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,with disappearance of lamina dura ~Height of alveolar bone is reduced ~Socket is obliterated 20 30 wk after extraction (Radiographically)

Inflammatory Diseases of Bone

Divided into 3 categories: Type Osteitis Osteomyelitis Periostitis Definition Localized inflam. of bone w/o progression trough marrow spaces > extensive inflam. of the interior of the bone, spreading trough marrow spaces Inflam. of periosteal surface of bone, may be associated with osteomyelitis

Diseases:

Osseointegrated Implants
Definition: healing of bone around an endosseous implant which results in intimate 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

1. 2. 3.

Alveolar Osteitis(Dry Socket) Focal Sclerosing(condensing) osteitis Osteomyelitis suppurative, sclerosing, chronic with proliferative periostitis

4. 5.

Chronic periostitis associated with hyaline bodies(pulse/vegetable granuloma) Radiation injury and osteoradionecrosis

2. 1. Intro Alveolar Osteitis (Dry Socket) Unpredictable complication of tooth extraction.(1-3 %) Mostly in: 1. Following molar extraction(L8) 2. Following difficult extractions 3. Tobacco users Localized infl. Of bone following either a)failure of blood clot to form in socket Pagets dis Osteopetrosis Radiotherapy >> use of VC in LA b)premature loss of disintegration of clot >> mouth rinsing Fibrinolysis by proteolytic bacteria Clinical Severe pain developing afew days after extraction Socket foul tasting smelling decomposing food debris W/o treatment, healing is slow Clinical Intro

Focal Sclerosing(condensing) osteitis

5.

Radiation injury and osteoradionecrosis

One of sequelae of periapical infl.

High grade irritations acute destruction results as ulcers low grade irritations chronic results as sclerosing, keratenisation .

Non-vital bone which results from reduction of blood supply is: Sterile asymptomatic 1. Radiotherapy for oral malignancy affects the bone vascularity Proliferation of intima of BV (endarteritis obliterans) Serious effects on mandible with its end-artery supply Inferior dental artery may become trombosed

Etiology

Etiology

Result from low-grade irritation / high tissue resistance

Here is increasing in the

2.
3.
number and the thickness of the bone trabeculae.why? Low grade irritation (from pulp to the periapical) and\or high tissue resistance

4.

Generally seen at root apex, most commonly 1st permanent molar. May remain after extraction. Usually asymptomatic.
Notice the abnormal

Extensive osteomyelitis with painful necrosis of bone, often associated with sloughing of overlying oral and sometimes facial soft tissues may occur, even years after radiotherapy.

Pathogenesis

1. 2. 3.

Food debris,saliva,and bact. Collect in empty socket Infection + necrosis Inflammatory rxn in adjacent marrow localizes infection to

Radiographical features

radiopaque area.

socket walls 4. Necrotic bone is gradually separated by osteoclast Slow healing + follows by granulation tissue proliferation surrounding vital bone

Histological features

Localized increase in no + thickness of bony trabeculae Scattered Lymphocytes + plasma cells surrounding scanty fibrosed marrow

Notice the sloughing of the soft tissue

5.

3. Osteomyelitis 1. Common complication of dental infection before advent of Ab. 2. Rare now 3. Variation in clinical + pathological features comprises a spectrum of infl. & reactive changes in bone and periosteoum 4. They reflect the balance bw: Nature and severity of irritant Host defenses Local + systemic predisposing fx Suppurative
Pathogenesis:

4. Chronic periostitis assc. with hyaline bodies Systemic Factors Impaired host defense Immune deficiency states Immunosuppression DM Malnutrition Extreme of age
An unusual form of chronic periostitis. Histologically, associated with hyaline ring-shaped bodies with foreign body reaction

Local Factors Decreased bone vitality Trauma Radiation injury Pagets dis Osteopetrosis Major vessel dis.

Sclerosing

Chronic with proliferative periostitis

(Garres osteomyelitis,Periostitis ossificans) It is a periosteal osteosclerosis in Mandible in children and young adult

Intro

Organism proliferate in marrow spaces acute infl. Tissue necrosis + suppuration Widespread of necrosis if ada thrombosis Marrow filled with pus adjacent marrow spacesperiosteum trough cortical bone Striping of periosteum compromises blood supply to cortical plate + predisposes tu further necrosis

A controversial condition: localized lesions are identical to focal sclerosing osteitis. some previously reported diffuse types probably represent infected florid cemento-osseous dysplasia.

Hyaline material is thought to represent vegetable material, especially pulses which may gain access to tissue via surgery,open root canal trauma Similar hyaline bodies are occasionally seen with apical granulomas + capsules of odontogenic cyst, thought to be due to impaction of food debris down to root canal

However, diffuse sclerosing lesions of the mandible as a complication of spread from contiguous focus of lowgrade infection/inflammation such as periapical granuloma have been reported. spread of low grade,chronic apical inflammation through the cortical bone then,stimulating a proliferative reaction of periosteum

Etiology

Source: 1. adjacent dental infection wide range of m/o (mainly staph.) polymicrobial,anaerobes 2. local trauma Divided clinically to acute + chronic(> 1 month ) > 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 circulation

Clinical

Bony hard swelling on the outer surface of mandible

This is presenting case for the

May be exfoliated through sinus/surgically removed

diffuse(it looks nearer than for localized)form.

Radiographical features

Normal in early stages. In 10-14 days, sufficient bone resorption occurs to produce irregular, moth-eaten areas of radiolucency. Sequestra may be seen. Sequestra, that presents in the isolated necrotic bone Bone resorption, which will be clear during 1014 days .it gives motheaten

Radigraphs show focal subperiosteal overgrowth of bone with smooth surface on outer cortical plate. The subperiosteal mass consists of irregular trabeculae of actively forming woven bone with scattered chronic inflammatory cells in fibrous marrow.

the overgrowth is composed of irregular trabeculae of actively formed woven bone

Histological features

Note the devitalized lamellar bone sequestrum with scalloped edges Absence of stainable osteocytes and osteoblasts. An osteoclast in a resorption area is seen.

There is focal subperiosteal overgrowth of the bone.

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

1.We can see sequestra with scalloped edges. 2. Notice the osteoclasts in resorption area.(near the scalloped area. 3. We can not see stainable osteocytes in isolated bone(central pink part)because this is dead bone