MODUL 5-Group J Ppt

8/13/2019 MODUL 5-Group J Ppt

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THE MEMBERS



Poor Oral Hygiene

Weakened Immune System Oral Microflora Increased (Gram +

and -)

Dental Plaque

Initiate Caries

Profunda Perforating

Caries

Plaque On Gingiva Sulcus (Junctional

Epithelium)

Chronic Gingivitis

Pocket Periodontal Infection

cause

Pulpitis

Inflammation and Destruction in

Attachment Apparatus of Teeth Migration to

Junctional

Epithelium

Periodontitis

Marginalis

DM Plaque Accumulation

Antibody Deficiency Focal Infection

Bacteraemia

SIRS

Immune System can’t

control

Microflora(Bacteria)invasion

Get Progressive

Worse and

UntreatedOral Sepsis

Sepsis to

Related

Tissue

Oral Infection

Hypersensitivity



In this case, a woman with 34 years old came

to the dentist with pain on the tooth 27.

After checking, the dentist found that there

is a hole and the gingiva surrounding thetooth is swollen.

She experience bleeding especially after

brushing her teeth. The tooth 27 before this

was treated by a dentist but still the woundwas not healed. She undergoes fever,

headache, flu, difficulty in breathing,

frequent urination and easily feels thirsty.



Periodontal disease, is the most common

disease in the world and the leading cause of

tooth loss in adults is a chronic infection that

slowly attacks and destroys the gums andbone that support the teeth.



In America, one-third of children ages 6-11

and two-thirds of adolescents have some

form of periodontal disease



Periodontal disease is caused by more than

200 species of bacteria. These bacteria form

masses of sticky film called plaque, which is

able to adhere to the surface of teeth andgums.

When left untreated, the bacteria begin to

spread to areas that are hard to reach with

normal brushing and flossing; for instance,areas below the gum line, thus causing

periodontal disease (periodontal).



Here as a dentist we should know what is

periodontal disease and how we can

responsible about that.



Bacteremia is usually defined as the

presence of viable bacteria in the blood

stream, as evidenced by blood cultures

(Young,2000). Bacteremia is usually classified according to

the microbial agent and an eventual

coexisting focus of infection, assessed on the

basis of microbiological and clinical findings



In this thesis we focused on community-

acquired bacteremia, as our aim was to

investigate diabetes as a risk factor for

bacteremia in the general population, notamong patients already hospitalized.



Pulpitis is the process of inflammation in

dental pulp tissue, which in general is a

continuation of the caries process. Pulp

tissue located within the dental hard tissuesso that when experiencing inflammation.



Based on the duration and severity Acute pulpitis

Sub acute pulpitis

Chronic pulpitis

Based on the presence or absence ofsymptoms Symptomatic pulpitis

Asymptomatic pulpitis

Based On Histo pathologic And ClinicalDiagnosis Reversible Pulpitis

Irreversible Pulpitis.



Irreversible pulpitis is an inflammatory

condition of persistent pulp, can be

symptomatic or asymptomatic due to a

stimulus / lesion, where the defense can nottackle pulp inflammation that occurs, and

the pulp can not return to its original or

normal.



On the pulpitis irreversible humoral immune

response seen increased IgG and IgM high,

but IgA decreased considerably indicating

that low mukosalnya resistance. The high IgG

and IgM showed high pulp tissue resistance to

microorganisms.



This is due to the wet zone products:

Drain of carious lesions

The product is absorbed by the venous

circulation or lymphatic spread to adjacent tissue

combination of the above ways that do not

increase blood pressure vessel

changes of irreversible symptomatic pulpitis

(acute) that are dormant.



The bone of the alveolar crest shows

resorption as demonstrated by the presence

of Hownship’s lacunae sometimes still

containing multinucleated osteoclasts. Caries

may add to the damage caused by

periodontitis by attacking the cementum

covering the exposed root surface.



Chronic gingivitis is asymptomatic, low grade

inflammation of the gingivae. The latter

become red and slightly swollen with

oedema.

Pressure on the gingival margins causes

bleeding, and sometimes pus can be

expressed from round the necks of the teeth.





Gingivitis is an inflammatory response to

plaque bacteria. By definition, inflammation

is restricted to the gingival margins and does

not affect the periodontal ligament or bone.

It must be appreciated that these stages are

artificially distinguished, being largely based

on animal studies. (DeBowes LJ. 2002)



Pregnancy gingivitis

Down's syndrome

Diabetes mellitus



Clinical features :Chronic periodontitis (the

'advanced lesion') is the chief cause of tooth

loss in later adult life, but symptoms are

typically minimal. Many patients remain

unaware of the disease until teeth become

loose. (Cawson, 2002)



Radiography :Bone resorption usually

progresses in a regular manner and its level

remains the same along a row of

teeth.Complex patterns of bone loss may

also be seen, but where alveolar bone is

thicker, partial destruction gives rise to

vertical or angular bone defects. (Cawson,

2002)



Plaque :Bacterial plaque, a dense mat of

bacteria, extends from the gingival margins

into pockets. (Cawson, 2002)

Subgingival calculus :Extension andcalcification of plaque leads to formation of

subgingival calculus within periodontal

pockets.

Chronic inflammation :Dense masses ofthese cells accumulate, especially under the

epithelium in the connective tissue apposed

to plaque and calculus. (Cawson, 2002)



Pocketing :Patients suffering from gingivitis

will have a pocket depth of 3mm; a normal

patient will have a pocket depth of less than

3mm (Hafernick). The second stage of

periodontal disease is periodontitis II; this is

characterized by puffy, bleeding gums with a

pocket depth of up to 5mm and the early

stages of bone loss (Hafernick).



Smokers have greater susceptibility to

periodontitis but paradoxically less gingivitis.

The reasons for this are not understood but

smoking is known to interfere with

inflammatory and immune reactions probably

by activating endothelial and inflammatory

cells inappropriately in the lungs and

circulation, and by inducing them to secrete

cytokines and other compounds.



The first response triggered by bacterial

infection is the innate immune response.

Bacteria are taken up by macrophages,

causing the macrophage to release cytokines.

The cytokines cause the inflammation

associated with periodontal disease.

Interleukin-8 (IL-8) is a chemoattractant for

neutrophils, therefore it is logical that

increased levels of IL-8 are found in gingival

cells.



Chronic periodontitis, once established, is

self-perpetuating. Pockets cannot drain

effectively and favour proliferation of

bacteria. The epithelial lining, plaque and

subgingival calculus effectively obstruct

healing.



Control of bacterial plaque

Establishment of healthy gingiva accessible

to plaque control

Minimisation of periodontal tissue lossUse of antibiotics in selected cases

Mucogingival surgery in selected cases



Subgingival scaling or root planing will not

remove subgingival plaque entirely and may

force pocket bacteria into the tissues.

However, competent performance of these

procedures reduces bacterial bulk, changes

the composition of the flora and frequently

produces clinical improvement. (Cawson,

2002)



In 1992, the American College of Chest

Physicians (ACCP) and the Society of Critical

Care Medicine (SCCM) introduced definitions

for systemic inflammatory response

syndrome (SIRS), sepsis, sepsis induced

hypotension, septic shock, and multiple

organ dysfunction syndrome (MODS).



SIRS is defined as 2 or more of the following

variables:

- Fever of more than 38°C or less than 36°C

- Heart rate of more than 90 beats perminute

- Respiratory rate of more than 20 breaths

per minute or a PaCO2 level less than 32 mm

Hg - Abnormal white blood cell count

(>12,000/@L or <4,000/@L or >10% bands)

(Abrahamson, 1993)



The most common causes of SIRS related to

infectious disease are as follows: bacterial

infection, wound infection (burns, surgical

wounds, diabetic foot and other infectious

complications), cholecystitis, cholangoitis,

other abdominal infections, pneumonia both

nosocomial or community acquired,

urogenital infections, meningitis and other

less frequent conditions Noninfectious



1. Fever

2. Hypotension

3.Tachykardia

4. Increase oxygen tissue supply increasedbreathing rate and hypocapnia

5.Changes of the leucocytes (WBC) count



Sepsis describes a complex clinical syndrome

that results from a harmful or damaging host

response to infection. As a result of a

concerted effort to understand the

underlying pathogenetic mechanisms, there

have been significant advances that have

illuminated not just the process of sepsis,

but also fundamental principles governing

bacterial–host interactions.



Determining the structural components of

bacteria that are responsible for initiating

the septic process has been important not

only in understanding the underlying

mechanisms, but also in identifying potential

therapeutic targets.



Diabetes mellitus is one of the oldest

diseases in humans. By the definition,the

definition of medical diabetes extends to a

collection of symptomps that arise in a

person that is caused by the presence of

elevated levels of blood glucose resulting

from insulin deficiency is either absolute or

relative nature.



Type 1 diabetes (b-cell destruction, usually

leading to absolute insulin deficiency)

Type 2 diabetes (ranging from predominantly

insulin resistance with relative insulindeficiency to predominantly an insulin

secretory defect with insulin resistance)



Vascular disease (diabetic angiopathy),

atherosclerosis, heart conditions and stroke:

These cardiovascular disorders are the

leading cause of death in people with

diabetes.

Kidney disease (diabetic nephropathy):

Diabetes is the chief cause of end-stage renal

disease, which requires treatment withdialysis or a kidney transplant.

Eye diseases: These include diabetic

retinopathy, glaucoma and cataracts.



Genetics and family history

Family medical history

Weight and body type

Sex Level of physical activity

Diet



Here we have found one of the main reasons

for this to happen is poor oral hygiene. The

poor oral hygiene will cause continual

accumulation of minerals from saliva on

plaque on the teeth. It is rough surface

provides an ideal medium for further plaque

formation, threatening the health of

the gingiva (gums). Once the plaque formed,

it is too hard and firmly attached to be

removed with a toothbrush.

http://en.wikipedia.org/wiki/Gingiva




The condition of too much plaque on the

teeth can be the reason of oral micro flora

increased. Oral micro flora is a colony of

bacteria in the mouth which can be aerobe

or anaerobe. The example is lactobacilli,

staphylococci, corynebacteria, streptococcus

mutans and various anaerobes in

particular bacteroides.

http://en.wikipedia.org/wiki/Anaerobe

http://en.wikipedia.org/wiki/Bacteroides

http://en.wikipedia.org/wiki/Bacteroides

http://en.wikipedia.org/wiki/Anaerobe



Another effect of increased bacteria is

plaque on gingiva sulcus (junctional

epithelium). This long time condition can

cause chronic gingivitis.

Gingivitis (inflammation of the gum tissue) is

a non - destructive periodontal disease. The

most common form of gingivitis, and the

most common form of periodontal

disease overall, is in response to

bacterial biofilms adherent to tooth surfaces,

termed plaque-induced gingivitis.

http://en.wikipedia.org/wiki/Inflammation


http://en.wikipedia.org/wiki/Periodontal_disease



http://en.wikipedia.org/wiki/Biofilms

http://en.wikipedia.org/wiki/Biofilms





http://en.wikipedia.org/wiki/Inflammation



Tooth decay disease is caused by specific

types of bacteria that produce acid in the

presence of fermentable carbohydrates such

as sucrose, fructose, and glucose. Another

effect of increased bacteria is plaque on

gingiva sulcus (junctional epithelium). This

long time condition can cause chronic

gingivitis. Chronic gingivitis makes a dental

pocket. Thus, chronic gingivitis and

junctional epithelium destruction together

lead a pocket periodontal that cause

periodontitis.

http://en.wikipedia.org/wiki/Acid

http://en.wikipedia.org/wiki/Fermentation_(food)

http://en.wikipedia.org/wiki/Carbohydrate

http://en.wikipedia.org/wiki/Sucrose

http://en.wikipedia.org/wiki/Fructose

http://en.wikipedia.org/wiki/Glucose

http://en.wikipedia.org/wiki/Glucose

http://en.wikipedia.org/wiki/Fructose

http://en.wikipedia.org/wiki/Sucrose

http://en.wikipedia.org/wiki/Carbohydrate

http://en.wikipedia.org/wiki/Fermentation_(food)

http://en.wikipedia.org/wiki/Acid



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MODUL 5-Group J Ppt