The Impact of Nutrition and Diet on Oral Health. Группа авторов

evidence suggesting that the incidence is increasing [12].

      The condition is seen in both the primary and permanent dentition, and it is a growing concern that dental erosion is now being detected and established at even younger ages. Among pre-school children, erosion was found on 6–50% of the deciduous teeth, while, in adolescents, 9–17 years of age, the prevalence ranged between 11 and 100% [12].

To a large extent, the increase in disease activity can be attributed to various dietary changes, especially the significant increase in the amount and frequency of acidic foods and soft drink consumption in populations throughout the world [13]. Early erosive wear in permanent teeth may compromise the entire dentition and cause considerable pain, and it may result in an increasing need for further comprehensive restorations, affecting the quality of life of the individual throughout his or her life.

      Aetiology and Pathogenesis

There are 2 causes of erosive tooth wear. The first is extrinsic factors, where the choices of diet/drinks and intake habits, beverages consumed during sporting activities, occupational factors or acidic medicines are examples of elements that may contribute to tooth mineral degradation [14, 15]. The individual’s choice of a healthier lifestyle often includes a diet with large amounts of fruit, vegetables and herbal teas, where the pH can be low, thus adding to the increase in erosion [16].

Intrinsic factors are the other cause, and gastro-oesophageal reflux disease and eating disorders also risk causing the chemical demineralisation of the enamel and dentine as a result of contact with the acidic contents of the stomach [17–19], while unhealthy lifestyles, such as alcoholism or the use of illegal designer drugs like ecstacy, have also been associated with an increase in the development of dental erosion [20]. Any accompanying form of excessive tooth wear, like attrition due to bruxism, adds considerably to the rate of hard-tissue loss [21].

The erosive damage to the dental hard tissues occurs after exposure to acidic substances and does not include the effects of bacteria or their products. The process involves an initial softening of the tooth surface, which is followed by a permanent loss of tooth substance. The degree of saturation of Ca²⁺, PO₄^3–, OH^– and F^– ions in the fluid that exists in the vicinity of the hydroxyapatite crystals, together with the critical pH for equilibrium and the erosive potential/chelating ability of the acid, are some factors that influence whether the minerals will dissolve or form deposits on the enamel surfaces [22]. To counteract the erosive processes, a satisfactory saliva secretion rate, composition and buffering capacity together with the formation of a protective dental biofilm shield, are considered to be influential protective biological parameters [23, 24].

      Future

      In the future, studies aiming to bring about the remineralisation of the affected dental tissues are needed. Increased awareness in the public and dental communities, early detection, change of behaviours associated with erosive tooth wear, applied preventive measures and continued targeted research are other plausible avenues to limit the expansion of dental erosion.

      Periodontal Diseases

      Introduction and Prevalence

Periodontal diseases comprise chronic, biofilm-initiated, inflammatory conditions including gingivitis and periodontitis [25]. They affect the tooth-supporting structures and may lead to masticatory dysfunction. Together with dental caries, they are the main cause of tooth loss. In its early stages, the disease may be restricted to the gingiva and be seen clinically as an inflammation indicated by bleeding upon probing. At this stage, it is possible for the gum tissues to return to a state of health, without the irreversible loss of tooth attachment, once the cause is removed. Further progression from gingivitis to periodontitis is manifested by attachment loss, clinically taking the form of deep periodontal pockets and gingival recession. Although periodontal disease may be identified in younger individuals, an increase in prevalence is seen with increasing age [26]. Even if signs of disease can be found in prehistoric samples, it is more common in the modern population. A substantial increase in periodontal health has taken place during the last 50 years. A reduction in gingivitis in Swedish individuals aged ≥20 years, from 40% in 1973 to 15% in 2013, has been seen [27]. A reduction in the frequency of individuals with a probing pocket depth of >4 mm, an increase in the number of individuals with no marginal bone loss and a reduction in the number of subjects with moderate alveolar bone loss have also been observed [27]. The peak incidence of severe periodontitis occurs between the age of 30 and 50 years, with the prevalence remaining basically the same afterwards [28, 29].

      Aetiology and Pathogenesis

Like dental caries, periodontal diseases are complex and of a multifactorial nature, including both inherited and acquired risk factors. A subgingival biofilm is required for the development of periodontitis, where the presence of proteolytic and anaerobic bacterial species plays a key role [30]. Differences in host response may determine disease onset, progression and severity, and several conditions may influence the interaction between the host and the bacterial biofilm. It has long been known that genetics contribute to periodontal diseases, with a likely risk estimated at up to 50%, and several different genes associated with chronic periodontitis have been identified [31]. A gender difference for periodontal diseases can be seen, but this is instead related to variations in lifestyle and is not genetically determined [32]. There is extensive support for smoking as a risk factor for periodontal disease where smoking, nicotine and its metabolites may have a negative effect on subgingival microflora, periodontal tissue and host response [33, 34]. Other risk factors for periodontal disease are diabetes, obesity, and other metabolic disorders; however, lifestyle factors such as alcohol and stress are also included [32, 34].

      Destructive inflammatory processes occurring around osseointegrated dental implants have been described by the term “peri-implantitis.” The disease process is very similar to that found in association with periodontal disease. In severe cases, peri-implantitis can lead to the disintegration and loss of implants and their supported prostheses.

      Disease Prevention

      Preventive strategies and maintenance focus on mechanisms, which directly or indirectly may have an impact on the amount and composition of the subgingival