Inflammatory Disease

8/3/2019 Inflammatory Disease

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Healing of an Extraction Socket

~ 6 wk after extraction:- regenerated epith. appears normal- supra-alveolar CT healed- socket filled with woven bone- sockets outline can still be discerned histologically / radiographycally

~Woven bone is remodeled with formation of cortical + cancellous bone,withdisappearance of lamina dura

~Height of alveolar bone is reduced

~Socket is obliterated 20 30 wk after extraction (Radiographically)

Osseointegrated Implants

Definition: healing of bone around an endosseous implant which results inintimate interface bw bone & implant

Healing Process:- similar to socket healing- involves osteogenesis + remodeling- several months of healing period before any load to allow for an intimate

interface

Failure if-Repeated small amounts of movements interfere with formation of interface &results in a zone of fibrous tissue bw implant and bone

Successful Healing Criteria- bone is separated from implant by an interfacial matrix zone up to ~100 nm

thick- should be intimate contact with alveolar CT- implants penetrate alveolar mucosa- dense collagen bundles run parallel to long axis of implant- Gingival epith forms a collar around implant post + attached to its surface

by basal lamina & Hemidesmosome- Epith not migrate apically along post surface

Inflammatory Diseases of Bone

Divided into 3 categories:

Type Definition

Osteitis Localized inflam. of bone w/o progression trough marrow spaces

Osteomyelitis > extensive inflam. of the interior of the bone, spreading trough

marrow spacesPeriostitis Inflam. of periosteal surface of bone, may be associated with

osteomyelitis

Diseases:

1. Alveolar Osteitis(Dry Socket)

2. Focal Sclerosing(condensing) osteitis

3. Osteomyelitis

- suppurative,- sclerosing,- chronic with proliferative periostitis

4. Chronic periostitis associated with hyaline bodies(pulse/vegetablegranuloma)

5. Radiation injury and osteoradionecrosis


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1. Alveolar Osteitis (Dry Socket)

2. Focal Sclerosing(condensing)osteitis

5. Radiation injury andosteoradionecrosis

Intro Unpredictable complication of toothextraction.(1-3 %)Mostly in:

1. Following molar extraction(L8)2. Following difficult extractions3. Tobacco users

Int ro One of sequelae of periapical infl.

High grade irritations acute destructionresults as ulcers

low grade irritations chronic results as

sclerosing, keratenisation .

Non-vital bone which results from reduction ofblood supply is:- Sterile- asymptomatic

Etiology Localized infl. Of bone following eithera)failure of blood clot to form in socket- Pagets dis- Osteopetrosis- Radiotherapy- >> use of VC in LA

b)premature loss of disintegration ofclot- >> mouth rinsing

Fibrinolysis by proteolytic bacteria

Etiology Result from low-grade irritation / hightissue resistance

Here is increasing in the

number and the thickness of the bonetrabeculae.why?Low grade irritation (from pulp to theperiapical) and\or high tissue resistance

1. Radiotherapy for oral malignancyaffects the bone vascularity

2. Proliferation of intima of BV (endarteritis

obliterans)

3. Serious effects on mandible with itsend-artery supply

4. Inferior dental artery may becometrombosed

Clinical Severe pain developing afew days after extraction

Socket- foul tasting- smelling decomposing food debris

W/o treatment, healing is slow

Clinical - Generally seen at root apex, mostcommonly 1st permanent molar.

- May remain after extraction.

- Usually asymptomatic.

Extensive osteomyelitis with painful necrosisof bone, often associated with sloughing ofoverlying oral and sometimes facial softtissues may occur, even years afterradiotherapy.

Pathogenesis1. Food debris,saliva,and bact.

Collect in empty socket

2. Infection + necrosis

3. Inflammatory rxn in adjacentmarrow localizes infection to

Radiographicalfeatures

Notice the abnormal

radiopaque area.


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socket walls

4. Necrotic bone is graduallyseparated by osteoclast

5. Slow healing + follows bygranulation tissue proliferation

surrounding vital bone

Histologicalfeatures

Localized increase in no + thickness ofbony trabeculae

Scattered Lymphocytes + plasma cellssurrounding scanty fibrosed marrow

3. Osteomyelitis 4. Chronic periostitis assc.with hyaline bodies

1. Common complication of dental infection before adventof Ab.

2. Rare now3. Variation in clinical + pathological features comprises a

spectrum of infl. & reactive changes in bone andperiosteoum

4. They reflect the balance bw:- Nature and severity of irritant- Host defenses- Local + systemic predisposing fx

Local Factors Systemic Factors

Decreased bone vitality- Trauma- Radiat ion injury- Pagets dis- Osteopet rosis- Major vessel dis.

Impaired host defense- Immune deficiency states- Immunosuppression- DM- Malnutrition- Extreme of age

An unusual form of chronicperiostitis.

Histologically, associated withhyaline ring-shaped bodies withforeign body reaction

Hyaline material is thought to

represent vegetable material,especially pulses which may gainaccess to tissue via surgery,openroot canal trauma

Similar hyaline bodies areoccasionally seen with apicalgranulomas + capsules ofodontogenic cyst, thought to bedue to impaction of food debrisdown to root canal

Suppurative Sclerosing Chronic with proliferative periostitis

Intro Pathogenesis:

- Organism proliferate in marrowspaces acute infl.

- Tissue necrosis + suppuration- Widespread of necrosis if ada

thrombosis

- Marrow filled with pus adjacentmarrow spacesperiosteumtrough cortical bone

- Str ip ing of per iosteumcompromises blood supply tocortical plate + predisposes tu

further necrosis

A controversial condition:- localized lesions are identical

to focal sclerosing osteitis.

- some previously reporteddiffuse types probablyrepresent infected floridcemento-osseous dysplasia.

However, diffuse sclerosing lesionsof the mandible as a complication ofspread from contiguous focus of low-grade infection/inflammation such as

periapical granuloma have beenreported.

(Garres osteomyelitis,Periostitis ossificans)

- It is a periosteal osteosclerosis

- in Mandible in children and young adult

Etiology Source:1. adjacent dental infection

- wide range of m/o (mainly staph.)- polymicrobial,anaerobes

2. local trauma

- spread of low grade,chronic apicalinflammation through the cortical bone

- then,stimulating a proliferative reaction ofperiosteum

Clinical Divided clinically to acute + chronic(> 1month )> in Mandible due to:- thick trabeculae & cortical plates- blood supply is derived from an

end artery(mand artery)< in Maxilla due to:

- rich of collateral circulationThis is presenting case for the

- Bony hard swelling on the outer surface ofmandible

Notice the sloughingof the soft tissue


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diffuse(it looks nearer than forlocalized)form.

Radiographicalfeatures

- Normal in early stages.

- In 10-14 days, suff icient bone

resorption occurs to produceirregular, moth-eaten areas ofradiolucency.

- Sequestra may be seen.

- Radigraphs show focal subperiostealovergrowth of bone with smooth surface onouter cortical plate.

- The subperiosteal mass consists ofirregular trabeculae of actively formingwoven bone with scattered chronicinflammatory cells in fibrous marrow.

the overgrowth is composed of irregulartrabeculae of actively formed woven bone

There is focal subperiosteal overgrowth of thebone.

- Periosteal new bone formation(periosteal reaction) / Onion-peel

appearance.

Histologicalfeatures

- Note the devitalized lamellarbone sequestrum with scallopededges

- Absence of stainable osteocytesand osteoblasts.

- An osteoclast in a resorption areais seen.

Bone

resorption,which will beclear during 10-14 days .itgives moth-eaten

Sequestra,that presentsin theisolatednecroticbone

May be exfoliatedthroughsinus/surgicallyremoved


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1.We can see sequestra with scallopededges.

2. Notice the osteoclasts in resorptionarea.(near the scalloped area.

3. We can not see stainable osteocytesin isolated bone(central pinkpart)because this is dead bone


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Inflammatory Disease