase in the probability of the disease occurring. [13, 14, 15, 16]. into modifiable and non-modifiable factors
Modifiable factors Non-modifiable factors
Acquired: Anatomical:
Smoking Diabetes Cardiovascular Disease Poor diet Osteoporosis Stress Malpositioned teeth Furcations Root grooves & concavities Enamel pearls Socioeconomic status Genetics Sex Race and gender Age
Non-modifiable risk factors
Socioeconomic status (SES). Studies exclusively focusing on trends in socioeconomic inequality of oral health status are relatively sparse. Groups of the population with low socioeconomic status (low income and/or education) are at a higher risk of having perio-dontal diseases than groups with high socio-economic status, and the increased risk level in this group seems to be attributed to behavioral and environmental factors. SES is a modifiable factor and it can be examined in multivariate models for the disease [18, 19, 20].
Genetics. Researchers believe up to 30 % of the population may have a genetic susceptibility to perio-dontal disease. Having a genetic susceptibility, however, doesn't mean gum disease is inevitable. Even people who are highly prone to periodontal disease because of their genetic make-up can prevent or control the disease with good oral care [21, 22, 23].
Sex. Numerous studies reported higher periodon-tal destruction among males compared to the female population. The reasons for these sex differences are not clear, but they are thought to be related to the ignorance of oral hygiene, which is usually observed among males. However, the relationship observed between sex and the disease is not apparent and is not considered as strong and consistent. Thus, sex may be a demographic factor, which may interfere with the effects of other factors and it must be controlled for investigating the disease [24, 25].
Race and gender. Destructive periodontitis is consistently more prevalent in males than females which could be due to lifestyle choices of males which include an increased alcohol and smoking consumption. PD also has been reported to be more prevalent amongst blacks than whites with a Brazilian study reporting that groups of blacks have a three times higher risk of periodontal destruction compared with whites of the same age cohort [26, 27].
Age. The prevalence of periodontal disease is seen to increase with age, while the extent and severity also increases with advancing age.
Periodontal disease is a chronic infection therefore symptoms of periodontitis such as attachment loss, bone loss, gingival recession can be the result of the cumulative effect rather than older age of a person [6, 13].
Modifiable factors
Anatomical. Malocclusion, as well as crooked and spaced teeth, can all contribute to periodontal disease. In these situations your teeth and gums are more difficult to clean and become breeding grounds for disease causing bacteria. Bad oral hygiene combined with these traits can greatly contribute to the development of periodontitis [28, 29, 30]. Installation of orthodontic appliances increases the amount of plaque, which results in formation of gingival hyperplasia and pseudopockets. This situation changes the subgingival ecosystem and facilitates the increasing of periodontal pathogens levels, which express virulence factors that stimulate host cells to release several types of inflammatory cytokines such as interleukin ip (IL-1P), interleukin 6 (IL -6) and interleukin 8, (IL-8) and growth factors such as tumor growth factor (TGF), which modulate the inflammatory response in periodontal tissues [31, 32, 33].
Acquired
Cigarette smoking has long been associated with periodontal disease and tooth loss. Nicotine was toxic ingredients contained in cigarettes which was known to have a harmful effect on periodontal tissue, it may alter host's tissue response or directly damage the cells of the normal periodontium. It has been demonstrated that there are differences in the oxygen saturation of hemoglobin in the gingiva of smokers and non-smokers, suggesting that smokers have functional impairments in the gingival microcirculation [34, 35, 36].
Nicotine was known to be able to inhibit cells splitting processes in osteoblast cultures by stimulating osteoblast alkaline phosphate activity in vitro. Nicotine might also alter the periodontal cells in vivo. This meaned that nicotine had a tendency to disturb reparative and generative potential of the periodontium [37]. Nicotine metabolism might cause vasoconstriction and suppress functional activity of polimorphonuclear (PMN) cells and macrophages. The quantity of neutro-phils in the peripheral blood increased and penetrated cappilary wall [38].
Vasoconstriction of peripheral blood vessels caused by smoking may also affect the periodontal tissues [39]. In addition, nicotine may suppress the production of pro-inflammatory cytokines interleukin 1 (IL-1) and tumor necrosis factor-alpha (TNF-a) which was considered as a key in regulating the host response against microbial infection [40].
The two-way relationship between diabetes and periodontal disease. It is proven beyond doubt that diabetes (poorly controlled) can lead to aggravation of periodontal infection and exaggerated bone loss and vice a versa is also true i.e. poorly controlled diabetes can be due to chronic periodontitis.
Control of periodontal infection is not only important for oral health, but also for general health in diabetic patient. Patients with diabetes have a hyperactive inflammatory response and the bacterial challenge of periodontal infection results in exaggerated inflammation and periodontal tissue destruction. Impaired functions such as impaired phagocytosis and neutrophil chemotaxis may predispose patients with diabetes to more severe periodontal disease.
Systemic inflammatory responses as seen in peri-odontal disease may contribute to insulin resistance and hyperglycemia. For example, TNFa can promote insulin resistance by interfering with insulin signaling mechanisms, reducing intake of glucose into cells. The systemic inflammatory response associated with perio-dontal disease thus many account, in part, for the effects of periodontal disease on poorer glycemic control and increased cardiovascular and renal complications in patients with both diseases [41, 42, 43, 44, 45].
Cardiovascular Disease. The biological plausibility of the association between periodontal diseases and cardio-vascular diseases is well studied and it includes some of the following possible mechanisms: high concentrations of cholesterol and the action of oral bacteria in the process of atherosclerosis or the participation of acute-phase proteins that may increase in chronic peri-odontitis.
Periodontal disease is capable of predisposing to vascular disease due to the rich source of subgingival microbial species and host's response. Furthermore, we must be aware that these diseases share many risk factors and there are evident similarities to the basic pathogenic mechanisms [46, 47, 48].
Nutrition. Nutrition can influence the growth, development and metabolic activities of the periodon-tium; the high rate of cell turnover in the periodontal tissues requires that essential nutrients are readily available. Iron deficiency has a deleterious effect on macrophages, cells that are intimately involved in the immune and inflammatory systems. Cells of the immune system have a high turnover rate, a high demand for the building blocks of DNA, and are vulnerable to folic acid deficiency. Zinc plays a significant role in the regulation of the inflammatory process and a deficiency could negatively influence host resistance to gingivitis.
An unhealthy diet - one high in processed foods and refined carbohydrates - increases the tendency for gums to become inflamed. In both gingivitis and perio-dontitis, this can lead to more swelling at the gum line and increased damage to the tooth-supporting structures. An unhealthy diet also increases the risk of diabetes, which can further exacerbate periodontitis. Nutrition is important for overall good health, including a working immune system and healthy gums and mouth [49].
Osteoporosis. Osteoporosis features systemic degenerative bone loss that leads to loss of skeletal can-cellous microstructure and subsequent fracture, whereas periodontitis involves local inflammatory bone loss, following an infectious breach of the alveolar cortical bone, and it may result in tooth loss. Most cross-sectional studies have confirmed the association of osteoporosis and periodontitis primarily on radiographic measurements and to a lesser degree on clinical parameters. Multiple shared risk factors include age, genetics, hormonal change, smoking, as well as calcium and vitamin D deficiency. Both diseases could also be risk factors for each other and have a mutual impact that requires concomitant management.[50, 51, 52].
Stress. Stress is linked to many serious conditions such as hypertension, cancer, and numerous other health problems. Stress also is a risk factor for perio-dontal disease. Research demonstrates that stress can make it more difficult for the body to fight off infection, including periodontal diseases.
Mental and emotional stress can weaken the immune system and lower the resistance of the gums to harmful bacteria. People with a weakened immune system may be more susceptible to gum disease. The resulting greater bacterial load adds to the unfavorable effect on an already compromised immune system. Individuals suffering from stress or depression may spend less time on their daily oral hygiene at home [53, 54, 55].
Conclusion
It is important to understand the etiological factors and the pathogenesis of periodontal disease to recognize and appreciate the associated risk factors. As peri-
odontal disease is multifactorial, effective disease management requires a clear understanding of all the associated risk factors.
In conclusion, it is imperative that the clinician looks beyond the oral cavity for factors of which to potentially recommend modification in order to help their patients reach their common goal of prevention or management of periodontal disease - and thereby possibly improve general health as well.
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АНАЛИЗ ОШИБОК, ДОПУСКАЕМЫХ ВРАЧАМИ-ПЕДИАТРАМИ В ЛЕЧЕНИИ ДЕТЕЙ С
ИНФЕКЦИОННЫМ КАШЛЕМ
Кузнецова М.А.,
Саратовский государственный медицинский университет имени В.И. Разумовского, ассистент кафедры педиатрии
Зрячкин Н.И.,
Саратовский государственный медицинский университет имени
В.И. Разумовского, профессор, заведующий кафедрой педиатрии
Елизарова Т.В.
Саратовский государственный медицинский университет имени В.И. Разумовского, доцент кафедры педиатрии
ANALYSIS OF ERRORS MADE BY PEDIATRICIANS IN THE TREATMENT OF CHILDREN WITH
INFECTIOUS COUGH
Kuznetsova M.,
Saratov State Medical University named after V.I. Razumovsky, Assistant of the Department of Pediatrics Zryachkin N.,
Saratov State Medical University named after V.I. Razumovsky, Professor, Head of the Department of Pediatrics
Elizarova T.
Saratov State Medical University named after V.I. Razumovsky, Associate Professor of the Department of Pediatrics
АННОТАЦИЯ
Кашель на фоне острых респираторных вирусных инфекций (ОРВИ) - один из основных симптомов, требующих адекватного лечения, поскольку является маркером несостоятельности мукоцилиарного клиренса. Разнообразие средств от кашля с разным механизмом действия и разным тропизмом к слизистой оболочке органов дыхания требует хорошего профессионального уровня как в плане диагностики разных вариантов кашля и разных клинических форм ОРВИ, так и современных подходов к терапии в свете национальных клинических рекомендаций.
ABSTRACT
Cough on the background of acute respiratory viral infections (ARVI) is one of the main symptoms that require adequate treatment, since it is a marker of the failure of mucociliary clearance. A variety of cough remedies with different mechanisms of action and different tropism to the mucous membrane of the respiratory system requires a good professional level both in terms of diagnosing different cough variants and different clinical forms of acute respiratory viral infections, and modern approaches to therapy in the light of national clinical recommendations.
Ключевые слова: дети, острая респираторная вирусная инфекция, кашель, врачи-педиатры, ошибки в лечении.
Keywords: children, acute respiratory viral infection, cough, pediatricians, treatment errors.
