Dental caries and periodontitis

1. Dental caries and periodontitis Medical oral microbiology I – ZLLM0421p Week 13 OndřejZahradníček Based upon the slideshow of assoc. prof. Vladana Woznicová

2. Dental caries and its history Archaeological findings conclude that dental caries is very old disease. On the other hand it is considered to be a civilisation disease. How it this possible? In the very ancient times caries existed, but was rare Increase in number of caries lesions during neolith was a result of increasing plant food and from this resulting increasing volume of saccharides in a diet Further increase was connected with rice-growing in South Asia. Also Sumerian texts about 5000 years B. C. describe „dental worms“ causing dental caries Today‘s dental caries are almost caused by high consumption of simple saccharides(with use of Wikipedia)

3. Genesis of caries and microbes Dental caries is defined as limited destruction of tissues of a tooth. From microbiological side of view it is a chronic infection, that is not caused by a pathogen from outside, but by the components of normal oral microflora. Microbes ferment saccharides, forming acids, and their effect leads to demineralisation of enamel. In further development it may lead to destroying of the dentin, eventually the inflammation may continue to pulpa (pulpitis)

4. Dental caries Obrázek z Wikimediacommons http://en.wikipedia.org/wiki/File:Toothdecay.png

5. Development of caries • Primary lesion of enamel is so called white chalky spot. The surface layer is relatively OK, but deeper layers are demineralised. This stage reversible, it can remineralise • After destruction of enamel, the process spreads to dentin and causes • inflammation of dentin • necrosis and gangrene of pulpa • formation of so calledperiapical acute or chronic inflammation (around apex of the tooth)

6. Dentoalveolar abscess (1) Dentoalveolar abscess usually develops as dental caries complication, when bacteria go through caries cavity into pulpa. Nevertheless, there exist also other possibilities, especially going through the tissues dividing the gingiva from the tooth (in this case it is rather complication of gingivitis or periodontal abscess – see later), eventually directly through periapical vessels. Next to the tip of dental apex we can see a sac with pus (a periapical abscess)

7. Dentoalveolar abscess(2) Further development of periapical pus may be different: In keeps localised – chronic abscess develops It spreads along soft tissues ( abscesses of soft tissues, cellullitis at spreading into dermis) It spreads into boles ( osteomyelitis) It spreads by blood way ( endocarditis or or metastatic abscess in other organs) It spreads along fascias and then the development depends on the direction

8. Factors influencing dental caries I • So called endogenous factors (tooth properties) • age, gender and genetic basis (tooth shape and position, enamel structure, quality of hard tissues of the teeth, etc.) • level of secretoryimmunoglobulins IgA • saliva – its quantity, flow and composition (buffer) – it washes and cleans the tooth and decreases the solubility of the enamel. In patients with decreased formation of saliva (hyposialia or asialia), caries frequency is much higher than in the healthy population

9. Factors influencing dental caries II • Effect of nutrition • saccharides intake: sucrose (saccharose) is the most cariogenic sugar, there is direct relation between sucrose and caries • sucrose diffuses easily to the plaque, it has excellent solubility, it diffuses to the plaque easily – cariogenic streptococci change it to insoluble glucanthat enables initial adhesion of microbes on the tooth surface; it is a source of nutrients and takes place in the intercellular matrix development • Tooth plaque microbes • almost all microbes in the dental plague have cariogenic effect thanks to their biochemical features • the most important in caries development –streptococci of the mutans group, lactobacilli, and actinomycetes • also combination of other microbes can start the cariogenic process

10. Streptococcus mutans and dental caries In man usually: S. mutans (serotypes c, e, and f) and S. sobrinus (serotypes d and g). Some strains seems to be more cariogenic. The relation of these streptococci to caries is still not completely clear Some facts concerning participation of these streptococci on the dental caries are nevertheless considered proven – see further

11. S. mutans ethiological role – facts: Numbers in the plaque and saliva correlates with caries prevalence and incidence Isolated from the tooth surface immediately before caries Immunisation of animals with S. mutans specific serotypes decreases caries incidence lesion progression and S. mutans numbers correlates are attached to the tooth surface and together by glucanes formed from saccharose they are the most efficient microbes in making caries in lab animals they are able to form acids and multiply in low pH reach pH needed to enamel demineralization quicker than other bacteria form reserves e. g. glycogen (in case of low levels of saccharides in food)

12. Lactobacilli and dental caries in high numbers in dental caries their numbers in saliva (and dental plaque) and caries activity correlate growth in pH lower than 5 + develop lactate biochemically active – extracellular and intracellular polysaccharides from sucrose some strains cause caries in microbe-free animals in healthy teeth – low numbers of lactobacilli

13. Lactobacilli Obrázek z WikimediaCommons (http://commons.wikimedia.org/wiki/File:Lactobacillus_sp_01.png)

14. Dental caries and more microbes • Actinomyces • related to root caries – especially Actinomyces viscosus • the role of actinomycetes in caries development is not elucidated completely • Veillonella • in high numbers in supragingival plague of most people • need lactate, are NOT able to use saccharides and use lactate developed by other microbes – transform it to less cariogenic organic acids • maybe even inter-species differences (V. dentocariosacommon in persons with caries, but V. rogosaerather in persons without caries) so in might eventually work even against caries – but it is nothing more than a hypothesis

15. Actinomyces Všechny obrázky pocházejí z Wikimediacommons

16. Protective factors Milk, diary products, milk proteins – buffer, increase of pH thanks to decarboxylation of amino acids from casein Milk casein – adsorption on the tooth surface, casein layer prevents S.mutans adhesion Calcium phosphate from casein boost enamel remineralisation Fluorides – boost tooth mineralization, diminish glycolyse, impair CM, and inactivate enzymes Xylitol– inhibition of bacterial growth

17. Treatment and prevention Standard treatment = ablation of impaired tooth tissue, preparation of cavity and filling Preventive measures = change of diet (low-carbohydrate diet), application of fluorides and proper dental care Ozone – low efficiency* *Műller, Eur J Oral Sci,2007; review: Azarpazhooh A, Limeback H. The application of ozone in dentistry: A systematic review of literature. J Dent. 2008 Feb;36(2):104-16.

18. Microbiology testing of risk of caries There exist kits enabling e. g. semiquantitativeevaluation of amount of streptococci S. mutans, evaluation of quantity of lactobacilli and testing of buffer capacity of saliva (Dentocult SM, Dentocult LB, Dentobuff) It is relativelly easy to use them

19. Dentocult SM http://www.i-zuby.cz/prevence/jak-na-bakterie-zubniho-kazu---prostredek-k-detekci-bakterii-streptococcus-mutans/

20. Changes of gingiva, periodontitis The dental plaque in the margin of gingiva leads to the fact that gingival tissue around sulcus gingivalis starts to be inflammatory. It leads to so called marginal gingivitis Site of infection is visited by anaerobic proteolytic bacteria. Also WBCs migrate here (polymorphonuclear granulocytes). The inflammation destroys the function of the junction epithelium, the plaque invades apically into the subgingival region. The symptoms are the stronger the older and more robust the plaque is

21. Microbes in cronic marginal gingivitis Clinical symptoms of the chronic marginal gingivitis mean especially temporary bleeding from gingiva, that is red and oedematous, but pain is minimal Early stage (one week): increase of capnophilic and strictly anaerobic microbes (Capnocytophaga, Actinomyces, anaerobic G– rods) Final stage: more microbes, anaerobes (Porphyromonas gingivalis, Prevotella intermedia, oral spirochets) Bleeding helps to the multiplication of black pigmented anaerobic rods (source of haemin)

22. Prevotella melaninogenica (black pigmentation) http://pharmacie.univ-lille2.fr

23. Changes in the periodontal pocket

24. Periodontitis (also „parodontitis“) Almost 80 % adults Inflammation of gums, scarcement of dentogingival junction Resorption of alveolar bone tissue A periodontal pocket develops in the place of gingival sulci, there is bleeding on probing, purulent content Dental plaque and tartar sediment on the cervical surface A teeth starts to move

25. Periodontitis (dog) http://commons.wikimedia.org/wiki/File:periodontitis_Hund.jpg

26. http://www.cassityimplants.com/gum_disease.htm

27. Influence of subgingival plaque – studies Strong correlation between plaque volume and prevalenceand severity of periodontal diseases Volunteers studies – poor dental hygiene = plaque growth and gingivitis – after plaque removal gingivitis heals Local application e.g. chlorhexidine diminish plaque and prevent gingivitis Microbe-free animal models - bacteria of „red complex“ from human plaque lead to periodontal infection and immunoinflammatory bone resorption (Kesavalu 2007)

28. Etiology of periodontitis Three main hypothesis about how dental plaque influences periodontal disease: • specific plaque hypothesis • non-specific plaque hypothesis • ecological plaque hypothesis http://www.intelligentdental.com/2012/02/19/is-dental-plaque-the-main-cause-of-dental-caries/

29. Specific plaque hypothesis Periodonitis, according to this hypothesis, is caused by particular specific microorganisms This hypothesis is valid only for some specific situations, e. g.: necrotizing ulcerative gingivitis – key bacteria arefusobacteria and spirochetes; therapeutic success with antimicrobials inhibiting anaerobes – e. g. metronidazole Another example: rapidly progreding juvenile periodontitis– key bacterium isAggregatibacter actinomycetemcomitans – susceptible to tetracycline – treatment by tetracycline leads to quick improvement

30. Non-specific plaque hypothesis According to this hypothesis, there are no „worse“ and „better“ bacteria. All is just a question of quantity – just large bacterial community leads to concentration of all virulence factors necessary to tissue destruction There is no specific role of individual species, if some are more frequent, they just substitute others, accidentally absent ones Plaque spreading under gingival level always cause the disease, not regarding the composition This hypothesis is supported by some studies, nevertheless, this theory cannot explain majority of cases of gingivitis

31. Ecological plaque hypothesis Recently the most supported theory Endogenous infection is caused by opportunist species = periodontitis caused by change in sulcarmicroflora based on changes of environment In the beginning, there is plaque development and spreading to sulcus gingivalis = macroorganism reacts by inflammation Increasing production of sulcar fluid increases supply of proteins – catabolised by proteolytic(= proteins decomposing)G- anaerobes easily Change of ration between bacterial species: number of G- anaerobes is growing, whereas facultative G+ anaerobes not – the first ones produce sufficient amount of virulence factors and break host immunity – destruction is a result

32. Therapeutic strategiesaccording to the hypothesis • Specific plaque hypothesis – therapy focused on specific pathogen removal, e.g. antibiotics administration • Both non- specific and ecological hypotheses – periodontal disease can be treated by instruments concentrated at reduction of the plaque volume • In any case, it should contain • Systematic removal of dental plaque (proper toothbrushing) • Proper removal of dental tartar • Repair of exogenous factors (improper dental plate etc.)

33. Microbiology of special types of gingivitis and periodontitis These are special types different from usual description Aggressive gingivitis and periodontitis types are particular, they use to develop quickly and have some specific. This group contains • Quickly progredingperiodontitis • Localised juvenile periodontitis • Prepubertalperiodontitis • periodontitis and gingivitis in HIV patients • Gingivitis in pregnancy • periodontal disease in diabetes

34. Quickly progredingperiodontis • Also post-juvenile periodontitis. Usually persons between teen age and 30 years, more commonly women. Typical loses of bone tissues with root resorption, sometimes worse, sometimes better, but finally the teeth use to be lost • As to microbiology, typical is high concentration of oral spirochetsplus G– anaerobes

35. Localised juvenile periodontis • Rare, usually starts in teen age. Women : men = approx. 4 : 1. Patients use to have good oral hygiene. • Disease attacks incisive teeth and first molars, it is painful • Important is inborn influence. As to microbes, important is A. actinomycetemcomitans in pockets • Treatment: tetracycline (effect to A. actinomycetemcomitans)  elimination of disease, eventually combination with metronidazole (for anaerobes). • In immunocompromised people generalized form of this disease may occur

36. Prepubertalperiodontitis • Based on a inherited WBC defect • It exists it both localized and generalized form • Not common in white persons • In periodontal pockets: common Gram-negative anaerobes in black colonies

37. Periodontitis and gingivitis in HIV infection • Bloody and painful atypical gingivitis and generalized periodontitis • Key microbes: Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum a Porphyromonas gingivalis, but also yeast Candida albicans • Dental surgery in these patients are risky, as they tend to bleed

38. C. albicans www.medmicro.info

39. Gingivitis in pregnant women and in diabetes • Gingivitis in pregnancy: • Serious gingivitis in pregnant women, but also at hormonal anticonceptionis explaind by presence of steroide hormones in sulcar liquid, that supports multiplying of Prevotella intermedia • Gingivitis at diabetes • Especially young patients with not sufficiently compensated diabetes mellitus have attacks of periodontal disease • Besides typical periodontal pathogens also Staphylococcus aureus

40. periodontal abscess • The periodontal pocket contains pyogene liquid (exsudate) • The gingiva over this pocket is red and oedematous, regional lymph nodes may be enlarged, temperature is increased • Typically endogenous (coming from inside the body) polymicrobial infections caused by subgingival plaque microbes (G– anaerobic rods, G+ anaerobic cocci, treponemas etc.) • Surgical treatment (incision), support of drainage, eventually even tooth extraction, eventually plus antimicrobial drugs (penicillin, erythromycin, metronidazole)

41. Nekrotising ulcerative gingivitis • Acute necrotizing ulcerative gingivitis (ANUG) is connected with bad oral hygiene and insufficient nutrition. • Treatment: stomatosurgical removal of attacked tissue, oral hygiene, topic treatment: chlorhexidine systemic treatment: metronidazole • Origin: polymicrobial, so called Plaut-Vincent fusospirochetal flora (Fusobacterium nucleatum + oral treponemas, especially Treponema denticola)

42. Noma • Noma (cancrumoris) is extremely serious form of ANUG • Typical situation: African children with poor nutrition and poor immunity, e. g. after measles; in Europe in history in concentration camps, now rare (immunodeficiencies) • Original necrotic lesions spread from gingiva to the face and this leads to the lost tissues (nomafaciei) • Microbiology: again Plaut-Vincent fusospirochetal flora

43. Key pathogens

44. Once more – bacteria and periodontitis V.parvula A.odontolyticus S.mutans S.oralis S.sanguis P.intermedia P.nigrescens P.micros F.nuc.nucleatum F.nuc.vincentii F.nuc.polymorphum F.periodontium P.gingivalis T.forsythia T.denticola E.corrodens C.gingivalis C.sputigena C.ochracea A.actinomyc. Zdroj: Socransky et al. 1998

45. Why „red complex“ has importance in periodontitis? • Virulence factors • Aggregation of bacteria • Interaction of bacteria

46. Treponema denticola • A spirochete (related to T. pallidum – causative agents of syphilis) • Strongly proteolytic • Colonises older children (in children aged 6–12 years 50 % has it, but it is only 0.5 % of microbial population) and adults • Ability of co-aggregation with fusobacteria, porfyromonas • It has close relations to Porphyromonas gingivalis

47. Porphyromonas gingivalis • It is highly proteolytic • Fimbriae – serve to adhesion and colonisation • Releases vesicles containing parts of outer membranes – proteins, LPS, capsule etc. • Vesicles – transport of toxins and enzymes, bacterial adhesion and aggregation, adheresion of thrombocytes • Black pigment = accumulated hemin – a source of iron (a growth factor)

48. Tanerella forsythia • Interaction between T. forythia a P. gingivalis • P. gingivalis supports adhesion to host cells and invasion • Epitelia with invading bacteria are the source of recurrent infection

49. Mutual relationshiphs inthe „red complex“ Porphyromonas gingivalis Treponema denticola Tanerella forsythia Nutrition, coaggregation support for adhesion a invasion adherence

50. Periodontitis – conclusion • Model polymicrobial disease • Oral biofilm and interaction of bacteria • Important microbes – Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola • Influences health widely