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Oral Pathology

Lectures
4- Diseases of the Pulp and
Periapical Tissues
( including spread of dental infection ,
cellulitis , dry socket and osteomyelitis )

Prepared by
Dr. Azzam A. Sultan
Post-Grad 1st part 2023
Faculty of Dentistry
University of Benghazi
prepared by dr. azzam sultan22
Diseases of the Pulp and Periapical Tissues
INTRODUCTION :
Definitions :
Notes :
 The most common cause of inflammatory swellings in oral and
paraoral tissues is infection
 The main source of infection is odontogenic in origin
Fate of infection :
1. Resolution
2. Localization ( chronocity )
3. Extension
4. Complications
Tissue Response to Irritation Depends on :
1. Number and virulence of micro-organisms
2. Types , severity and duration of irritant (chemical / microbial)
3. Resistant of the patient
4. State of tissue before the infection and its anatomy .
2 1
Diseases of the Pulp ( Pulpitis )
 Definitions :
 Aetiology :
 Types ( Classification ) :

 Clinical Features :
 Diagnosis :
 Histopathology and Prognosis
 Treatment :
prepared by dr. azzam sultan22
Diseases of the Pulp ( Pulpitis )

Definitions :
Aetiology :

1.Microbial ( Bacterial ) :
a. dental caries ( most common )
b. chronic periodontitis ( occasionally )
c. cracked or fractured tooth ( possible )
d. blood-born ( haematogenous ) ( uncommon )
2.Chemical :
3.Thermal : prepared by dr. azzam sultan22
Types of Pulpitis ( Classification ) :
On histopathological and clinical bases :
1. Focal reversible pulpitis ( pulp hyperemia )
2. Acute pulpitis
3. Chronic pulpitis

- Chronic hyperplastic pulpitis ( pulp polyp)

4. Pulp necrosis

- Partial ( focal ) or Complete ( total ) .

prepared by dr. azzam sultan22


Clinical Features :
- depends on the type

Diagnosis :
1. History pain
2. Clinical examination
3. Pulp testing (electrical, cold , heat)

Histopathology and Treatment :

- depends on the type .


azzam sultan19 / 20
prepared by dr. azzam sultan22
Table 1 : Pulpitis
Character Thermal
Pain and Radiographic Microscopical Treatment
Type Electrical al
1- Focal - Mild.
- Not spontaneous -Dilatation of blood vessels - Eliminate the
Reversible (initiated by stimulus) - Sensitive - No. PA change ( hyperemia ) cause
Pulpitis - Not tender to - Edema fluid - Reversible
(Pulp Hyperemia ) percussion.

- Sever ( lancinating )
- Constant (if closed) , Sensitive - Dilatation of blood vessels
or or - No PA change - Fluid edema - Pulpotomy or
2- Acute Pulpitis -Dull , throbbing - Hyper - Polymorph nuclear leuc. - RCT
( if open ) sensitive - Destruction of - Extraction
- Spontaneous or odontoblasts
initiated by stimulus
- Not tender

-
- More destruction of
- Mild , - Less
3- Chronic Pulpitis - Intermittent sensitive - No PA change.
odontoblast.
- RCT or
- Lymphocytes and plasma
( the pain is not - Extraction
cells
a prominent feature)
- Fibrosis
- Not tender

4- Chronic - Granulation tissue ( c. t.


- None Non fibers , capillaries , chronic
Hyperplastic ( asymptomatic ) or - No PA change inflammatory cells and may - RCT or
Pulpititis - Not tender less sensitive shows epithelial lining ) - Extraction
( Pulp Polyp )
1- FOCAL REVERSIBLE PULPITIS
( Pulp Hyperemia )
 Localized , early , transient pulpitis
Aetiology :
Clinical Features :
1. Pain mild to moderate ,
intermittent ,
not spontaneous ,
evoked by temperature and
relieved after removal of stimulus.
2. Usually associated with restored deep dental caries
with inadequate lining .
3. Reversible : if the cause is removed .
4. Sensitive : to thermal changes.
Histopathology : prepared by dr. azzam sultan22
Histopathology :

1. dilatation of blood vessels ( hyperemia ) .

2. exudation of plasma proteins ( edema fluid ) .

3. extravasation of RBCs and some WBCs. .

prepared by dr. azzam sultan22


Treatment :

1. Identification and elimination of the cause .

2. Correction of the defect .

Prognosis :

If the cause removed return to normal


If untreated further progress

prepared by dr. azzam sultan22


2- ACUTE PULPITIS
- It is a sequela of focal reversible pulpitis OR
- as acute exacerbation of chronic inflammatory process .
Aetiology :
Clinical Features :
1. Pain - sudden onset ,
- spontaneous OR in response to stimuli ,
- sever , sharp throbbing ,
- lasts for few hours or days ,
- poor localization ,
- the pain persist after removal of stimulus ,
- respond to traditional therapy ,
- may referred to other jaw or radiated to
distant areas, e.g. ear.
( pain may be dull throbbing , if there is a large open cavity )
prepared by dr. azzam sultan22
2. Sensitive to thermal changes .

3. React to lower level of current by electrical pulp tester

4. The tooth not tender to percussion.

5.The patient is extremely uncomfortable .

prepared by dr. azzam sultan22


Histopathology :
1. vascular dilatation

2. exudation of plasma proteins

3. polymorphnuclear leucocytes

4. destruction of odontoblasts

5. may be a localized destruction , and small abscess


( pulp abscess ) may occur

6. in some cases , this process may involve most of the

pulp , so the entire odontoblastic layer degenerate ,

and the pulp may undergoes liquifaction degeneration

and necrosis prepared by dr. azzam sultan22


Treatment :

1. Pulpotomy.

2. Root canal treatment ( may be ).

Prognosis :

- If most of the pulp involved the damage is irreparable

- If untreated further progress

prepared by dr. azzam sultan22


3- CHRONIC PULPITIS
- May arise from onset OR
- May as a sequel of acute pulpitis
- May classify into open and closed chronic pulpitis
Aetiology :
Clinical Features :
1.pain - not a prominent feature ,
- but sometimes , mild , dull ,
- intermittent ,
- long duration ( months ) ,
- resist traditional therapy

2. less sensitive to thermal changes


3. may react at a higher current level by electric pulp
tester ( degeneration of nerve tissue )
Histopathology: prepared by dr. azzam sultan22
Histopathology:

1. Chronic Inflammatory cells ( mainly lymphocytes and

plasma cells) ,

2. Prominent capillaries ( usually )

3. fibroblastic activity ( collagen fibers ) , in an

attempt to wall-off the infection . .


prepared by dr. azzam sultan22
Treatment :

1. RCT

2. Extraction

Prognosis :

- acute exacerbation

- pulp abscess

- pulp necrosis .

prepared by dr. azzam sultan22


CHRONIC HYPERPLASTIC PULPITIS (Pulp Polyp)
- A specific form of chronic pulpitis
- An excessive proliferation of chronically

inflamed dental pulp tissue extruded through


pulp exposure ( known as pulp polyp ).
- Arises as a chronic lesion from the onset or from acute
pulpitis
Clinical Features :
1. Children and young adults.
2. Deciduous molars and first permanent molars
3. Large , open carious cavity.
4. Appears as pinkish-red mass protruded from the pulp
chamber , soft , may be easily bleed.
5. Symptomless. .
prepared by dr. azzam sultan22
Histopathology:
The granulation tissue is made of :

1. delicate c. t. fibers with variable number


of small capillaries

2. chronic Inflammatory cells , mainly lymphocytes ,


plasma cells.

3. commonly becomes epithelized ( st. sq. in type ).

- Pulp polyp , should be differentiated from

gingival polyp
Treatment :

1. RCT
2. extraction

Prognosis :

may persist as such for several months and years. .

prepared by dr. azzam sultan22


4- PULP NECROSIS

- Untreated pulpitis ( acute or chronic ) ,

results in complete necrosis of the pulp.

Liquefactive type of necrosis:

Coaqulative type of necrosis:

- The tooth usually discolored .

prepared by dr. azzam sultan22


Periapical Periodontitis
 Definitions :
 Aetiology :
 Types Classification ) :

 Clinical Features :
 Diagnosis :
 Histopathology and Prognosis
 Treatment :
prepared by dr. azzam sultan22
PERIAPICAL PERIODONTITIS
Definition :
Aetiology :
1. Pulpitis and pulp necrosis

2. Trauma ( high restoration , orthodontic


treatment , or direct blow ) .

3. Endodontic treatment ( mechanical instrumentation


through root apex, or chemical irritant from
root filling materials ) .
Types :
1. Acute p. p.
2. Ch. p. p. ( periapical granuloma )
3. Periapical abscess ( acute or chronic ) .
Clinical features : depends
Diagnosis: depends on 1- History, 2- Examination ,and 3-Radiographs
Histologically : Treatment & Prognosis :
prepared by dr. azzam sultan 20
prepared by dr. azzam sultan22

Table 2 : Periapical Periodontitis


Character Thermal
Type Pain and Radiographical Microscopical Treatment
Electrical

- Severe , elicited - No change in early - Acute infl. cells - In case of


1- Acute by light touch stage , or ( in acute periapical periapical
- None periodontitis ) , or abscess
periapical - Tender to - Widening of
periodontitis percussion periodontal - In case of acute - Drainage
and ligament space peirapical abscess ( RCT or
Acute presence of a cavity ( Extraction )
periapical as a result of pus ) ,
abscess surrounded by acute - Antibiotic
infl. cells ( mainly
neutrophils ) , b.v.

- None to mild - Widening of - Granulation tissue ,


2- Periapical ( mainly periodontal chronic inf. cells , - RCT or
asymptomatic ) - None ligament space cholesterol clefts ,
Granuloma hemosidren , - Extraction
( Ch. P. P. ) - May be tender or multinucleated giant
to percution cells , foam cells , c.t.
- A radiolucent area capsule , osteoclasts
of variable size . ( occasional )
1- ACUTE PERIAPICAL PERIODONTITIS

Aetiology :
Clinical Features :
1. Pain ---- elicited by light touch ,
2. Tender to percussion
3. the patient feels the tooth elevated
4. not sensitive to thermal stimuli
5. the condition may be transient, and
soon resolved , if it is due to acute trauma ( without
infection )
Radiographiccal :
1. Often normal ( in early stage ) OR
2. May shows slight widening of periodontal ligament
space and the lamina dura may be faint at the apex . .
Histopathology :
1. Vascular dilataion,
2. Exudate ( mainly neutrophils ),
3. Oedema fluid

Treatment :
1. RCT
2. Extraction

Prognosis :
If untreated chronic periapical periodontitis , or
acute or chronic periapical abscess ( dentoalveolar
abscess ). .

prepared by dr. azzam sultan22


2- CHRONIC PERIAPICAL PERIODONTITIS
( PERIAPICAL GRANULOMA )
Aetiology:
Clinical Features :
1. Mainly asymptomatic ( unless
acute exacerbation )
2. Occassionally tender to
percussion
3. The patient may feels the tooth is elevated
Radiographically:

1. Widening of periodontal ligament space at apex OR


2. As a periapical radiolucent area of variable size
( usually well circumscribed ) .

prepared by dr. azzam sultan22


azzam sultan19 / 20
Histopathology :
A mass of granulation tissue , consists of :
1. Chronic Inflammatory cells (lymphocytes
and plasma cells )
2. Cholesterol crystals ( seen as clefts or
empty needle- like spaces )
3. Hemosiderin , and mulinucleated foreign body giant
cells
4. Foci of lipid laden macrophages ( foam cells )
5. Epithelial proliferation ( often forming anastomosing
cords , arranged in loops or arcades )
6. c. t. capsule
7. Osteoclasts ( occasional )
8. Microcyst ( may be )
Cholesterol Multinucleate
Cleft d Giant Cells
prepared by dr. azzam sultan22
Treatment :

1. RCT ( with or without apicectomy )


2. Extraction
Prognosis:

If untreated may undergoes to periapical periodontal


abscess , periapical cyst. .

prepared by dr. azzam sultan22


3- PERIAPICAL ABSCESS
( Dento-alveolar abscess or alveolar abscess )
- May develop from acute or chronic perapical periodontitis
Aetiology :
pulpitis pulp necrosis irritation of periapical tissue
( either bacterial , mechanical or chemical )

Clinical Features : ( of acute periapical abscess )


1- Pain---- extremely painful
2- the tooth slightly elevated
3- Tender to percussion or palpation
4- Not sensitive to elecrical or thermal changes
5- Regional lymphadenitis and fever
( rarely systemic manifestations )
6- Most abscesses in 6 5 4__22 4 5 6 point bucally, or palatally
7- abscess in molar region ( max. , mand. ) , may perforate the
bone above or below the attachment of buccinator muscle
may spread into soft tissues of surgical spaces ( such as
masseteric , infratemporal and parapharyngeal spaces ) .
8- Root apices of 87654 45678 may related to maxillary
sinus ( account 20% of sinusitis )
9- Chronic periapical abscess , may be no clinical feature ,
except in acute exacerbation
Radiographically :
1- Only widening of periodontal ligament
space OR
2- Radiolucent area at the apex
Histopathology :
1- a zone of liquefaction ( space or cavity ) necrosis
2- dilated blood vessels , and neutrophilic
infiltrate surrounding the zone
3- the adjacent marrow spaces may shows
inflammatory cells infiltrate
Treatment :
1- drainage ( RCT , or extraction )
2- antibiotic .
Prognosis / spread of dental infections :
I f untreated : may
1- remain localized
2- drain through the :
a. root canal ( into the mouth )
b. periodontal ligament space ( into gingival sulcus)
3- perforate the bone and point buccally, liabially ,
palaltally or lingually
4- extend into maxillary sinuses in case of upper teeth
5- form subperiosteal abscess
6- mucosal or skin sinus
7- spread (above or below the attachment of mylohyoid
or buccinator muscles ) into soft tissues
a. Cellulitis , Ludwig’s angina
b. Surgical spaces infection ( e.g. masteric ,
infratemporal parapharyngeal )
8- osteomyelitis OR
9- other complications : such as :
bacterimia , septicemia , cavernous sinus thrombosis .
Non-bacterial Normal Pulp Bacterial
( e.g. trauma ) ( e.g. caries )
Pulpitis

acute chronic

periapical periodontitis

acute p. p. chronic p. p.

acute p. absces periapical granuloma


blood sream chronicity
1.bacteremia 1. ch. P abscess
2.cavernous s. 2. ch. osteomyelitis
thrombosis spread through the jaws
penetration 1. osteomyelitis pathological fracture?
1.mucosal sinus 2. periostitis
2.skin sinus
spread to soft tissues periapical cyst ( radiculr cyst )
1.absces ( dento alv.abs. )
2.cellulitis , 3. Ludwig’s angina 4. surgical spaces infection
Sequelae of Pulpitis and / or Periapical Inflammation
Buccinator
muscle

Mylohyoid
muscle

prepared by dr. azzam sultan22


Cellulitis
CELLULITIS
It is a painfull , diffuse, tense , and rapidly spreading swelling of
acute inflammation of soft tissue . Particularly associated with virulent
organisms ( streptococcal infection ) that produce enzymes such as
streptokinase and hyaluronidase.
Aetiology :
Spreading of untreated p. abscess into soft tissue
Clinical Features :
1- Sudden-onset diffuse , tense , painful soft tissue swelling
(infl. edema )
2- Usually associated with malaise , fever

3- Cellulitis associated with :


a. Upper teeth initially involve upper half of the face ( may
extend into the eye risk of cavernous sinus thrombosis )
b. Lower teeth initially involve lower half of the face ( may
extend into submandibular and cervical tissues risk of
respiratory embarrassment )
4- Cellulitis spreading into deeper surgical spaces usually
presents clinically as pain and trismus rather than facial
swelling.
Ludwig’s Angina :
- It is a sever form of cellulitis , involving :
1- submandibular ,
2- sublingual , and
3- submental spaces .
- Usually as a result of involvement of the submandibular
space .

Cllinically : seen as :
1- A firm swelling of the floor of the mouth
2- The tongue being elevated and displaced posteriorly
3- Difficulty in eating , swallowing and breathing
4- Risk of death by suffocation ( may occur )

( as a result of involvement of pharynx , and larynx , oedema of


glottis ) .
Osteomyelitis
Healing of Extraction Socket ( Wound )

Dry Socket
HEALING OF EXTRACTION SOCKET ( Wound )
A- Immediate reaction following ( after ) tooth extraction :
1. Blood fills the socket , then coagulates ( clots )

B- During the first and second week after extraction :


1. The blood clot begins to undergo organization
2. At the same time , the epithelium at the periphery of the wound start
proliferation
3. Also resorption of the alveolar crest going-on ( by osteoclasts )

C- During the third week :


1. The clot appears almost completely organized
2. The surface of the wound ( socket ) become completely epithelized
3. Very young trabeculae ( woven bone ) forming from the wall of the
socket )

D- During the fourth week:


1. The wound ( socket ) begins the final stage of healing by :
- continued deposition and resorption of bone ( remodeling )
- and this process continue for several weeks .

prepared by dr. azzam sultan 20


4th week and soon 3ed week 1st and 2nd week immediately
after extraction

4 3 2 1
prepared by dr. azzam sultan

azzam sultan19 / 20
HEALING OF EXTRACTION SOCKET ( Wound )

At about 4 weeks At about 1 week


1- DRY SOCKET ( Alveolar Osteitis )

- It is a localized inflammation of bone without

progression through the bone marrow

- It is unpredictable complication in the healing of

extraction wounds ( sockets )

- Usually associated with difficult or traumatic


extractions

- Anaerobic bacteria are likely to play the major role


prepared by dr. azzam sultan 20
Aetiology : may be due to :
1. Failure of blood clot to form in the socket:
a. Impaired or Poor blood supply to bone ( e.g. dense
bone )
b. Following radiotherapy
c. Excessive use of vasoconstriction in local anesthesia

2. Premature loss of blood clot :

a. Washing away of blood clot by excessive mouth rinsing

3. Disintegration of blood clot :


a. Due to local proteolytic activity of bacteria , or
b. Due to release of fibrinolytic activity from adjacent bone
and soft tissue
c. Increase serum fibrinolytic activity
4. Food debris , saliva and bacteria :
a. Collected in the empty socket
b. Then become infected and necrotic .
prepared by dr. azzam sultan 20
Clinical Features :

1. Sever pain (main symptom)

2. Foul odor and tasting

3. Tenderness and redness of the adjacent

mucosa

4. Whitish dead bone ( which can be seen or felt

by probing )

Treatment :
.
prepared by dr. azzam sultan 20
2- OSTEOMYELITIS
Definition :

It is an inflammation of the bone involving the

bone marrow.
Aetiology :
1- May be as a complication of odontogenic infection
( infected wound )
2- Other variety of situations

3- Predisposing factors e.g. systemic diseases,

patient’s resistance , etc. (may be present) .


prepared by dr. azzam sultan 20
Normal Bone

Spongy bone Compact bone


Classification ( Types ) :
1- SUPPURATIVE :

a. Acute suppurative osteomyelitis

b. Chronic suppurative osteomyelitis

2- CHRONIC SCLEROSING :

a. Focal sclerosing osteomyelitis ( condensing or sclerosing osteitis )

b. Diffuse sclerosing osteomyelitis


c. Chronic osteomyelitis with proliferative periostitis ( Garre’s disease
or periostitis ossificans )
3- SPECIAL TYPES :
a. Radiation osteomyelitis ( osteoradionecrosis )
b. Chemical osteomyelitis
c. Osteomyelitis of new-born infants ( neo-natal maxilitis )
d. Osteomyelitis of specific infections:
i- Tuberculus osteomyelitis
ii- Syphilitic osteomyelitis
iii- Actinomycotic osteomyelitis . prepared by dr. azzam sultan 20
Clinical Features:

Presents a different clinical features


depending upon :
1. Virulence of organism involved , and
2. Status of the patient

Diagnosis :

Histopathology :

Treatment and Prognosis :


Table 3a : Osteomyelitis
Character
Clinical Features Radiographical Microscopical Treatment
Type
- Bone marrow infiltrated by - Drainage ( eliminate
1. Acute Supurative - Pain - May be no change ( in early stage) PMNs
Osteomyelitis - Mandible ( common ) the cause )
- Paresthesis or anaesthesia - ( Moth eaten ) after 10-14 days. - Sequestrum. - Antibiotic
- Mobility and Tenderness of teeth - Degenerated osteocytes.
- Fever ,  WBC’s , lymphadenitis and osteoblasts - Surgery ( may be ) .

- Radiolucent area with focal zones - Bone marrow infiltrated by - Same as acute.
2. Chronic - Same as acute, but milder  except
acute exacerbation. of opacifications. with indistinct chronic inflammatory cells. - Hyperbaric oxygen
Suppurative - Pathological fracture ( may be ) margins ( often ) - More destruction. ( may be ) .
Osteomyelitis

- Asymptomatic ( commonly ) - localized increased in density -


3. Focal - Associated with infected pulp. - Well circumscribed radiopaque of bone trabeculae. No treatment , except
Sclerosing
- Common at apices of lower 3rd and mass of sclerotic bone , below the - Few active osteoblasts. elimination of the
osteomyelitis
2nd molars apex of the root . - Bone marrow infiltrated with cause.
- Before 20 years of age. few lymphocytes.

- Dense , irregular , bone -


4. Diffuse - Asymptomatic
trabeculae, Eliminate the cause.
Sclerosing - Common in mandible may bilateral. - Diffuse sclerosis may be bilateral - Bone marrow fibrous , few - Antibiotic in acute
Osteomyelitis
- Older persons, negroes.
lympocytes and plasma cells. phase.
- may shows mosaic pattern.

- Asymptomatic , May be mild pain - Subperiosteal reaction


5. Chronic - Only remove the
- Common in molar area - Occlusal view shows duplication ( new bone formation ) cause.
Osteomyelitis of cortical layer. - - No surgical
- Bony hard swelling - Bone marrow fibrotic, with
with intervention.
Proliferative - Unilateral ( usually ) scattered chronic
Periosteitis - Before age 25 years. inflammatory cells.
Table 3b : Special Types Osteomyelits .
Character
Type Clinical Features Radiographical Microscopical Treatment

- Occur when the bone exposed to heavily radiation , as a - Radiolucent - Necrosed bone - Treatment of
result of death of some cells and affected blood vessels areas with ( dead bone , the infection
- Mandible more affected than maxilla radiopacites sequestrum ) Sequestrectomy
1- Radiation - The bone becomes very susceptible to infection , and the ( moth eaten - Degenerated
Osteomyelitis infection spread rapidly , leading to extensive painful appearance ) . osteocytes and - May be
( osteoradionecrosis ) necrosis bone osteoblasts treated by
- Sequestration and sloughing of bone and overlying oral - Narrowing and hyperbaric
mucosa , and occasionally facial soft tissues obliteration of oxygen
- Teeth may be mobile blood vessels
- Modern methods of radiotherapy have reduce this ( endarteritis
condition very greatly obliterans )

2- Chemical - Very rare these days


Osteomyelitis - May follow incorrect use of some local medications used in endodontic treatment ( very rare )

3- Osteomyelitis - Occur in Infants , Uncommon ( Rare )


of - More common in maxilla
New-Born - Probably results from infections introduced during delivery or feeding , or haematogenous
and Infants - Usually , it is acute suppurative in type , Seen as a red swollen and painful maxilla with multiple
( Neonatal Maxilitis ) draining sinuses , the developing teeth may be sequestrated and the infant usually seriously ill

- Due to specific micro-organisms such as


4- Osteomyelitis i - Tuberculous osteomyelitis
due to ii - Syphilitic osteomyelitis
Specific Infections iii - Actinomysis osteomyelitis
- Difficult to differentiate from other osteomyelitis and further investigations are needed
1- SUPPURATIVE

a. Acute Suppurative Oseomyelitis


Aetiology : ( may be due to ) :

1. Dental abscess if untreated ( most common cause )


2. Physical injury such as extraction , fracture, and
penetrating wounds (the second most common cause)
3. Haematogenic such as tonsilitis
4. The organisms often implicated are staph. aureus and
staph. albus , also various streptococci ( mixed
organisms ). also spesific infection such as
T.B., syphilis, actinomycosis ( may occur )
5. Predisposing factors may be present such as
systemic diseases , patint’s resistance, anatomical
location , and irradiated bone .
Clinical Featurres:
1. Sever pain ( is the primary feature )

2. Common in mandible

3. Mobility and tenderness of the teeth ( if involved )

4. Swelling ? ( only if there is periostitis )

5. Paresthesia or anaesthesia of lip ( mandible )

6. Sinus tract may be seen with sequestrum

7. Pyrexia

8. Lymphadenitis ( regional )

9. Leucocytosis
Radiographically:
1. No change ( in early stage )
2. Bone resorption --- moth-eaten area of radiolucency
( later after 10---14 days ) .
Histopathology:
Bone marrow:
1. Infilitrated by acute inflammatory cells, mainly neutrophilis

2. Destroyed and replaced by pus and inflammatory cells


Bone trabeculae:

1. Sequestrum ( dead bone ) may exfoliate through the sinus


2. Osteocytes ( appear as a dark , empty spaces )
3. Osteoblasts degenerate ( or not present )
Treatement:
1. Antibiotic ( culture sensitivity test )

2. Drainage (and / or removal of the cause such as carious


tooth )
3. Surgery ( may be part of treatement , range from a simple
sequestrectomy to bone replacement )
4. Each case should be judged individually

Prognosis: If untreated

periostitis , cellulitis , and pathological fracture may occure .


Pathogenesis :
1. Entry of micro-organisms into bone marrow
2. Proliferate in marrow spaces
3.Give raise to acute inflammatory reaction
4. Tissue necrosis and suppuration may rapidly occure

5. Because of thrombosis of neighboring vessels, necrsis and

suppuration continue (marrow spaces become filled with pus )

6. Sequestrum ( necrotic bone ) bathed in pus , may exfoliated


through the sinus
7. Invlucrum ( new bone ) may be formed ( raise periosteum )

8. Healing by proliferation of granulation tissue with new bone


formation, and then remodeling of bone, leading to normal
architecture of bone

9. Fibrous tissue in marrow spaces may remain as the only


evidence of previous inflammation .
b. Chronic Suppurative Osteomyelitis

Aetiology :
1. May develop after acute phase

2. May occure from the onset ( de novo )

Clinical Features :
1. Similar to those of acute phase , except all signs & symptoms
are milder
2. Acute exacerbation occur periodically
3. Swelling of the jaw ( commone )
4. Fistulous tract may be seen

Radiographically :
1. Radiolucent lesion that may shows focal zones of opacification
2. May be very extensive with indistinct margin ( often ) .
prepared by dr. azzam sultan 20
Histopathology:

Vary from mild to intense

1. Marrow spaces contains chronically inflammed

granulation tissue

2. Extensive bone resorption ( may occur )

3. Acute exacerbation may arise periodically,

and may be associated with formation and

discharge of pus

Treatment :

1. On the same principles of acute phase

2. Hyperbaric oxygen ( may be used ) .


azzam sultan19 / 20
2- CHRONIC SCLEROSING
a. Focal (local) Sclerosing Osteomyelitis
(condensing osteitis )
A relatively common phenomenon , represents a local bony
reaction to low-grade inflammatory
stimulus and a high tissue resistance.
Aetiology :
Low-grade infection
( carious tooth ), coupled with high tissue resistance
Clincal Features :
1. Any age , but most in young persons
2. Usually asymptomatic ( or may be mild pain )
3. The majority are found at the apices of the lower ( mandible )
6, 7, then 4 and 5
4. Chance finding ( radiographically )
5. May remain as a sclerotic area of bone after extraction .
prepared by dr. azzam sultan 20
Radiographically :
Seen as a dense radiopaque mass of sclerotic
bone , below the root apex , well circumscribed
Histopathology :
1. A localized increase in the bone trabeculae with
little marrow tiusse
2. If soft tissue ( marrow ) present, it is generally fibrotic and
infiltrated by few ch. Iflammatory cells
3. Few active oteoblasts may be present on the surface of bone
marrow
D/D:
Periapical cemental dysplasia , Osteoma , Cementoblastoma ,
Hypercementosis ( diagnosis confirmed by histologic and
radiographic features )

Treatment and Prognosis :


- No treatment ( reactive lesion ) , only the causative factor should
be treated
- The lesion remain as a sclerotic area of bone after extraction .
b. Chronic Diffuse Sclerosing Oseomyelitis
Aetiology :
1. Mild ( low-grade ) infection coupled with high tissue resistance
2. Periodontal disease ( most common )
3. Haematogenous origin ( has been suggested )
Clinical Features :

1. Any age , but most common in older persons


2. More common in mandible , and may be bilateral
3. More common in Negroes

4. Asymptomatic , except in acute exacerbation may results

in mild vague pain , discomfort, suppuration and sinus tract

5. May be enlargement of the mandible ( due to subperiosteal new


bone formation ) .
prepared by dr. azzam sultan 20
Radiographically
As the name suggests :
1. Diffuse ( generalized ) sclerosis of bone
2. Both maxllla and mand. may be involved , and may be bilateral
3. May mimic osteitis deformans ( Paget’s disease of bone )

D/D:
- Paget’s disease of bne
Histopathology :

1. Dense, irrigular trabeculae of bone , some bordered by ostoblasts

2.Bone in some areas may shows ‘mosaic’ patter ( indicate periods


of resorption followed by repair )

3. The soft tissue ( marrow ) is fibrosed and may shows small


capillaries and few collections of lymphocytes and plasma
cells ( except in acute exacerbation ) .
Treatment :

1. Eliminate the causative factor

2. Antibiotic ( in acute cases )

Prognosis :

- Slowly progressing , may undergo acute

exacerbation

- Rarely cause any complication .

prepared by dr. azzam sultan 20


c. Chronic Osteomyelitis with Proliferative Periostitis
( Garre’s Disease or Periostitis Ossificans )
It is a subtype of ch. osteomyelitis in which there is an

additional periosteal reaction .


Aetiology :

1. Dental infection ( low-grade )


2. Overlying soft tissue infection

Clinical Features :
1. Almost entirely in children and young adult ( before age of 20 )

2. Common in mandible , molar area

3. Usually unilateral
4. Seen as a bony hard swelling on outer surfsce of the mand.
( usually asymptomatic , and may be with pain ) .
Radiographically :

Occlusal view ( of the lower jaw ) --- shows focal overgrowth of

bone on outer surface of the mandible ( described as a duplication


of the cortical layer of bone )

Histopathology :
1. Reactive new bone ( sub-periosteal reaction )
2. Osteoblastic activity ( bordering many trabeculae )
3. Marrow spaces cotains fibrous tissue with scattered
lymphocytes and plasma cells
Treatment :
1. Elimination of the causative factor
2. No surgical intervention ( except for biopsy ) , because
gradual remodeling of the jaw occur ( after removal of the
cause such as extraction ) .
prepared by dr. azzam sultan 20
SPECIAL TYPES OSTEOMYELITIS

a. Radiation Osteomyelitis (Oseoradionecrosis )

b. Chemical Osteomyelitis

c. Osteomyelitis of New-Born and Infants


( Neonatal Maxilitis )
d. Osteomyelitis due to Specific Infections
1. Due to specific micro-organisms such as :

I - Tuberculous osteomyelitis
ii - Syphilitic osteomyelitis
iii - Actinomysis osteomyelitis
prepared by dr. azzam sultan 20
3- SPECIAL TYPES
a. Radiation Osteomyelitis (Oseoradionecrosis )
1. Following heavy radiation of bone as
a part of oral, head and neck malignancies
2. Results in death of some cells , narrowing
and obliteration of blood vessels in the I
ntimal layer ( endarteritis obliterans )

3. Then the bone become necrosed ( non-vital )

4. So the bone become very susceptible to infection ( e.g. from teeth,


periodontal diseases )
5. The infection spread rapidly -- leading to extensive , painful
necrosis of bone
6. Sequestration and sloughing of the overlying oral mucosa , and
occasionally facial soft tissue
7. Mandible more affected than maxilla
8. Modern methods of radiotherapy have reduce this condition very
greatly
9. May be treated by hyperbaric oxygen .
prepared by dr. azzam sultan 20
b. Chemical Osteomyelitis
1. Now days are rare

2. Was seen in some chemical workers without


precaution such as phosphours and mercury
3. May follow incorrect use of some local medications
such as paraformaldehde containing compounds
used in endodontic treatment
c. Osteomyelitis of New-Born and Infants
(Neonatal Maxilitis )
1. Uncommon ( rare )

2. common in infants ( young children )

3. More common in maxilla

4. Probably results from infections introduced during


delivery or feeding , or haematogenous .
5. Usually , it is acute suppurative in type
6. Seen as a red swollen and painful maxilla with
multiple draining sinuses
7. The developing teeth may be sequestrated
8. The infant usually seriously ill , and may not
survive the disease

d. Osteomyelitis due to Specific Infections


1. Due to specific micro-organisms such as :
i - Tuberculous osteomyelitis
ii - Syphilitic osteomyelitis
iii - Actinomysis osteomyelitis
2. Dificult to differentiate from other osteomyelitis

( further investigations are needed) .


prepared by dr. azzam sultan 20

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