IN THE NAME OF GOD - PowerPoint Presentation

Slide1

IN THE NAME OF GODSlide2

Pulpal and

Periapical

Disease

CHAPTER 3

Dr

.

Kheirandish

Oral

and maxillofacial pathologySlide3

Pulpitis

Periapical

Granuloma

Periapical Cyst

OsteomyelitisOsteomyelitis with Proliferative Periostitis

Alveolar

OsteitisSlide4

PULPITIS

Mechanical damage

Traumatic accidents, iatrogenic damage, attrition, abrasion

2. Thermal injuryLarge

uninsulated metallic restorations, dental procedures (cavity preparation, polishing) 3. Chemical irritation

Erosion , acidic dental materials

4. Bacterial effects

toxins or directly (caries)Slide5

Reversible pulpitis

Irreversible pulpitis

PULPITIS

Mimic

pulpalgia

:

Myofascial

pain

Trigeminal neuralgia

Atypical facial neuralgia

Migraine headaches

Cluster headaches

Nasal or sinus

pathoses

Angina pectorisSlide6

Reversible pulpitis

Temperature extremes

: short duration /mild-to-moderate pain.

Cold,sweet or sour : pain

The pain does not occur without

stimulation

and subsides

within seconds after the stimulus is removed.

Electric pulp testing :

lower levels

Mobility and sensitivity :

absent.

Without treatment :

IirreversibleSlide7

Irreversible pulpitis

Early stages :

Sharp, severe pain on

thermal stimulation

Pain continues after the stimulus is removed

Cold and heat

Spontaneous or continuous pain

Lies down

Electric pulp testing :

lower

levels

Early stages : localized pain / increasing discomfort : unable to identify the offending tooth

Early

stages

Later

stagesSlide8

Later stages :

Increases pain

Throbbing

pressure Awake at night.

Heat increases the painCold decrease pain

Electric pulp testing :

higher levels / -

Mobility and sensitivity:

absent

Drainage

(crown fracture, fistula formation) : symptoms resolveSlide9

CHRONIC HYPERPLASTIC PULPITIS (pulp polyp)

Pulpal inflammation

Children and young adults

Large pulp exposures

Deciduous or succedaneous molars

Asymptomatic

(masticatory function)Slide10
Slide11

HISTOPATHOLOGIC FEATURES

Reversible pulpitis :

Hyperemia

EdemaFew inflammatory cells Irreversible pulpitis :Congestion of the

venulesChronic hyperplastic pulpitis :

Inflamed

granulation tissue

Histopathologically

resembles

a pyogenic

granulomaSlide12

TREATMENT AND PROGNOSIS

Reversible pulpitis

Removal the local irritant

Irreversible and chronic hyperplastic

puIpitis Root canal therapy

Extraction

Slide13

PERIAPICAL GRANULOMA (CHRONIC APICAL PERIODONTITIS)

Chronically inflamed granulation tissue

Apex of a

nonvital

toothNot

true granulomatous inflammation microscopically

Apical periodontitis

Bacterial ( Yeasts / Cytomegalovirus / Epstein-Barr virus )

75

%

of apical

inflammatory

lesions Slide14

Early stages

Acute

apical periodontitisConstant dull / Throbbing painVitality test :

- / delayed positivePain : biting or percussionRadiographic : -

Neutrophils

Prostaglandins ( activate osteoclasts ) Slide15

Late stages

Asymptomatic

Radiographic : +Response to thermal or electric pulp tests : -

Mobility or significant sensitivity to percussionChronic inflammatory cells (lymphocytes)

Reduce

osteoclastic

activity

Fibroblastic activity

Periapical

cyst formation Slide16

Routine

radiographic examination

Radiographic features are

not diagnosticVariable radiolucencies Loss of apical

lamina duraCircumscribed or ill-defined

Root

resorption

RGSlide17
Slide18
Slide19

Phoenix abscess :

Secondary acute inflammatory changes within a

periapical granuloma

Unable to distinguish periapical granulomas from periapical cysts

Greater than 200 mm2 : periapical cystsPeriapical

inflammatory disease is

not static

and granulomas can transform into cysts or abscesses Slide20

HISTOPATHOLOGIC FEATURES

Inflamed granulation tissue

Surrounded

by a fibrous connective tissue wallLymphocytes

( neutrophils. plasma cells. Histiocytes )

Plasma

cells

:

Eosinophilic

globules

of gamma globulin

(Russell bodies)

Basophilic particles

(

Pyronine

bodies)

Not

specific

Slide21

Rests

of

Malassez

Giant cells Red blood cell extravasationHemosiderin pigmentation

Cholesterol clefts Source

of the

cholesterol clefts

is

unclear (dying inflammatory Cells / disintegrating red blood

cells / degenerating

cystic epithelium)Slide22
Slide23

TREATMENT AND PROGNOSIS

Root

canal therapy

Goal of endodontics : reduce the microbial load

Extraction and curettageSlide24

Fail

to

heal :

Cyst formation Persistent pulpal infection

Accumulation of endogenous debris

Associated

periodontal disease

Penetration

of the adjacent maxillary

sinus

Fibrous

scar

formationSlide25

Periapical

surgery:larger than 2 cm

Endodontic therapy : -All soft tissue removed during periapical

surgical procedures should be submitted for histopathologic examination.

Periapical

fibrous

scars :

facial

and lingual cortical plates have been

lost and lesions fill

with dense collagenous

tissue rather

than normal

bone( Surgery - )Slide26

PERIAPICAL CYST

(

RADICULAR CYST;

APICAL PERIODONTAL CYST)Prevalence : 15%

Epithelium at the apex of a nonvital tooth presumably can be stimulated by inflammation to form a true

epithelium-lined cyst

(

periapical

cyst ).

Keratinocyte

growth factor

(increased

proliferation of normally

quiescent Epithelium) Slide27

Source of the epithelium :

Rest

of

Malassez Crevicular epitheliumSinus liningEpithelial lining of fistulous

tractsPeriapical

pocket

cysts

incomplete epithelial lining

Periapical

true

cysts

complete epithelium lined (baglike structure)

PERIAPICAL CYST Slide28

Lateral radicular cyst

Along

the lateral aspect

Rests of Malassez Pulpal necrosis

Radiographically : mimic developmental lateral periodontal cysts

Residual

periapical

cyst

Dystrophic

calcification /

radiopacitySlide29
Slide30
Slide31
Slide32

Grow slowly

Nonvital

No symptoms

large size (swelling and mild sensitivity)Mobility

of adjacent teethRadiographic : resemble periapical granuloma

Greater size than

periapical

granulomas

Loss of lamina

dura

Root

resorption

is common

Significant

growth Slide33
Slide34
Slide35

Stratified squamous epithelium

Exocytosis

Spongiosis

Hyperplasia Mucous cells

Ciliated pseudostratified columnar epithelium

HISTOPATHOLOGIC

FEATURESSlide36
Slide37

Rushton bodies

(Arch-shaped calcifications)

Dystrophic calcification

Cholesterol clefts Multinucleated giant cells

Red blood cellsHemosiderin

Inflammatory infiltration (

lymphocytes,neutrophils,plasma

cells,histiocytes,mast

cells and

eosinophils

)

Hyaline bodies

(pulse

granuloma,giant

-cell

hyaline

angiopathy

)

Chronic

intraosseous

inflammationSlide38
Slide39

TREATMENT AND PROGNOSIS

Nonsurgical

Surgical

Extraction

Biopsy is indicatedSlide40

OSTEOMYELITIS

Osteomyelitis is an

acute or chronic

inflammatory process in the medullary spaces or cortical surfaces of bone

that extends away from the initial site of involvement.Bacterial infections

Lytic

destruction of

the involved bone

All ages

Male

Mandible Slide41

Osteoradionecrosis

(hypoxia,hypocellularity

and hypovascularity)Uncommon in developed countries Developd

countries : Odontogenic infections or traumatic fracture

Africa : acute necrotizing ulcerative gingivitis (ANUG) or

NOMA.Slide42

Predispose

people to

osteomyelitis:

Chronic

systemic diseasesImmunocompromised status

Disorders

associated with decreased vascularity

Tobacco

Alcohol

IV

drug

abuse

Diabetes mellitus

Malaria

Sickle cell anemia

Malnutrition

Malignancy

AIDS

Radiation

Diseases

(e.g.,

osteopetrosis

,

late

Paget's disease, end-stage

cementoosseous

dysplasia

) Slide43

Acute suppurative

osteomyelitis

Young patients

Signs and symptoms

Acute inflammatory process 1 month in

duration

Swelling: may be present

Fever

Leukocytosis

Lymphadenopathy

Significant sensitivitySlide44

Radiographs : unremarkable / ill-defined radiolucency

Paresthesia

of the lower lip

Necrotic boneSequestrum

Fragment of necrotic boneSpontaneous exfoliation

Involucrum

Necrotic

bone surrounded by new vital boneSlide45
Slide46

Chronic suppurative

osteomyelitis

If acute osteomyelitis is not resolved or primarily without a previous acute episode.

Granulation tissueDense scar

tissueSwellingSlide47

Pain

Sequestrum

formation

Tooth lossPathologic fractureRadiographs : patchy, ragged. and ill-defined radiolucency (central radiopaque)Slide48
Slide49

HISTOPATHOLOGIC FEATURES

ACUTE SUPPURATIVE OSTEOMYELITIS

Biopsy not

common (lack of a soft tissue component)Necrotic bone

Loss of the osteocytesPeripheral

resorption

Bacterial

colonization

Acute

inflammatory

cells

CHRONIC SUPPURATIVE OSTEOMYELITIS

Significant

soft tissue component

Chronically inflamed fibrous

connective

Scattered

sequestra

Abscess formationSlide50
Slide51

TREATMENT AND PROGNOSIS

ACUTE

SUPPURATIVE OSTEOMYELITIS

Antibiotic therapy

CHRONIC

SUPPURATIVE OSTEOMYELITIS

Surgical Intervention

Antibiotic

therapy Slide52

OSTEOMYELITIS

WITH PROLIFERATIVE PERIOSTITIS (PERIOSTITIS

OSSIFICANS)

Garre

sosteomyelitis Periosteal reaction to the presence of inflammation

Periosteum

: Several rows of reactive

vital

bone that

parallel

each other

Children and young adults (13 y/o)

premolar and molar (mandible)

Radiopaque laminations of bone (NO=1 to 12 )Slide53
Slide54

Dental caries

(

periapical inflammatory disease, Periodontal infections, fractures

, buccal bifurcation cysts, and nonodontogenic infections)

Causes of periosteal new bone formation :Osteomyelitis Trauma

Cysts

Fluorosis

Avitaminosis

C

Congenital syphilis

Neoplasms

(Ewing

sarcoma,

Langerhans cell

histiocytosis

, and

osteogenic

sarcoma)Slide55

CT

scanning

Panoramic Lateral obliqueOcclusal

posteroanteriorSlide56

ALVEOLAR OSTEITIS

(

DRY

SOCKET; FIBRINOLYTIC

ALVEOLITIS

)

Destruction

of the initial

clot

( plasminogen to plasmin)

Mandible (posterior areas

)

:Impacted

mandibular

third molars

20

- 40

y/o

Poor

oral

hygiene

Inexperienced surgeons

Traumatic extractions

Oral contraceptive

Presurgical

infections

Tobacco Slide57

Dirty

gray clot

Bare bony socket

Sensitive bone Severe painFoul odor

3 to 4 days10 to 40

daysSlide58

High risk patients :

Oral contraceptives

Smoke

Pericoronitis Traumatic extractionsHistory of alveolar osteitisSlide59

TREATMENT AND PROGNOSIS

Curettage of the socket is

not recommended,

Eugenol (every 24 hours for the first 3 days

)Slide60