Loading presentation...

Present Remotely

Send the link below via email or IM


Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.


oral diseases

No description

Alzahra Alshayeb

on 15 December 2012

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of oral diseases

Alzahra Alshayeb
Tania Salam
Yasser Alrauji Oral bacterial diseases Oral cavity Dental Plaque Periodontitis Is characterized by destruction of the supporting tissues of the teeth, including of alveolar bone, by inflammation.
Antiseptic mouthwash
Dental sealant
Oral irrigator Introduction Dental Plaque Periodontal Disease Conclusion Important
Details Notes Host immune response determine severity and extent of the disease Other host factors (acquired):
- systemic disease e.g. diabetes mellitus (DM)
- Medication: phenytoin, nifedipine, and cyclosporine.
- Immunosuppresssive disease such as HIV
- Smoking Etiology Several oral microbes (indigenous) have been implicated in periodontitis including "red-complex" - Porphyromonas gingivalis
- Tannerella forsythia
- Treponema denticola Porphyromonas gingivalis is the keystone species One out of every two
American adults
aged 30 and over has
periodontal disease Predisposing factors (genes):
(for risk assessment, not for diagnosis) Diagnosis: Dental plaque is occurred by complex of microorganisms and their products being accumulated on the teeth surface.

It is associated in formation of dental caries ( tooth decay).

Most common bacterium cause dental plaque is Streptococcus mutans that gram positive. Dental Plaque VIRULENCE FACTORS
The main virulence factors of S. mutans are:
-ability to utilize sucrose: promote adhesion
-Also, acidogenicity: S. mutans consists complete glycolytic pathway and can produce lactate, formate, acetate, and ethanol as fermentation products. The certain distribution of fermentation products depend on growth conditions with lactate being the main product when glucose is sufficient.

-Acid tolerance: S. mutans remain glycolytic capabilities even at low pH levels( as low as pH 4) which are growth inhibitory. Acid- tolerance might aid by the synthesis of water-insoluble glucan and the formation of biofilm. Therefore, S. mutans cell with biofilm are able to survive an acid challenge than other grown bacteria CAUSES AND SYMPTOMS
Organisms are normally found in mouth cavity such as S mutans that converts foods such as sugar into acids.

There may not be any symptoms unless dental plaque progress and lead to further disease. Immune response: - Generally, the plaque is not immunogenic.

-Researchers at an Indiana University School of Dentistry, led by Dr. Michael Kowolik,. They found that dental plaque accumulation did not result in a change in total white blood count (WBC), however in African American men, shows increase in WBC but not in women or white people. (The Journal of the American Dental Association November 2009 vol. 140 no. 11 1351 ). FURTHER DISEASE CAN CAUSE - S. Mutans isolated from cases of infective endocarditis. In addition, 20% of the endocarditis cases attributed to S. mutans

- It is not certain whether the frequency of causation parallels prevalence of the organism in the oral cavity or is influenced by the variety of virulence factors.

- Also, bacteria leads to oral diseases such as dental caries, gingivitis, and periodontitis. DIAGNOSIS
Two methods:

1. Tablet stain : Chew one tablet that contain a red stain then dye over the teeth and gums . Then rinse the mouth with water and examine the teeth to identify plaque.

2. Plaque light: after gurgle special fluorescent solution then rinse with water and examine the teeth and gums by UV light.
Brushing the teeth
Maintain good oral hygiene
Gargle with warm saltwater three time pre day
See the dentist every 6 months Prevention VACCINE
There is vaccine against S. mutans for dental caries which is the progress stage of dental plaque, but it is still in the early stage. Treatment presence or absence of clinical signs of inflammation.
Identifying the pathogens is helpful in determine target therapy, not in diagnosis.

- Probing depths.
- Extent and pattern of loss of bone attachment.
- Patient's medical and dental history.
- Radiography
- Gingval cervicular fluid (GCF).
- Asparate Aminotransferase (ASA) released by dead and dying host cells
- non- specific neural proteinaese released by nutrophils. Probing depths Every smile makes you a day younger Mucous membrane epithelium:
-Masticatory mucosa: Gingiva and hard palate.
-Specialized mucosa: tongue
-Lining mucosa: e.g soft palate http://www.sciencedirect.com/science/article/pii/S1931312811003349# http://www.sciencedirect.com/science/article/pii/S1349007912000771 Hundreds of bacterial species inhabit the oral cavity
- Fluoride is still the most effective caries-preventive agent
- Identifying specific pathogens is no longer that important. The focus is now moved to overall functionality of the oral microbiota rather than biofilm composition.
- Antimicrobials generally have a limited capacity to eliminate bacteria deep into biofilms,
- exploiting ‘good’ bacteria, probiotics, to promote health flora might be more successful than eliminating pathogenic microbiota

Photos courtesy of Center for Medical Biofilm Research, University of Southern California. Bacteria beginning to adhere
Formation of a microcolony
Formation of a macrocolony
Bacteria macrocolonies spread and overlap, resulting in full biofilm.
Resistance to antibiotics Biofilm forms over 24-hour period Oral Disease
Risk Factors
Oral flora
Progression of the disease
Plaque: Streptococcus mutans
Periodontitis:Porphyromonas gingivalis
Secondary condition
Conclusion Objectives: Oral Disease Oral health is essential part of our life.
The ability of speak, eat and taste, smell, smile, chew, swallow and facial expression depends on the maintenance of oral health.
Oral disease can be ranged from cavities to oral cancer. Cause Oral disease causes tooth decay
Bacterial colonization
Bacteria changes carbohydrates in to acids.
Plaque that stays on the teeth for more than two or three days can become harder under the gum line and turn into tartar or calculus.
Tartar makes plaque more difficult to remove and this creates a protective shield for bacterial growth (Martins, et al. 2012). Carbohydrate such as sugar and starches
Poor hygiene
Tobacco and Alcohol Risk Factors Data According to World Health Organization (WHO),
Dental Cavities:
60 to 90 % of children.
~ 100 % of the adults .
Periodontal disease:
15 to 20 % of middle-age adults.
Dental cavities and periodontal diseases:
30 % of population worldwide have total tooth loss.
Oral cancer:
10 cases per 100,000 people.
Tobacco and alcohols are the major cause of Oral disease.
According to CDC (Center for Disease Control and Prevention),
7800 people dies from oral cancer every year.
36500 new cases of oral cancer being diagnosed. Oral Disease Dental cavities
Plaque formation
Periodentitis also known as gum disease.
Without treatment this conditions can lead to more severe diseases such as
Oral cancer,
Heart Disease,
and many more. List of Oral Microorganisms http://www.landesbioscience.com/journals/virulence/HuangVIRU2-5.pdf Bacterial interactions. Solid lines indicate inhibition while dashed lines indicate facilitation. The direction of the arrow indicates the direction
of inhibition or facilitation. http://www.nature.com/ijos/journal/v4/n3/fig_tab/ijos201254f4.html#figure-title
doi:10.1038/ijos.2012.54 Alkali prevents Dental caries http://atlantadentalspa.com/oral_dna.html Secondary conditions http://www.healthanddentistry.org/oralimmunesystem.html Cont. Streptococcus tigurinus
http://ijs.sgmjournals.org/content/early/2012/01/16/ijs.0.038299-0 A recent study done by Andrea Zbinden and his colleague published an article in International Journal of Systematic and Evolutionary Microbiology in January, 2012.
A new kind of streptococcus species where isolated from patient with endocarditis, meningitish and spongylodiscitis.
Sequencing 16s rRNA gene sequencing,
98.6% similarities to Streptococcus mitis
DNA-DNA hybridization analysis,
low re-association value with streptococcus mitis.

Streptococcus tigurinus.
Resembles to oral bacteria.
Bleeding gums -possible route of entry into the bloodstream.
Future research
How common this bacteria are in oral cavity and rish factors are yet to be determined. Bacteria and oral disease
secondary condition Flouride:

Dental hard tissue contains mineralized enamel
Plaque = acid formation= demineralization.
fluoridation prevents tooth decay.
Fluoride ion has the ability to penetrate bellow the enamel surface and stimulate remineralization of the enamel and allow precipitation of mineral incorporating fluoride which are fluoridated apatite and calcium fluoride in active form. (Lussi, et al, 2012)

According CDC website,
In New York, fluoridization reduced tooth decay 25 % in children and adult
72.2 percent of the population receives fluoridated drinking water.
In Connecticut fluoridization became law in May 18, 1965. Prevention Other ways,
Lowering carbohydrate intake and balancing nutritional intake to prevent tooth decay and premature tooth loss,
Oral cancer can be prevented by intake of fruit and vegetable,
Reducing the usage of tobacco and alcohol,
Maintaining proper hygiene; brushing and flossing regularly. Prevention Oral Flora A new study was published on Sep. 2012, in Journal of Oral Science,
contribution of alkali generation in dental biofilm that inhibits the initiation and progression of dental caries.
Dental Biofilm maintains the balance of pH and reminerilzation and de mineralization (Liu, 2012) Primary source of alkali generation,
Hydrolysis of Urea by enzyme
Streptococcus salivarius, Actinomyces naeslundii and oral haemophili produce the enzyme that hydrolyzes Urea.
Metabolism of arginine
Arginine catabolism is provided by oral flora that colonizes teeth and soft tissue are Streptococcus sanguinis, Streptococcus gordonii, Streptococcus parasanguis and Streptococcus mitis (LiU, et al., 2012) Cont. Oral organisms generate alkali to form protection against acid damage and enhancement of cell growth.
S. mutants and S. sobrinus have no enzyme to breakdown Urea or arginine.
alkali generation favor the health associated bacteria and discourage the growth of carcinogenic bacteria which prefers low pH to grow such as S. mutans (LiU, et al., 2012)
a mice was injected with S. mutant. A gene that encodes for urease enzyme was inserted into the S. mutant gene. Results shows that S. mutant produces high level of urease producing ammonia and increasing pH of the solution and form fewer caries than those with the normal gene (LiU, et al., 2012). Cont. Steptococcus mutans
Porphyromonas gingivalis
Treponema Denticola
Streptococcus mitis
Streptococcus oralis
Streptococcus sanguis
Streptoccocus gordinis
Staphylococcus aureus
Staphylococcus epidermidis
Veillonella spp
Neisseria sicca
Actinomyces spp.
Corynebacterium spp.,
Prevotella spp.
Streptococcus sanguis
Psudomonas aeruginosa
Fusobacterium nucleatum
Treponema spp.
Tannerella forsythensis
Aggregatibacter actinomycetemcomitans Treatment: Reduce and eliminate the resultant inflammation and halt disease progression. Gingivitis : cleaning by general dentist with maintain oral hygiene.
Periodentitis: depends on severity Nonsurgical treatment: Deep cleaning (scaling and root planning)
a- control risk factors: such as smoking and diabetes.
b-systemic antibiotics especially in invasion lesion.
c-Modulation of host response: slow down of the inflammatory enzymes and tissue destruction.

Surgical treatment:
gum surgery- access to some roots and bones areas that are normally inaccessible by nonsurgical treatments.
Eliminates all bacterial accumulation and prevent disease recurrence. Symptoms : - Gingival swelling
- Bleeding on brushing
-Bad mouth odor
-Purulent exudate
-May experience pain Bacteria alone can't cause disease and count only for 20% of the risk of developing sever periodontitis. Heredity alone accounts for 50% of the enhance risk for sever periodontitis: - TNF-alpha promoter: increase production enhance susceptibility to oral infections.
- Adult with increase production of IL-1 have 20 time more risk to develop sever periodentitis Periodontitis during pregnancy Maternal infection is responsible for 30 to 50% of all preterm low birth weight (PTLBW).

Inflammatory cytokines or oral infection may trigger preterm labor (PTL )and PTLBW.

Treating periodontitis during pregnancy significantly reduce rate of PTL.

Porphyromonas gingivalis agar (P. GING) is an enriched selective medium for the isolation and presumptive identification of Porphyromonas gingivalis. This medium is prepared, stored and dispensed under oxygen-free conditions to prevent the formation of oxidized products prior to use. Identification:
- Culture base studies.
- Whole-genomic DNA probes. Most studied oral bacterium Circular representation of P. gingivalls genome, Each color shows the prediction for coded region and divided in 8 categories: e.g ninth circle shows tRNA (green) and rRNA (black) Virulence factors: Tissue degradation occurs due to inflammatory response P. gengivalis continue growing because it have the ability to escape from immune response by manipulating the key components of innate immunity (disable host response) - Inhibit complement activation by digestion C3
- Degradate TLR coreceptores (CD14), Cytokines (IL-12, IL-6, and IFN-gamma)
- Make C5aR-TLR2 crosstalk which inhibit phagocyte killing ability
-Hijaking C4b-binding proteins Lipopolysaccharide (LPS):
- resist complement-mediate lysis

Fambriae: (adhesive hair-like structure on bacterial surface):
-Inhibite phagncyte killing
- bind to CR3 which suppress production of IL-12
- Insure intracellular survival by CR3 mediate entry

- Counteraction of oxidation damage
- Resistance to environmental oxidative stress and oxidative killing by phagocyte Biofilm EBV DNA was found in gingival crevicular fluid and saliva of periodontal patients:
- 60%–80% of aggressive periodontal lesions
- 15%–20% of gingival lesions or normal periodontal sites. Higher concentrations of P. gingivalis bacilli were found in EBV-positive periodontal patients EBV reactivation may facilitate progression of periodontal disease in infected individuals http://www.pgingivalis.org/ http://www.ncbi.nlm.nih.gov/pubmed/12949112 http://wishart.biology.ualberta.ca/BacMap/includes/species/Porphyromonas_gingivalis.png http://www.anaerobesystems.com/Home/pras-mono-plated-media/Porphyromonas-Gingivalis-Agar http://www.sandquistdds.com/images/uploads/toothdiagram.gif http://gloriagilbere.typepad.com/.a/6a01156fb2e48a970c0133ec685076970b-320wi http://www.aafp.org/afp/2008/0315/afp20080315p797-f5.jpg http://frisco-dentist-blog.com/wp-content/uploads/2012/09/gum-disease3.jpg http://www.perio.org/consumer/cdc-study.htm http://www.cancer.gov/images/cdr/live/CDR716338-571.jpg http://mpkb.org/_media/home/publications/marshall_autoimmunity_2010/2010ai_marshall_slide10.jpg?w=640 gram-negative anaerobic rod Gingipains: References: References: Streptococcus mutans is the most common bacterium that cause dental plaque. The presence of effective vaccine my help reduce the prevalence of dental cavities and other dental diseases. Porphyromonas gingivalis is the key species for periodentitis. The progression of the disease should be stopped as early as possible to prevent other serious complication such as endocarditis s The oral cavity is a normal habitat for thousand of microorganisms, not all of them are pathogenic. - "Dental Plaque Prevention." Dental Plaque: Prevention. N.p., n.d. Web. 27 Nov. 2012. <http://www.freemd.com/dental-plaque/prevention.htm>.
- "Health Guide." Dental Cavities. N.p., n.d. Web. 21 Nov. 2012. http://health.nytimes.com/health/guides/disease/dental-cavities/overview.html
- "Health Guide." Dental Plaque Identification at Home. N.p., n.d. Web. 26 Nov. 2012. <http://health.nytimes.com/health/guides/test/dental-plaque-identification-at-home/overview.html>.
- "Result Filters." National Center for Biotechnology Information. U.S. National Library of Medicine, n.d. Web. 27 Nov. 2012. <http://www.ncbi.nlm.nih.gov/pubmed/14977543>
- "The Journal of the American Dental Association." INFLAMMATORY RESPONSE TO DENTAL PLAQUE ACCUMULATION VARIES BY SEX, RACE. N.p., n.d. Web. 25 Nov. 2012. <http://jada.ada.org/content/140/11/1351.1.full>.
- “Bacteriology at UW-Madison”. 2008. The microbial world: Microbes and Dental Disease. Kenneth Todar University of Wisconsin-Medison Department of Bacteriology. Available at: http://www.textbookofbacteriology.net/themicrobialworld/dental.html
- American academy of periodontology. 2003. Diagnosis of periodontal diseases. Journal of Periodontol 37:1237-1247.
- Duncan, M., Dewhirst, F., & Chen, T. 2012. Porphyromonas gingivalis: Pathogenesis studies. Department of Molecular Genetics, The Forsyth Institute. http://www.pgingivalis.org/pathogenesis.htm
- Eke, P. I., Dye, B. A., Wei, L., Thornton-Evans, G. O., and Genco, R. J. 2012. Prevalence of periodontitis in adults in the United States: 2009 and 2010. Journal of Dental Research. 91(12)
- Hajishengallis, G. 2011. Immune evasion strategies of prophyromonase gingivalis.Journal of Oral Biosciences 53(3):233-24
- Honda, K. 2011. Porphyromonas gingivalis Sinks Teeth into the Oral Microbiota and Periodontal Disease. Cell Host & Microbe, 12(5): 605-730.
- Huang,R., Li, M. & Gregory, R. L. 2011. Bacterial interactions in dental biofilm. Virulence 2 (5): 435-444.
- Huang,R., Li, M. & Gregory, R. L. 2011. Bacterial interactions in dental biofilm. Virulence 2 (5): 435-444.
- Imai, K., Ogata, Y. & Ochiai, K. 2012. Microbiat intreaction of periodontontopathic bacteria and Epstein-Barr virus and their implication of periodontal diseases. Journal of Oral Biosciences 54(3): 164-168
- Kawar, N. & Alrayyes, S. 2011. Periodontitis in pregnancy: The risk of pregnancy labor and low birth weight. Dis Mon 57: 192-202
- Liu, Y. L, Nascimento, M. & Burne, R. A. 2012. Progress toward understanding the contribution of alkali generation in dental biofilms to inhibition of dental caries. International Journal of Oral Scienece 4: 135-140 - Ljubljana, S. 2010. Presentation - Olmesartan overcomes antibiotic resistance, inducing recovery from advanced autoimmune disease. The Marshall Protocol Knowledge Base. http://mpkb.org/home/publications/marshall_autoimmunity_2010
- Lussi, A., Hellwig, E. & Klimek, J. 2012. Fluorides – Mode of action and recommendations for use. Journal of Research and Science. 122: 130-136
- Lussi, A., Hellwig, E. & Klimek, J. 2012. Fluorides – Mode of action and recommendations for use. Journal of Research and Science. 122: 130-136
- Martins, C., Siqueira, W. L., Oliveira, E., Nicolau, J., Primo, L. G. 2012. Dental calculus formation in children and adolescents undergoing hemodialysis. Journal of Pediatric Nephrology 10: 1961- 1966
- N.p., n.d. Web. 27 Nov. 2012. http://www.ijdr.in/article.asp?issn=0970-9290;year=2009;volume=20;issue=1;spage=99;epage=106;aulast=Shivakumar
- Najjar, T. & James, W. D. Bacterial mouth infection. Medscape Reference. Updated: May 23, 2012. Available at: http://emedicine.medscape.com/article/1081424-overview
- Nelson, K. E., Fleuschman, R. D., DeBoy, R. T., Paulsen, I. T., Fouts, D. E., Eisen, J. A., Daugherty, S. C., Dodson, R. J., Durkin, S., Gwinn, M., Haft, D. H., Kolonay, J. F., Nelson, W. C, Mason, T., Tallon, L., Gray, J., Granger, D., Tettelin, H., Dong, H., Galvin, J. L., Duncan, M. J., Dewhirst, F. E. & Fraser, C. M. 2003. Complete genome sequence of the oral pathogeic bacterium Prophyromonas gingivalis strain W83. Journal of Bacteriology 185(18): 5591-5601.
- Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: An Introduction. 11th ed. Redwood City, CA: Benjamin/Cummings Pub., 1995. Print.
- Zbinden, A., Mueller, N. J. , Tarr, P. E., Sproer, C. , Keller, P. M. , Bloemberg, G. V. 2012 Streptococcus tigurinus sp. nov., isolated from blood of patients with endocarditis, meningitis and spondylodiscitis. International Journal of Systematic and Evolutionary Microbiology 62(11):
- Zbinden, A., Mueller, N. J. , Tarr, P. E., Sproer, C. , Keller, P. M. , Bloemberg, G. V. 2012 Streptococcus tigurinus sp. nov., isolated from blood of patients with endocarditis, meningitis and spondylodiscitis. International Journal of Systematic and Evolutionary Microbiology 62(11)
-Kawar, N., Gajendarddy, P. K., Hart, T. C., Nouneh, R. & Alrayyes, S. 2011, April. Periodontal disease for the primary care physician. Dis Mon 57:174-183.
-Martins, C., Siqueira, W. L., Oliveira, E., Nicolau, J., Primo, L. G. 2012. Dental calculus formation in children and adolescents undergoing hemodialysis. Journal of Pediatric Nephrology 10: 1961- 1966. Gingivitis Periodontitis
Full transcript