diseases of pulp & periapical tissues (1)

Diseases Of Pulp & Diseases Of Pulp & Periapical TissuesPeriapical Tissues

By SMIJAL

Diseases Diseases Of Of Dental Dental PulpPulp

Etiology:Etiology:PHYSICAL INJURYPHYSICAL INJURY CHEMICAL INJURYCHEMICAL INJURY MICROBIAL MICROBIAL

FACTORSFACTORS

FACTORSFACTORS

Acute Injury•Injury on tooth•Cavity preparation without water spray•Vigorous polishing •Root planning in PDL therapy•Restoration – improper insulationChronic Injury•Attrition -abrasive food & bruxism•Abrasion -abnormal tooth brushing

•Medicaments or materials applied to dentin diffuses through dentinal tubules.

Bacterial invasion by:

•Dental caries•Fractured tooth where exposed pulp • Anachoretic infection due to presence of bacteria in circulating blood stream.

Classification Of PulpitisClassification Of Pulpitis1.1. Acute & ChronicAcute & Chronic2. Based on extend - Partial pulpitis - Partial pulpitis (confined a portion of pulp)

- Subtotal pulpitis - Subtotal pulpitis

3. i. If inflammatory process confined within a portion: - Focal /Partial pulpitisFocal /Partial pulpitis ii. If most of pulp diseased:-Total /Generalized Total /Generalized

pulpitispulpitis 4. Another classification of acute & chronic based on

presence or absence of direct communication between pulp & oral environment:

-- Open pulpitis (pulpitis aperta)Open pulpitis (pulpitis aperta) communicated exist. - Closed pulpitis (pulpitis clausa) - Closed pulpitis (pulpitis clausa) no communication

exist.

Focal Reversible PulpitisFocal Reversible Pulpitis (Pulp

Hyperemia)Mild, transient, localized inflammatory response.

CLINICAL FEATURES:CLINICAL FEATURES:Tooth is sensitive to thermal changes, especially cold.

Pain - short duration, disappears on withdrawal of thermal irritant.

Affected tooth responds to stimulation of electric pulp tester at lower level of current indicating low pain threshold.

Teeth usually show deep caries, metallic restoration with defective margins.

HISTOLOGICAL FEATURES:HISTOLOGICAL FEATURES:Dilation of pulp blood vessels.

Edema fluid collection due to damage of vessel wall & allowing extravasations of RBC or diapedesis of WBC.

Slowing of blood flow & hemoconcentration due to transudation can cause thrombosis.

Reparative or reactionary dentin in adjacent dentinal wall.

TREATMENT & PROGNOSIS:TREATMENT & PROGNOSIS:Carious lesion should be excised & restored or defective filling is replaced.

If primary cause is not corrected, extensive pulpitis may result in death of pulp.

Dilation of blood vessels

Inflammatory cell infiltrate

Dentin

Acute PulpitisAcute PulpitisIrreversible condition characterized by acute, intense inflammatory response in pulp.

CLINICAL FEATURES:CLINICAL FEATURES:Teeth extremely sensitive to thermal changes.

Hot or cold stimuli cause increase in pain intensity & persists.

Pain - poorly localized since pulp of individual tooth is not represented in sensory cortex.

Intrapulpal abscess formation cause severe pain lancinating or throbbing type. (10 – 15mins)

Intensity of pain can increase when patient lies down.

Acute pulpitis withIntrapulpal abscess

Pulp vitality test indicats increased sensitivity at low level of current.

Pulpal pain is due to:

- pressure built up due to lack of exudate escape.

- pain producing substances from inflammation.

Pain subsides when drainage is established or when pulp undergoes complete necrosis.

The tooth is not tendered to percussion unless the pulpal inflammation has spread beyond the root apex into the periapical region.

HISTOLOGIC FEATURES:HISTOLOGIC FEATURES:

Edema in pulp with vasodilation.

Infiltration of polymorphonuclear leukocytes along vascular channels & migrate through endothelium lined structures.

Destruction of odontoblasts at pulp dentin border.

Rise in pressure due to inflammatory exudate local collapse of venous part of circulation Tissue hypoxia & anoxia Destruction of pulp & abscess formation.

Abscess consists pus, leukocytes & bacteria.

Numerous abscess formation cause pulp liquefaction & necrosis. (acute suppurative pulpitis)

TREATMENT & PROGNOSIS:TREATMENT & PROGNOSIS:

Drainage of exudate from pulp chamber.

Pulpotomy & placing calcium hydroxide over entrance of root canal.

Root canal treatment.

Extraction of tooth.

Chronic PulpitisChronic PulpitisPersistent inflammatory reaction in pulp with little or non constitutional symptoms.

CLINICAL FEATURES:CLINICAL FEATURES:Pain is not prominent, mild, dull ache which is intermittent.

Reaction to thermal changes is reduced because of degeneration of nerves.

Response to pulp vitality tester is reduced.

Wide open carious lesion & with exposure of pulp cause relatively little pain.

Manipulation with small instruments often elicits bleeding but with little pain.


Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective tissue reaction.

Capillaries are prominent; fibroblastic activity & collagen fibers in bundles.

When granulation tissue formation occurs in wide open exposed pulp surface – ulcerative pulpitis. (with bacterial stains & micro org. in carious lesion)

If pulpal reaction vacillates between an acute & chronic phase causes pulp abscess formation, which is surrounded by fibrous CT wall, which is called Pyogenic Pyogenic MemberaneMemberane


Root canal therapy

Extraction of tooth.

Chronic Hyperplastic PulpitisChronic Hyperplastic Pulpitis (pulp (pulp polyp)polyp)

Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass..

CLINICAL FEATURES:CLINICAL FEATURES:

Children & young adults with high degree of tissue resistance & reactivity & responds to proliferative lesions.

Pulp - pinkish red globule of tissue protruding from chamber & extend beyond caries.

Most commonly affected are deciduous molar & Ist permanent molars.

Pulp is relatively insensitive because few nerves in hyperplastic tissue.

Lesion bleeds profusely upon provocation.

Due to excellent blood supply high tissue resistance & reactivity in young persons leads to unusual proliferative property of pulp.

Some cases, gingival tissue adjacent, may proliferate into carious lesion & superficially resemble hyperplastic pulpitis.

- So careful examination is made to determine whether connection is with pulp or gingiva.


Hyperplastic tissue is basically granulation tissue, consisting delicate CT fibers & young blood capillaries.

Inflammatory infiltrates – lymphocytes, plasma cells & polymorphs.

Stratified sq. epithelium covering polyp

Granulation tissue

Pulpal tissue

Carious tooth

Stratified squamous type epithelial lining resembles oral mucosa with well formed rete pegs.

Grafted epithelial cells are believed to be desquamated epith. Cells, which carried by saliva.

Origin of these cells is unknown. They are degenerated superficial squames, which ’ve lost dividing capacity.

When pulp polyp is present for a long time, persistent rubbing of buccal mucosa may help in grafting of epith. cells..


Extraction of tooth or pulp extripation.

Untreated pulpitis results complete necrosis of pulp.

As this is associated with bacterial infection – pulp gangrene.

It is associated with foul odor when pulp is opened for endodontic treatment.

In sickle cell anemia, blockage of pulp vessels be defective RBC results pulp necrosis.

Non vital pulp maintain general histology being non purulent.

This may be due to trauma or infarct.

Gangrenous Necrosis of PulpGangrenous Necrosis of Pulp

Necrosis of pulp

REVERSIBLE PULPITISREVERSIBLE PULPITIS

• Mild – moderate inflammatory condition.

• Nature of pain is mild & diffuse.

• Brief duration & can be produce cold stimuli that elicits the pain mostly, although hot, sweet or sour food may also initiate the pain.

• Once stimulus is removed, pain is usually subsides.

• Tooth responds to electric pulp tester at lower currents.

• Reversible pulpitis if allowed to progress can led to irreversible pulpitis.

IRREVERSIBLE PULPITISIRREVERSIBLE PULPITIS

• Sharp, severe, radiating pain of long duration & varying intensity.

• Pain continues even after the stimulus is removed.

• Pain may exacerbate with bending over or lying down.

• It may progress to more severe pain that is gnawing or throbbing.

• Increased by stimulus, like heat & at times relieved by cold although the cold may intensify the pain.

• When infection extends into PDL - apical periodontitis.

Diseases Diseases Of Of PeriapicPeriapical al TissuesTissues

Pulpitis

Acute chronic

Apical peiodontitisAcute chronic

Periapical abscess Periapical granuloma

Periodontal cyst

Acute chronic

Osteomyelitis

Periosteitis

Cellulitis Abscess

Acute chronic

Focal Diffuse

Inflammation of PDL around apical portion of root.

Cause: spread of infection following pulp necrosis, occlusal trauma, inadvertent endodontic procedures etc.

Types: 1.Acute Apical Periodontitis

2.Chronic Apical Periodontitis

Apical PeriodontitisApical Periodontitis


• Thermal changes does not induce pain.

• Slight extrusion of tooth from socket.

• Cause tenderness on mastication due to inflammatory edema collected in PDL.

• Due to external pressure, forcing of edema fluid against already sensitized nerve endings results in severe pain.

RADIOGRAPHIC FEATURES:RADIOGRAPHIC FEATURES:

• Appear normal except for widening of PDL space.

Acute Apical PeriodontitisAcute Apical Periodontitis


• PDL shows signs of inflammation -vascular dilation

-infiltration of PMNs

• Inflammation is transient, if caused by acute trauma.

• If irritant not removed, progress into surrounding bone resorption.

• Abscess formation may occur if it is associated with bacterial infection Acute periapical abscess / Alveolar abscessAcute periapical abscess / Alveolar abscess..


• Selective grinding if inflammation due to occlusal trauma.

• Extraction & endodontic treatment be done to drain exudate.

Chronic Apical PeriodontitisChronic Apical Periodontitis (Periapical Granuloma)(Periapical Granuloma)Most common sequelae of pulpitis or apical periodontitis.

If acute (exudative) left untreated chronic (proliferative).

Periapical granuloma is localized mass of chronic granulation tissue formed in response to infection.

But term is not accurate since it doesn’t shows true granulomatous inflammation microscopically.


Tooth involved is non vital / slightly tender on percussion.

Percussion may produce dull sound instead metallic due to granulation tissue at apex.

Mild pain on chewing on solid food.

Tooth may be slightly elongated in socket.

Sensitivity is due to hyperemia, edema & inflammation of PDL.

In many cases, asymptomatic.

Fully developed granuloma seldom presents more severe clinical symptoms.

No perforation of bone & oral mucosa forming fistulous tract unless undergoes acute exacerbation.


Thickening of PDL at root apex.

As concomoitent bone resorption & proliferation of granulation tissue appears to be radiolucent area.

Thin radiopaque line or zone of sclerotic bone sometimes seen outlining lesion.

Long standing lesion may show varying degrees of root resorption.

HISTOLOGIC FEATURES:HISTOLOGIC FEATURES:Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous immature blood capillaries with bone resorption.Capillaries lined with swollen endothelial cells.

Its is relatively homogenous lesion composed of macrophages, lymphocytes & plasma cells.

Lymphocytes produces IgG, IgA, IgM & IgE modulators of disease activity.modulators of disease activity.

Plasma cells containing Russels bodyRussels body are found extracellularly.

T lymphocytes produce cytotoxic lymphokines, collagenase & other enzymes & destructive lymphokines.

Collection of cholesterol clefts, with multinuclear gaint cells.

Epithelial rests of Malassez may proliferate in response to chronic inflammation & may undergo cystification.

Bacteriologic Features:Bacteriologic Features:

Strep. viridans, strep. Hemolyticus, non hemolytic strep, staph. aureus, staph. Albus, E coli & pnemococci are isolated from lesion.


Extraction & RCT with / without apicoetomy.

If untreated apical periodontal cyst formation.

Root Apex

Granulation Tissue

Periapical GranulomaPeriapical Granuloma

Residual CystResidual Cyst Type of inflammatory odont. cyst in edentulous alveolar ridge.

Occur due to extraction of tooth, leaving periapical pathology untreated or incomplete removal of periapical granuloma /cyst.


Round /ovoid radiolucency in alveolar ridge.

Lumen may show radiopacity - dystrophic calcification


Cyst should curetted & lining should be subjected to histopathological examination.

Developed from acute periodontitis / periapical granuloma.

Acute exacerbation of chronic lesion Phoenix AbscessPhoenix Abscess

Cause due to – pulp infection, traumatic injury pulp necrosis, irritation of periapical tissues ( endo procedures).

CLINICAL FEATURES:CLINICAL FEATURES:Features of acute inflammation.Tenderness of tooth, which relives after pressure application.

Extreme painful tooth extrude from socket.

Systemic manifestations like lymphadenitis & fever may present.

Periapical AbscessPeriapical Abscess(Dento-Alveolar abscess, Alveolar Abscess)(Dento-Alveolar abscess, Alveolar Abscess)

Periapical Periapical abscessabscess

Extension to bone marrow spaces produce osteomyelitis, but clinically considered as Dento-Alveolar abscess Dento-Alveolar abscess – – swelling of tissues.

Chronic abscess generally presents no features, since it is mild, well circumscribed area of suppuration which spread from local area.

RADIOGRAPHIC FEATURES:RADIOGRAPHIC FEATURES:Slight thickening of PDL space.Radiolucent area at apex of root.

HISTOLOGIC FEATURES:HISTOLOGIC FEATURES:Area of suppuration composed of PMN leukocytes, lymphocytes, cellular debris, necrotic materials & bacterial colonies.Dilation of blood vessels in PDL & bone marrow space.

Periapical Periapical abscessabscess

Inflammatory infiltrate, cellular debris, necrotic materials etc..

Marrow space show inflammatory infiltrates.

Tissue around area show suppuration containing serous exudate.


Drainage of abscess by opening pulp chamber or extraction.

RCT.

If untreated, causes osteomyelitis, cellulites & bacteremia & formation of fistulous tract opening to oral mucosa.

Cavernous sinus thrombosis has been reported.

OsteomyelitisOsteomyelitisInflammation of bone & marrow contents.

Secondary changes due to inflammation of soft tissue content of bone.

Predisposing Factors:Predisposing Factors: - trauma, accidents, gunshot wounds,

radiation damage, Paget’s disease & osteoporosis.

- systemic conditions like malnutrition, acute leukemia, uncontrolled DM, sickle cell anemia & chronic alcoholism.

Types: 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis: i. Chronic Focal Sclerosing

Osteomyelitis ii. Chronic Diffuse Sclerosing

Osteomyelitis

Acute osteomyelitisAcute osteomyelitis Serious sequelae of

periapical infection, results in spread into medullary spaces with necrosis of bone.

Chronic Chronic OsteomyelitisOsteomyelitis

Develops from untreated, acute osteo. Or arise from dental infection without preceeding acute stage.

CLINICAL FEATURESCLINICAL FEATURES

Acute & subacute osteo. involve either maxilla/mandible.

Some osteo. refered as neonatal maxillitis in infants & young children - hematogenous origin.

Clinical features are similar to acute, except:

Signs & symptoms – milder, with less pain.

Infants – seriously ill & may not survive disease.

Adults - severe pain, trismus & parasthesia of lips in mand. & elevated temperature with regional lymphadenopathy.

WBC count elevated.

Teeth involved is loose, eating difficult.

Pus exudate from gingival margins.

Until periostitis, no swelling or no reddening on skin /mucosa.

Leucocytes slightly greater than normal.

Teeth may not be loose & sore, so mastication is possible even though jaw may not be perfectly comfortable.

Acute exacerbation may occur periodically.

Temperature still elevated, but mild.

Suppuration may perforate bone & overlying skin or mucosa to form fistulous tract & empty on surface.

RADIOGRAPHIC FEATURESRADIOGRAPHIC FEATURES

Evidence until disease for 1-2weeks.

Loss of continuity of lamina dura.

Trabeculae - fuzzy, indistinct & radiolucent.

Saucer shaped irregular margins.

Moth eaten appearance.

Single /multiple radiolucencies.

Irregular margins.

Root resorption.

Lamina dura less apparent, blends with surrounding granular sclerotic bone.

Chronic OsteomyelitisChronic Osteomyelitis:

Ill defined area of radiolucency of right body of mandible on extracton site.

Acute OsteomyelitisAcute Osteomyelitis:

Ill defined area of radiolucency of right body of mandible.

Inflam. Exudate in medullary spaces.

Inflam. Cells – neutrophillic PMnuclear leucocytes, occasional lymphocytes & plasma cells.

Destroyed osteoblasts lining bony trabeculae.

Depending duration of process – trabeculae loss viability & undergo slow resorption.

HISTOLOGIC FEATURESHISTOLOGIC FEATURES

Chronic inflam. Reaction in bone - exudate & pus accumulation in medullary spaces.

Lymphocytes, plasma cells & macrophages.

Osteoblastic & osteoclastic activity occur parallely with irregular bony trabeculae formation with reversal lines.

Later stages - Sequestrum may develop

Acute OsteomyelitisAcute Osteomyelitis

Nonvital bone shows absence of osteocytes in lacunae.

Peripheral resorption, bacterial colonisation & inflam. Response.

Chronic Chronic OsteomyelitisOsteomyelitis

Chronic inflamation & reactive fibrous CT filling intertrabecular spaces.


Drainage, debridement & antimicrobial therapy.

When intensity of disease attenuated – sequestrum seperates from living bone & gradually exfoliates through mucosa.

If large – surgical removal.

Acute SO may preceed to develop periosteitis, soft tissue abscess /cellulitis.

Chr.Focal Sclerosing OChr.Focal Sclerosing O A reaction to mild

bacterial infection entering bone through carious tooth in persons ’ving higher degree of tissue resistance & tissue reactivity.

Chr.Diffuse Sclerosing Chr.Diffuse Sclerosing OO

Due to diffuse periodontal disease.

CLINICAL FEATURESCLINICAL FEATURES Commonly in children

& young adults & rarely old age.

Common tooth: mand Ist molar.

No other signs & symptoms other than mild pain.

Common in older, with edentulous mandibular jaw.

On exacerbation: vague pain, unpleasant taste & mild suppuration many times with fistula formation opening to mucosa & drains.

Well circumscribes radiopaque mass of sclerotic bone extending below apex on roots.

Root outline nearly visible with intact lamina dura.

PDL space widened & is important to distinguish cementoblastoma.

Lesion border: abutting normal bone, may smooth & distinct or appear to blend into surrounding bone in contrast to focal cemento osseus dysplasia.

Radiopacity stands out indistnct, contrast to normal trabaculae.

RADIOGRAPHIC FEATURESRADIOGRAPHIC FEATURES Cotton wool

appearance.

Sometimes bilateral.

Bilateral involvement in both maxilla & mandible.

Border between sclerosis & normal bone is indistinct.

Pattern may actually mimic Paget’s disease or cemento osseus dysplasia.

Focal sclerosing osteomyelitis

Diffuse sclerosing osteomyelitis

HISTOLOGIC FEATURESHISTOLOGIC FEATURES Dense mass of bony

trabeculae with little interstitial marrow tissue.

Osteocytic lacunae is empty.

Trabeculae show reversal & resting lines giving Pagetoid appearance.

If interstitial soft tissue present – fibrotic & inflitrate of few lymphocytes .

Osteoblastic activity ‘ve completely subsided.

Dense irregular trabeculae, some borderd by active layer of osteoblasts.

Mosaic pattern, indicates periodic resorption & repair.

Soft tissue in between trabeculae – fibrous & show proliferating fibroblast, capillaries with lymphocytes & plasma cells.

PMN leucocytes present, if lesion is in acute phase.

Sometimes, inflam component is completely burned out, leaving sclerotic bone & fibrosis.

Focal sclerosing osteomyelitis

Diffuse sclerosing osteomyelitis

Endodontic treatment

Extraction

Surgical removal of sclerotic lesion is not indicated unless symptomatic.

TREATMENT & PROGNOSISTREATMENT & PROGNOSIS Surgical removal

If tooth is present, must extracted.

Sometimes sclerosed bone will remain after resolution & remodelling.

Common odontogenic cyst encountered.

True cyst, since consits of pathological cavity lined by epithelium &fluid filled.

Epithelium may be derived from:

-respiratory epith (communicating with maxillary sinus)

-oral epith fibrous tract

-oral epith proliferating apically from PDL pocket

Apical Periodontal CystApical Periodontal Cyst((Radicular Cyst, Periapical Cyst, Root End Radicular Cyst, Periapical Cyst, Root End Cyst)Cyst)

EtiopathogenisiEtiopathogenisiss

Caries, trauma, periodontal disease

Pulp death

Apical bone inflammation

Granuloma formation

Stimulation, then proliferation of epithelial cell rests of Malassez

Cystification

CLINICAL FEATURES:

• Most cases are Assymptomatic

• Age: commonly 20-60 yrs, decidous teeth.

• Common tooth maxillary anteriors.

• Non vital tooth/deep caries/restoration which is painfull on percussion.

• In some cases, cyst may undergo acute exacerbation & develop abscess that may proceed to cellulitis/ fistula.


• Radolucency – round/ ovoid with a narrow opaque margin which is continuous with lamina dura.

• In long standing cyst bone resorption of affected teeth & occasional resorption of adj. teeth may be seen.

HISTOPATHOLOGYHISTOPATHOLOGY

• Lined by non keratinized stratified sq epith.

• Newly formed cyst - Epith lining thickness is uneven, due to hyperplasia

• In established cyst – lining thickness is even.

• Presence of Mucous secreting goblest cells in cyst lining.

• Transmigration of inflam. Infiltrate through epithelium.

• Supporting CT – focally/diffusely infiltrated with a mixed inflam. Cell population.

• Foci of dystrophic calcification, cholestrol clefts & multinucleated foreign body gaint cell seen on cyst wall.

• Rushton bodies are found in cyst lining or CT.

• Russels bodies (plasma cell surrounded by immunoglobulin) seen.

Cyst lumen consist of watery, straw colored, blood tinged fluid to semi fluid materials, with low conc. Of protien.


Extraction & curettage of apical zone.

RCT with apicoectomy.

Surgery

If left untreated – slowly increase in size & undergo bone resorption but seldom there is a remarkable compensating expansion of cortical plates.

Apical periodontal cyst

Sclerotic Cemental MassesSclerotic Cemental MassesBenign fibro-osseous jaw lesions of unknown etiology, occurring Benign fibro-osseous jaw lesions of unknown etiology, occurring

predominantly in middle-aged black females; lesions present as large predominantly in middle-aged black females; lesions present as large painless radiopaque masses usually involving several quadrants of the jaw painless radiopaque masses usually involving several quadrants of the jaw


Just same as in Diffuse sclerosing osteomyelitis – present with Just same as in Diffuse sclerosing osteomyelitis – present with multiple symmetric lesion, pain, drainage & localized expansion.multiple symmetric lesion, pain, drainage & localized expansion.

RADIOGRAPHIC FEATURES:RADIOGRAPHIC FEATURES:• Same as in DSO Same as in DSO - - Lesions appear as multiple sclerotic masses, located in Lesions appear as multiple sclerotic masses, located in

two or more quadrants, usually in the tooth-bearing regions.two or more quadrants, usually in the tooth-bearing regions.HISTOLOGIC FEATURES:HISTOLOGIC FEATURES:

Differences:Differences:• Cemental masses instead of sclerotic boneCemental masses instead of sclerotic bone

Cementum – large solid masses with smooth, lobulated margins, with Cementum – large solid masses with smooth, lobulated margins, with globular accretion patternglobular accretion pattern..

Florid Osseus DysplasiaFlorid Osseus DysplasiaAnother disease similar to DSO & Sclerotic cemental masses; described by Melrose & his associates.

characterized by lesions in upper/ lower jaw that occur when normal bone is replaced with a mix of CT and abnormal bone. It affect middle age Black and Asian women .

Cause – obstruction of normal interstitial fluid by fibro osseus proliferation.


FOD appears as well-defined mixed (radiolucent-radiopaque) or totally radiopaque & has a radiolucent periphery & surrounding sclerosing border similar to Periapical Cemental Dysplasia.

“cotton wool” appearance or large amorphous regions of calcifications.

TREATMENT:TREATMENT:

Usually no treatment necessary.Usually no treatment necessary.

Chronic Osteomyelitis with Chronic Osteomyelitis with Proliferative PeriosteitisProliferative Periosteitis

(Garre’s Chronic nonsuppurative sclerosing Garre’s Chronic nonsuppurative sclerosing osteitis, periosteitis ossificans)osteitis, periosteitis ossificans)A distinctive type of osteomyelitis with focal gross thickening of periosteum, & peripheral reactive bone formation resulting from mild infection or irritation.

It is essentially a periosteal osteosclerosis analogous to chronic focal endosteal sclerosis & diffuse sclerosing osteomyelitis.


young age <25yrs, mostly involve anterior of tibia.

Greater opportunity for infection enter maxilla & mandible, due to peculiar anatomic arrangement of teeth.

Cases in jaws; occurs in mandible bicuspid & molar region - children & young adults.

Maxilla is seldom affected, reason not clear.

Toothache or jaw pain & bony hard swelling on outer surface of jaw – usually for several weeks duration.

Due to overlying soft tissue infection/ cellulitis that involves periosteum cause reactive periosteitis.


Reveals a carious tooth opp: to hard bony mass.

Occlusal radiograph: focal overgrowth of bone on outer surface of cortex, which described as duplication of cortical layer.

Mass is smooth & well calcified & may show thin but definite cortical layer.

Firm swelling on lateral & inferior border of right mandible

CT scan of new proliferative periosteitis with onion skin laminations.


• Supracortical but subperiosteal mass is composed of much reactive new bone & ostoeid, with osteoblast bordering many trabeculae.

• Trabeculae orient perpendicular to cortex, with trabeculae arranged in parellel to each other or reticular form.

• CT between bony trabeculae is rather fibrous & show diffuse or patchy sprinkling of lymphocytes & plasma cells.

• Periosteal reaction – infection from caries perforating cortical plate & become attenuated, stimulating periosteum rather than producing usual suppurative periosteitis.

TREATMENT & PROGNOSISTREATMENT & PROGNOSIS:

• Endodontic treatment or extraction, with no surgical intervention for periosteal lesion except for biopsy.

Periosteal bone formation /neoperiosteosis may occur in variety of other conditions & care must be taken to exclude them from diagonosis.

Include infantile cortical hyperosteosis (Caffey’s disease), hypervitaminosis A, syphilis, leukemia, Ewing’s sarcoma, metastatic neuroblastoma & even a fracture callus.

diseases of pulp & periapical tissues (1)

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