Patogenesis Penyakit

Infeksi Pada Rongga

Mulut
Drg. Rachmi Fanani Hakim MSi
 Host (inang): manusia

SAKIT/ SEHAT
Infectious agents Environment

(bacteria, fungi) (mulut dan semua

unsur biologis)

 Keterkaitan antara keadaan sakit dan sehat Dinamis

 Keberadaan agen tidak selalu mengakibatkan host menjadi sakit

 Keseimbangan: tergantung mekanisme resistensi/ kerentanan host dan

virulensi agents, dan faktor lingkungan yang mempengaruhi keseimbangan
interaksi tersebut
 Oral cavity

Dental material

Somatic cells (tissue):

- Epithel Microorganism Neuro-
- Fibroblast endocrine
- osteoblast
system

Immune
system:
- Spesific
- Non-spesific
 Principal Infectious Agents

“Our mouth is an ecosystem, not a sterile object.”

• Viruses
All are the source of molecules:
• Bacteria
• Fungi Protein, glycoprotein, lipoprotein

• Protozoa
Prinsip: organisme (host dan agent) harus survive

Host : menolak, mentolerir/ kompromi keberadaan agen

Simtom klinis:
Non-spesifik
inflamasi
Sistem imun
spesifik
gejala pada
Agen : phenotipe komensal seluruh tubuh/

pathogen / virulensi gejala lokal

u/ survive: antigenic variation Perubahan karakter antigen

(gene rearrangement)
 PERJALANAN INFEKSI
 Karies,
 abrasi,
 atrisi,

 erosi,

 trauma
YANG TIDAK DI RAWAT
PERJALANAN INFEKSI
 Perjalanan infeksi
• Once bacteria and their products reach the apical area they
encounter Polymorphonuclear neutrophils (PMNs) and
macrophages.
• If this process is allowed to continue, chronic inflammatory
cells, lymphocytes, plasma cells, and fibroblasts wall off the
irritating agents. If the irritant is removed (i.e., if the canal is
cleaned, shaped,and filled), then healing should occur similar
to healing after the splinter is removed.

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• Zona infeksi : PMN
• Zona kontaminasi: Sel kronis
• Zona iritasi: histiosit + osteoklas
• Zona stimulasi: fibroblas, kapiler, osteoblas

• It was felt that bacteria only got past the apical foramen in an
acute alveolar abscess, where the body is temporarily
overwhelmed by the bacteria.

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• polymicrobial infections dominated by anaerobic species
• it was better to have these irritants outside the tooth, where
the blood supply is richer and the body's own defense
mechanism can neutralize the antigenic material
• With the persistence of a periapical lesion after conventional
endodontic therapy, it becomes apparent that the body's own
defense mechanism may not always be capable of healing
these lesions.

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 Perjalanan infeksi
• The periapex of the tooth becomes involved when bacteria
invade the pulp, rendering it partially to totally necrotic.
• The study demonstrated that without bacteria and their
products, periapical lesions of endodontic origin do not occur.
• periapical disease is the result of bacteria, their products, and
the host response to them.

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 HOST RESPONSE
• Inflammation
• The basic disease process in both pulp and
periapical disease is infection.
• The host responds to the infection with
inflammation.
• Inflammation defined as the complex
vascular,lymphatic, and local tissue reaction of
a higher organism to an irritant

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 Vascular Changes

• The initial vascular change in inflammation is a transient contraction of

the microcirculation followed almost immediately by dilatation blood
flow slows.
• The red blood cells move to the middle of the vessel (rouleaux
formation) and the white blood cells move to the periphery and stick to
the endothelial wall
• The vasculature in the postcapillary venules becomes leaky owing to
contraction of endothelial cells under the influence of histamine, which
allows plasma to escape into the tissue spaces. Because of this
leakage, edema results, causing increased tissue pressure.
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 Electron micrograph of a portion of a large vessel showing margination of two
leukocytes (arrows). (Original magnification, x 11,000). B, Smaller vessel with PMNS about
to squeeze through the wall .

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 Phagocytosis

• In the inflammatory process both PMNs and macrophages function

as phagocytes. The process of phagocytosis involves three stages:
1. Attachment of the phagocytic cell to the target cell orantigen. This
is facilitated by opsonization by IgG, IgM,or C3b (from the
complement system).
2. Ingestion of the cell or antigen. A cellular membrane extension
envelops the opsonized antigenic material to form a phagosome.
The phagosome fuses with cytoplasmic lysosomes that release
their digestive enzymes in a process called degranulation.

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3. Breakdown or degradation of the bacteria or antigen by:
a. Lysosomal hydrolytic enzymes
b. An acid pH in the vacuole
c. Cationic proteins
d. Lactoferrin
e. Superoxide anion
f. Hydrogen peroxide
g. Peroxide-halide-myeloperoxidase
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12-8 Electron micrograph of a large macrophage (M) with a full
phagosome in the cytoplasm.
The cell is surrounded by PMNs
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 Mediators
• Mediators are chemical substances that control the
inflammatory response. Mediators may be exogenous (as from
baclerial products) or endogenous. Endogenous mediators are
classified as either plasma or tissue mediators. Mediators
released from plasma include:
1. Bradykinin from the kinin system
2. Complement from the complement system
3. Factors from the clotting system

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 Mediators released from tissue include:

1. Vasoactive amines (released from mast cells and basophils).

These arc released in response to:
a. Physical injury (i.e., trauma)
b. Chemicals (i.e., neutrophilic lysosomal cationic protein)
c. IgE-sensitized cells
d. Exposure to complement C3a and C5a (anaphylatoxin)
2. Acidic lipids (i.e., prostaglandins, which are
metabolites of arachidonic acid)
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3. Lysosomal components
a. Cationic proteins
b. Acid proteases
c. Neutral proteases
4. Lymphocyte products (i.e., lymphokines from T cells)
Microscopically, the picture includes PMNs, macrophages,
and the tissue response as a result of these chemical
mediators.
On the clinical level we can now account for the five
cardinal signs of inflammation

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1. Redness (increased dilatation of the vessels)
2. Swelling (escape of vascular fluid into the tissues causing
edema)
3. Pain (release of pain mediators such as bradykinin and tissue
pressure due to hyperemia and edema)
4. Heat (increased blood supply to the injured tissues)
5. Loss of function (due to pain and swelling)

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 ACUTE INFLAMMATION
• The diagnosis of acute inflammation is both a histologic and a
clinical one.
• Histologically, polymorphonuclear leukocytes and
macrophages constitute the predominant acute inflammatory
cells, but clinically the presence of pain usually denotes an
acute condition.
• The other cardinal signs of acute inflammation may also be
present: swelling, heat, redness, and loss of function.

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 Acute Apical Periodontitis
• Acute apical inflammation is a very painful response that
occurs before alveolar bone is resorbed
• Apically, the vascular response to the antigens within the pulp
produces edema.
• The edema and PMNs rapidly fill the periodontal ligament
between the tooth and bone.

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• Because the fluid is not compressible,any external pressure on
the tooth forces the fluid against already sensitized nerve
endings, resulting in exquisite pain.
• The tooth remains painful until the bone begins to be resorbed
and space is created to accommodate the edema fluid.

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 Acute apical abscess
• An acute apical abscess may result when large numbers of bacteria
get past the apex and elicit a severe inflammatory response.
• This response is acute, the predominant cell being the
polymorphonuclear leukocyte.
• With the release of PMN lysosomal enzymes into the tissue space
and the concomitant tissue degradation, an abscess forms
• An abscess is defined as a localized collection of pus which,
microscopically, is composed of dead cells, debris, PMNs, and
macrophages.

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 Phoenix Abscess
• If a periapical radiolucency is present and an acute
inflammatory
• response is superimposed on this preexisting chronic lesion it is
termed a phoenix abscess (i.e., an acute exacerbation of an
existing chronic inflammation)

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 Healing

• Healing can occur by either regeneration or repair. This

distinction is important when considering what type of tissue
forms after the antigenic agents are gone.
• If the tissue returns to its original state, it is called
regeneration.
• If the original tissue is replaced with dense fibrous connective
tissue, it is called repair.

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• Several cell types are involved in healing. Macrophages clean
up the debris, fibroblasts repair the damage, and differentiated
or undifferentiated cells regenerate the damaged tissues.
• Because of the increased oxygen demands during healing,
proliferation of capillary buds also occurs.

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 Chronic Inflammation
• If the acute process does not heal but persists, the response
becomes chronic. This is a change in both time and cell
composition.
• The acute inflammatory process is an exudative response,
whereas the chronic process is proliferative response.
• Microscopically, proliferation of fibroblasts, vascular
elements,and the infiltration of macrophages and lymphocytes
are characteristic.

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 the chronic inflammatory response
• macrophages and lymphocytes elicit an immune response.
• The purpose of the immune system is to neutralize, inactivate,
or destroy a stimulus (antigen or bacteria). This is
accomplished by
1. Direct neutralization by antibody binding to the stimulus
and/or destruction of the stimulus by sensitized lymphocytes.
2. Activation of biochemical and cellular mediator systems that
can destroy the antigen.

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 Chronic hyperplastic pulpitis

• Pulp polyp
• Large exposure
• Children or youth
• Deciduous teeth
• Hyperplastic granulation tissue that can become
epithelialized from shedding epithelial cells
• Open apex decreases the chances of pulpal necrosis
 Periapical Extension of Pulpal Inflammation
Periapical inflammation may begin before the pulp is totally
necrotic. Bacterial products, mediators of inflammation, and
deteriorating pulp tissue leak past the apex and evoke a
chronic inflammatory response from the vessels in the
periodontal ligament.
This explains why it is possible to have a periapical
radiolucency while some vital tissue remains in the apical canal

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• The periapical inflammatory response is an
extension of the pulpal inflammatory
response.

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 Chronic Apical Periodontitis (Granuloma)
• Chronic apical inflammation is a relatively low-grade, longstanding
response to canal bacteria and irritants.
• Clinically, this lesion is usually asymptomatic and is revealed by an apical
radiolucency.
• Microscopically the lesion is characterized by a predominance of
lymphocytes, plasma cells, and macrophages surrounded by a relatively
uninflamed fibrous capsule made up of collagen, fibroblasts, and capillary
buds
• In the inflammatory area large, amorphous circles with very pale staining
may be seen.

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• These arc Russell bodies and arc thought to be associated with
plasma cells that no longer have the capability to produce
antibodies
• Cords or strands of proliferating epithelium may or may not be
present. This lesion is usually not purely chronic in nature,
since some PMNs may be seen scattered throughout the lesion

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 Suppurative Apical Periodontitis
(Granuloma with Fistulation)
• An apical lesion that has established drainage through a sinus
tract is termed suppurative inflammation
• Clinically, the patient may complain of a "gum boil" or a bad
taste in the mouth. Pus may be expressed through the opening
by gentle pressure. A radiograph should be exposed with a
gutta-percha probe inserted into the tract to determine the
cause of the lesion. Microscopically the tract may be filled with
PMNs or pus. Chronic inflammatory cells may line the
periphery, and, in later stages, epithelium may be present
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• Studies estimate that epithelium lines the tract 10% to 30%of
the time.
• Valderhaug has stated that the longer the tract persists the
more likely it is to have an epithelial lining.

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 Role of epithelium
• One of the normal components of the lateral and apical
periodontal ligament is the epithelial rests of Malassez.
• The term rests is misleading in that it evokes a vision of discrete
islands of epithelial cells.
• It has been shown that these rests are actually a fishnet-like,
three-dimensional network of epithelial cells.
• In many periapical lesions epithelium is not present and is
presumed to have been destroyed

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• If the rests remain, they may respond to the stimulus by
proliferating in an attempt to wall off the irritants.  periapical
cyst
• The epithelium is Surrounded by chronic inflammation, and
this lesion is termed an epitheliated granuloma (a granuloma
containing epithelium)

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 Foreign body reaction
• A foreign body response may occur to many types of
substances.
• The reaction can be acute and/or chronic. What usually
distinguishes these lesions microscopically is the presence of
multinucleate giant cells surrounding a foreign material

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• If the material is soluble in the solutions used to prepare the
histologic section the giant cells will appear to be surrounding
a space. Usually the giant cells are surrounded by a chronic
inflammatory infiltrate. The giant cells are thought to be
formed by the fusion of several macrophages, creating a
multinuclear cell

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• These lesions may or may not be symptomatic. The cause is
now beyond the apex, so surgery may be necessary to remove
the foreign material and effect healing.

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 Osteosclerosis or condensing osteitis
• The inflammatory response depends on the quality, duration,
and virulence of the irritant.
• A very low-grade, subclinical response may lead to an increase
in the bone density rather than resorption and Iucency.
• This lesion may be clinically asymptomatic and
radiographically can demonstrate increased trabeculation and
opacity

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• Microscopically, dense bone with growth lines is prevalent with
a mild chronic inflammatory infiltrate in the marrow spaces.
• Not much is known about this lesion, but if it is associated with
a necrotic or diseased pulp endodontic therapy may lead to
healing.

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 Acute Osteomyelitis
• Acute osteomyelitis can arise directly from an endodontic
infection.
• Live bacteria are past the apex and now are multiplying in the
marrow spaces and soft tissue of the bone.
• Osteomyelitis may be a serious progression of periapical
infection that results in diffuse spread through the medullary
spaces ultimately leading to necrosis of bone.

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• Acute osteomyelitis may be localized or spread throughout
large areas of bone
• the medullary spaces are filled predominately with neutrophils.
• There may or may not be pus formation. Other microscopic
findings include bone resorption due to vigorous activity of the
osteoclasts and the lack of osteoblasts.

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• If untreated, the acute form may progress to chronic disease.
• Clinically, chronic suppurative osteomyelitis is the same as acute
except the symptoms are milder and radiographically diffuse bone
resorption is evident.
• Osteomyelitis is a very serious extension of periapical disease and
must be treated promptly and agressively
• This can be a disease of endodontic origin; however, the etiologic
agent (bacteria) is now beyond the confines of the pulp and in the
surrounding tissues.
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 Cellulitis

• Spread of abscess in fascial planes of soft tissues

• Ludwig’s angina
– Submandibular region
– Lower molars
– Trauma, lacerations, peritonsillar infections
– Extension to pharyngeal and mediastinal spaces
• Cavernous sinus thrombosis
– Maxillary molars and premolars
– Maxillary sinus, infratemporal fossa, orbit 􀃆
cavernous sinus at the cranial vault
 Cellulitis

• Spread of abscess in fascial planes of soft tissues

• Ludwig’s angina
– Swelling: floor of mouth, tongue, submandibular region
– Woody tongue and bull neck
• Cavernous sinus thrombosis
– Edematous periorbital enlargement
– Protrusion and fixation of eyelid and pupil dilatation
• Blindness
– CNS involvement, sometimes brain abscess
– Deepening stupor, delirium
 Cellulitis

• Ludwig’s angina
– Maintenance of airway
– Antibiotic treatment
– Surgical drainage
– Tracheostomy
• Cavernous sinus thrombosis
– Antibiotics
– Extraction of tooth