Dent 356-11 Disorders of Bone II

Healing of Bone Inflammatory Diseases of Bone Metabolic & Endocrine Disorders of Bone

Healing of Bone

Healing of an extraction socket Osseointegrated implants

Healing of an Extraction Socket

Immediately after extraction, socket rapidly fills with blood which clots. Clot is organized to form granulation tissue.

Osteoclastic resorption of crestal bone and small detached bony fragments commences.

Healing of an Extraction Socket

~6 weeks after extraction: - regenerated epithelium appears normal - supra-alveolar connective tissues have healed - socket is filled with woven bone - outline of socket, however, can still be discerned histologically and radiographically.

Healing of an Extraction Socket

Woven bone is remodeled with formation of cortical and cancellous bone, with disappearance lamina dura. Height of alveolar bone is reduced during remodeling. Radiographically, socket is obliterated 20-30 weeks after extraction.

Osseointegrated Implants

Osseointegration: healing of bone around an endosseous implant which results in intimate interface between bone and implant. Healing process is similar to that in a healing socket, it involves osteogenesis and remodeling.

Osseointegrated Implants

A healing period of several months is required before applying load to implant to allow for an intimate interface. Repeated small amounts of movements are likely to interfere with formation of interface and result in a zone of fibrous tissue between implant and bone.

Osseointegrated Implants

In successful osseointegration, bone is separated from implant only by an interfacial matrix zone up to ~100 nm thick. Implants penetrate alveolar mucosa, the interface between it and soft tissues has a barrier function similar to dentogingival tissues. A successful implant should be in intimate contact with alveolar connective tissue.

Osseointegrated Implants

Dense collagen bundles run predominantly parallel to long axis of implant. Gingival epithelium forms a collar around the implant post, and is attached to its surface by a basal lamina and hemidesmosomes. Epithelium does not migrate apically along post surface.

Osseointegrated Implants

Plaque accumulation can lead to inflammation around the implant and to alveolar bone loss similar to chronic periodontal disease, especially if there is excessive load. Microbiological examination of plaque associated with implants shows a similar range of microorganisms to that found with chronic periodontal disease.

Inflammatory Diseases of Bone

Alveolar osteitis (dry socket) Focal sclerosing (condensing) osteitis

Osteomyelitis - Suppurative osteomyelitis - Sclerosing osteomyelitis - Chronic osteomyelitis with proliferative periostitis (Garrs osteomyelitis, periostitis ossificans)

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

Alveolar Osteitis (Dry Socket)

Unpredictable complication of tooth extraction (~1-3%). Localized inflammation of bone following either failure of blood clot to form in socket, or premature loss or disintegration of clot.

Alveolar Osteitis (Dry Socket)

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Most frequent: following molar extraction, particularly mandibular3rd molars. following difficult extractions. in tobacco users.

Alveolar Osteitis (Dry Socket)

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Failure of blood clot formation may be due to poor blood supply as in: Pagets disease. Osteopetrosis. Following radiotherapy. Excessive use of vasoconstrictor in local anesthesia. Premature loss of blood clot may be due to: Excessive mouth rinsing. Fibrinolysis by proteolytic bacteria.

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Alveolar Osteitis (Dry Socket): Clinical Features

Severe pain developing a few days after extraction.

Socket often contains foul tasting and smelling decomposing food debris which can be washed away to reveal denuded bone.
Without treatment, healing is extremely slow.

Focal Sclerosing (Condensing) Osteitis

Osteoscelrosis is one of the sequelae of periapical inflammation. May result from low-grade irritation and/or high tissue resistance.

Focal Sclerosing (Condensing) Osteitis

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

Focal Sclerosing (Condensing) Osteitis: Histopathologic Features

Histologically, localized increase in number and thickness of bony trabeculae is seen.

There may be scattered lymphocytes and plasma cells in surrounding scanty fibrosed marrow.

Osteomyelitis

Used to be a common complication of dental infection before advent of antibiotics, now a rare disease.

Variation in clinical and pathological features comprises a spectrum of inflammatory and reactive changes in bone and periosteum.
They reflect the balance between: Nature and severity of irritant. Host defenses. Local and systemic predisposing factors. It is usual to distinguish between suppurative and sclerotic forms of osteomyelitis.

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Osteomyelitis of the Jaws: Predisposing Factors

Local Factors Decreased vascularity/ vitality of bone: Trauma Radiation injury Pagets disease Osteopetrosis Major vessel disease Systemic Factors Impaired host defense: Immune deficiency states Immunosuppression Diabetes mellitus Malnutrition Extremes of age

Suppurative Osteomyelitis

Usually divided clinically into acute and chronic types depending on severity and course of disease. When it persists > 1 month, it is referred to as chronic. Usual source is adjacent focus of dental infection or local trauma. Wide range of microorganisms, unlike other bones (mainly staphylococcal), osteomyelitis of the jaws is polymicrobial. Anaerobes predominate.

Suppurative Osteomyelitis
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The mandible is much more frequently involved then the maxilla due to: thick trabeculae and cortical plates blood supply is derived from an end artery, the mandiblar artery.

Thrombosis of mandibular artery or of its branching loops can lead to extensive necrosis.
In contrast, the maxilla has a rich collateral circulation, and osteomyelitis there is rare.

Suppurative Osteomyelitis

Organisms proliferate in marrow spaces causing acute inflammation. Tissue necrosis and suppuration rapidly ensue. Necrosis may be widespread because of thrombosis of blood vessels.

Suppurative Osteomyelitis

Marrow spaces fill with pus and suppurative infection spreads through adjacent marrow spaces and may extend though cortical bone to periosteum. Stripping of periostium compromises blood supply to cortical plate and predisposes to further necrosis.

Suppurative Osteomyelitis

Eventually, a mass of necrotic bone (sequestrum) floating in pus becomes separated from surrounding vital bone by osteoclasts. It may be exfoliated through a sinus or have to be surgically removed to enhance healing.

Suppurative Osteomyelitis: Clinical Features

Acute: Pain, swelling, pyrexia, and malaise. Trismus is frequent. There may be paresthesia of lip and mobility of teeth. Chronic: Swelling and pain associated with chronic suppuration. Discharge of pus through one or more intraoral or extraoral sinuses.

Suppurative Osteomyelitis: Clinical Features

Chronic: Discharge of pus through one or more intraoral or extraoral sinuses.

Suppurative Osteomyelitis: Radiographic 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.

Suppurative Osteomyelitis: Radiographic 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.

Suppurative Osteomyelitis: Histopathologic Features*

Devitalized lamellar bone sequestrum with scalloped edges and absence of stainable osteocytes and osteoblasts. An osteoclast in a resorption area is seen.

Chronic Sclerosing Osteomyelitis

A controversial condition:

- localized lesions are identical to focal sclerosing osteitis.

- some previously reported diffuse types probably represent infected florid cemento-osseous dysplasia.

Chronic Sclerosing Osteomyelitis

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.

Chronic Sclerosing Osteomyelitis

A controversial condition: - identical to focal sclerosing osteitis. - infected florid cementoosseous dysplasia

- spread from contiguous focus of low-grade infection/inflammation such as periapical granuloma

Chronic Osteomyelitis with Proliferative Periostitis (Garrs Osteomyelitis, Periostitis Ossificans)

Seen almost exclusively in mandible in children and young adults. Essentially a periosteal osteoscelrosis thought to result from spread of low grade chronic apical inflammation through cortex. Proliferative periostitis may occasionally develop from overlying soft tissue infection, or from mechanical irritation of denture. Bony hard swelling on outer surface of mandible.

Chronic Osteomyelitis with Proliferative Periostitis (Garrs Osteomyelitis, Periostitis Ossificans)

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

Chronic Periostitis Associated with Hyaline Bodies (Pulse Granuloma, Vegetable Granuloma)

An unusual from of chronic periostitis in the jaws.

Histologically associated with hyaline ring-shaped bodies with foreign body reaction.
Hyaline material is thought to represent vegetable material, especially pulses which may gain access to tissues via surgery, open root canal or trauma. Similar hyaline bodies are occasionally seen with apical granulomas and capsules of odontogenic cysts, thought to be due to impaction of food debris down a root canal.

Radiation Injury and Osteoradionecrosis

Radiotherapy for oral malignancy affects the vascularity of bone. It causes proliferation of intima of blood vessels (endarteritis obliterans). This can cause serious consequences in the mandible due to its readily compromised blood supply.

Radiation Injury and Osteoradionecrosis

The non-vital bone which results from reduction in blood supply is sterile and asymptomatic. It is, however, very susceptible to infection and trauma e.g. from a denture.

Radiation Injury and Osteoradionecrosis

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. Modern methods of radiotherapy have greatly reduced its incidence.

Metabolic and Endocrine Disorders of Bone

Osteoporosis
Primary hyperparathyroidism Secondary hyperparathyroidism Rickets and osteomalacia Acromegaly

Osteoporosis

Bone is in a state of constant turnover. Bone loss gradually predominates over apposition in adult life. It results either when bone loss is excessive, or when apposition is reduced.

Osteoporosis

Presents most frequently in postmenopausal females who lose 1-2% of bone mineral per year. In of cases, there is more rapid rate, up to 58% per year. The rate of loss is twice as fast in women as in men. It is accentuated in other diseases such as Cushing syndrome, thyrotoxicosis, and primary hyperparathyroidim.

Osteoporosis
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Other risk factors are identified: Genetic. Reduced calcium intake. Lack of exercise. Smoking.

Osteoporosis

Osteoporotic bone is of normal composition but is reduced in quantity. There is increased radiolucency of bone, cortex is thinned. There are more marrow spaces in cancellous bone with thin trabeculae.

Osteoporosis

The jaws may be involved. In edentulous patients, it may leave the mandible as a thin fragile strip of bone which can be easily fractured. It has been suggested that osteoporosis is a risk factor in chronic periodontitis, but evidence is still little.

Rickets and Osteomalacia

Classically, rickets and its adult counterpart, osteomalacia are due to deficiency of, or resistance to the action of vitamin D. Deficiency may be due to lack of exposure to sunlight or dietary causes.

Hypocalcemia due to renal failure or malabsorption may be associated with osteomalacla.

Rickets and Osteomalacia

Radiographic changes are similar to osteoporosis, but in contrast, there is failure if mineralization of osteoid and cartilage. Histologically, bony trabeculae in rickets and osteomalacia are characterized by wide seams of uncalcified osteoid.

Rickets and Osteomalacia Clinical Features*

Affected children are apathetic and irritable with a short attention span.

Rickets and Osteomalacia Clinical Features*

Children with rickets suffer from skeletal defects including: Flattening of skull with frontal bossing and conspicuous suture lines. Chest shows the classic rachitic rosary, a grossly beaded appearance of costochondral junctions resulting from enlargement of costal cartilage. An outer curvature of the sternum (pigeon breast deformity). Deformities of spine and limbs.

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Rickets and Osteomalacia Clinical Features*

Rickets and Osteomalacia Clinical Features*

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Dental abnormalities in rickets include: Delayed eruption. Enamel hypoplasia. Increased width of predentin. Large amounts of interglobular dentin.

In rickets and osteomalacia jaw involvement has been reported.

In rickets, deficient growth of condylar cartilage may lead to lack of vertical growth of the mandibular ramus.

Acromegaly

Caused by prolonged and excessive secretion of growth hormone usually due to an adenoma of anterior lobe of pituitary developing after epiphyses have closed. There is renewed growth of bones of the jaws, hands, and feet with overgrowth of some soft tissues, including the lips and nose. Reactivation of condylar growth center of mandible causes enlargement, protrusion, and spacing of teeth.