DISEASES OF PERIRADICULAR TISSUES

PRESENTED BY Anubhuti Gupta

UNDER THE GUIDANCE OF

Dr. Sarika

Dr. Umesh

CONTENTS

Microbiology Pathways of infection Classification Periapical lesions

Etiology Clinical features Radiographic features Histopathological features Treatment

MICRO-ORGANISMS ASSOCIATED WITH ENDODONTIC DISEASE Endodontic infections are polymicrobial

with a majority being anaerobes.

Sundquist GK (1976) & Bystorm et al (1987) have shown a positive correlation between the number of bacteria in the infected root canal and the size of periradicular radiolucencies.

Sundquist et al (1989) had showed that

when intact teeth with necrotic pulps were cultured, over 90% of the bacteria were strict anaerobes.

Role of other microbes including viruses and fungi has been recently investigated by Glick, Trope, Pliskin (1989, 1991); Nair PNR et al (1990); Sen, Safavi & Spanberg (1997).

A much less likely pathway for bacteria for endodontic infections is anachoresis. This phenomenon was demonstrated by Robinson & Boling (1941); Gier & Mitchell (1968); Allard et al (1979).

COMMONLY FOUND ANAEROBES ARE:

Fusobacterium nucleatum Bacteroides species Peptostreptococcus Prevotella intermedia Fusobacterium species Actinomycetes species Capnocytophaga Propionobacterium propionicum Porphyromonas

PATHWAYS OF PULPAL INFECTION Dental caries is the most common

pathway to the root canal system for microbes

When the tooth is intact, enamel and dentine protect it against invasion of the pulp space

As caries approaches the pulp, reparative dentine is laid down to avert exposure but this rarely can prevent microbial entry

When a healthy vital pulp is exposed to caries, bacterial penetration proceeds relatively slowly

ANATOMIC CONSIDERATIONS

There is an intimate relationship between the periodontium and pulpal tissues

As the tooth develops and the root is formed, 3 main avenues for communication are created:

1. Apical Foramen2. Lateral and Accessory Canals3. Dentinal Tubules

APICAL FORAMEN

SEM of the apical third of a root. Note the opening of an accessory canal at ninety degrees from the main canal

LATERAL CANALS

DENTINAL TUBULES

Scanning electron micrograph of open dentinal tubules

PERIRADICULAR TISSUES

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Periradicular tissue consists of

Cementum - covers the roots of teeth

Alveolar process - forms the bony troughs containing the roots of teeth

PDL - whose collagen fibers, embedded in the cementum of the roots and in the alveolar processes, attach the roots to the surrounding tissues.

PG 50 GROSSMAN

In periradicular area, portals of entry and exit between root canals and surrounding tissues are located and pathological reactions to diseases of pulp are manifested.

DISEASES OF PERIRADICULAR TISSUES

Because of interrelationship between the pulp and periradicular tissues, pulpal inflammation causes inflammatory changes in the PDL even before the pulp becomes totally necrotic.

Bacteria and their toxins, immunological agents, tissue debris and products of tissue necrosis from the pulp reach the periradicular area through the various foramina of root canals and give rise to inflammatory and immunological reactions.

CLASSIFICATION OF PERIRADICULAR DISEASES

INGLE’S CLASSIFICATION

GROSSMAN’S CLASSIFICATION

Acute periradicular diseases -Acute alveolar abscess -Acute apical periodontitis

Chronic periradicular diseases

-Chronic alveolar abscess -Granuloma

-Cyst Condensing osteitis External root resorption Periradicular diseases of non endodontic origin

ACUTE ALVEOLAR ABSCESS

Definition: Localized collection of pus in the alveolar bone at the root apex of a tooth following death of pulp, with extension of infection through the apical foramen into the periradicular tissues.

It is continuance of the disease process beginning in the pulp and progressing to the periradicular tissues, which in turn, react severely to infection.

                                            

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ETIOLOGY

May be result of trauma, chemical or mechanical irritation

The immediate cause is generally bacterial invasion of dental pulp tissue.

Because the dental pulp tissue is solidly enclosed, no drainage is possible, and the infection continues to extend in the direction of least resistance that is through the apical foramen and thereby involves the PDL and periradicular bone.

CLINICAL FEATURES

Clinical and histopathological features of these conditions appear to be related to

the concentration and toxicity of the irritant or

the local proliferation of the invading organisms with their destructive activities.

Patient may or may not have swelling. If present swelling may be localized or diffuse.

Varying degree of palpation and percussion

Severe throbbing pain. Tooth becomes elongated and mobile as the swelling becomes more pronounced.

No reaction to heat, cold or electrical stimuli as the involved tooth has necrotic pulp.

RADIOGRAPHIC FEATURES

Vary from thickening of PDL space to the presence of a frank periradicular lesion.

Because the lesion has been present for a short period of time and is confined to medullary bone, radiograph does not show destruction of alveolar bone.

HISTOLOGICAL FEATURES

Shows a localized destruction of liquefaction necrosis containing numerous disintegrating PMNs, debris and cell remnants and accumulation of purulent exudate.

Differential diagnosis AAA should be differentiated from

periodontal abscess Percussion Vitality Location

SYMPTOMATIC APICAL PERIODONTITIS

Definition: it is a localized inflammation of the periodontal ligament in the apical region.

Causes :May occur in vital or non

vital tooth.In case of vital tooth Occlusal trauma

By abnormal occlusal contact High restoration Wedging of foreign object in

between the teeth Blow to the tooth

In non vital teeth - it is the sequelae of pulpal diseases and result from diffusion of bacteria and noxious products from inflamed or necrotic pulp.

may be iatrogenic e.g during root canal instrumentation forcing bacteria apically or over instrumentation .

CLINICAL FEATURES

Principal feature: sensitivity to percussion Pain –pathognomonic, varies from slight

tenderness to excruciating. Tooth may or may not respond to vitality

tests depending on the cause.

X-RAY FEATURE

May show slight thickening of PDL.

HISTOPATHOLOGY

An inflammatory reaction occurs in the apical PDL.

Bld vessels are dilated. Presence of PMNs. Distention of PDL due to accumulation of

exudate from bld vessels

CHRONIC ALVEOLAR ABSCESS

Synonym: chronic suppurative apical periodontitis

Definition: it is a long standing, low grade infection of the periradicular alveolar bone.

Cause: – Sequelae of death of pulp with extension

of infection periapically .– May result from pre existing acute abscess

SYMPTOMS

Tooth is generally asymptomatic. Usually associated with sinus formation. Vitality tests are negative.

GRANULOMA

A dental granuloma is a growth of granulomatous tissue continuous with the PDL resulting from death of the pulp and the diffusion of bacteria and bacterial toxins from the root canal into the surrounding periradicular tissue through the apical and lateral foramina.

Etiology :Further sequelae of infection from necrotic

pulp.It is chronic low grade defensive reaction of the

alveolar bone to irritation from the root canal.

CLINICAL FEATURES

May or may not produce any subjective symptom.

Mild pain may be present Can be sensitive to percussion.

RADIOGRAPHIC FEATURES

Earliest feature-thickening of PDL

Later on there is radiolucency at periapical region. Lucency may be well circumscribed or diffuse.

If well circumscribed, zone of sclerotic bone or thin opaque line is seen. it indicates slow progressive lesion.

Diffuse lesion suggest more acute phase.

HISTOLOGICAL FEATURE

Dense fibrous tissue capsule surrounding the C.T   

Central zone of granulation tissue with macrophages with a foamy cytoplasm   

May have some cholesterol crystals surrounded by multinucleated giant cells   

Irregular islands of epithelium

APICAL PERIODONTITIS (GRANULOMA) WITH CONTAINEDEPITHELIUM. EPITHELIAL CELLS OF PERIODONTAL LIGAMENT HAVE PROLIFERATEDWITHIN NEW INFLAMMATORY TISSUE. THE EPITHELIUM TENDS TO RAMIFY IN ARETICULAR PATTERN (STRAIGHT ARROW) TOWARD RECEDING BONE. IT ALSO MAY,AS IN THIS CASE, APPLY ITSELF WIDELY TO THE ROOT SURFACE (CURVED ARROW).INFILTRATION OF EPITHELIUM BY ROUND CELLS IS EVERYWHERE APPARENT.HUMAN TOOTH.

RADICULAR CYSTCyst: a cyst is a closed cavity or sac

internally lined by epithelium, the center of which is filled with fluid or semi solid material.

Radicular or alveolar cyst: it is slowly progressive epithelial sac at the apex of tooth that lines a pathological cavity in the alveolar bone, lumen of which is filled with low concentration of proteinaceous fluid.

About 75% of all cysts occur in maxilla and about 25% occur in mandible.

ETIOLOGY

A radicular cyst presupposes physical, chemical or bacterial injury resulting in death of pulp, followed by stimulation of the epithelial cell rests of malassez which are normally present in PDL.

PATHOGENESIS

•Inflammation in periapical granuloma or some products of dead pulp and it evokes a reaction•Local changes in supporting connective tissue which may activate the cell rests of malassez.

Initiation

•Proliferation of epithelial rests in periapical area•Proliferation of epithelium to line a pre-existing cavity formed through focal necrosis & degeneration of CT in periapical granuloma

Cyst formation

•Plasma protein exudate, hyaluronic acid, products of cell breakdown --> high osmotic pressure of cystic fluid on walls•Resorption of bone & enlargement of cyst

Cyst enlargemen

t

CLINICAL FEATURES

Majority are asymptomatic Tooth is seldom painful May undergo acute

exacerbation and thus can form abscess or a draining fistula.

                

              

 

                

              

Identical to that of granuloma except the size.

Cyst is usually of larger size

HISTOLOGICAL FEATURES

Cyst is lined by epithelium which is usually stratified squamous in nature.

Hyaline body or Ruston bodies are often found in epithelium. These hyaline bodies are tiny, linear and appear eosinophilic.

C.T is composed of collagen fibers, fibroblasts and bld vessels and inflammatory infiltrate .

In some cases cholesterol slits are also found in the wall of cyst.

Lumen of cyst contains fluid with low conc. of protein.

RADIOGRAPHIC FEATURES

Similar to periapical granuloma

May be of greater size than granuloma

               

               

 

             

       

TREATMENT

Excision of cyst & curettage of periapical tissue.

Sometimes involved tooth may have to be removed along with cyst.

CONDENSING OSTEITIS

Definition:-it is the response to a low grade, chronic inflammation of the periradicular area as a result of a mild irritation through the root canal.

Cause:- it is the result of any mild irritation from the pulpal disease that stimulates the osteoblastic activity in the alveolar bone.

SYMPTOMS

Age- usually in young adults who have a high degree of tissue resistance.

Usually asymptomatic. Most common in mandibular molars.

RADIOGRAPHIC FEATURES

Well circumscribed radio opaque mass of sclerotic bone surrounding the apex of tooth.

The entire root out line is clearly visible.

It is an important feature to distinguish condensing osteitis from benign cementoblastoma in which root outline appear to blend into bone.

APICAL CONDENSING OSTEITIS THAT DEVELOPED IN RESPONSE TOCHRONIC PULPITIS. ADDITIONAL BONY TRABECULAE HAVE BEEN FORMED AND

MARROW SPACES HAVE BEEN REDUCED TO A MINIMUM. THE PERIODONTAL LIGAMENT

SPACE IS VISIBLE, DESPITE INCREASED RADIOPACITY OF NEARBY BONE.

HISTOLOGY Appears an area of dense bone with trabecular

borders lined with osteoblasts. Chronic inflammatory cells, plasma cells and

lymphocytes are seen in bone marrow.

Treatment Endodontic treatment Extraction

Definition:-

It is a lytic irreversible process resulting in loss of enamel, dentin and cementum.

External Resorption

Etiology

Not fully understood

Possible causes are -Trauma -Ortho treatment -Bruxism - Developmental defects -Intracoronal bleaching

Symptoms Usually asymptomatic

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RADIOGRAPHIC APPEARANCE

Characteristic appearance:-– radiolucent with

indistinct border– Outline of pulp chamber

visible Varying x-ray angle will

move the lesion on the root.

NONENDODONTIC PERIRADICULAR LESIONS

Imp to differentiate between pulpal pathology and non-endodontic origins of alterations in bone morphology.

Differentiating between lesions of endodontic and nonendodontic origin is usually not difficult. Pulp vitality testing, when done with accuracy, is the primary method of determination; nearly all nonendodontic lesions are in the region of vital teeth, whereas endodontic lesions are usually associated with pulp necrosis, giving negative vitality responses. Except by coincidence, nonendodontic lesions are rarely associated with pulpless teeth.

Never assume a radiolucency is pulpal pathology.

NONENDODONTIC PERIRADICULAR LESIONS

Lesions of the jaws categorized as odontogenic or nonodontogenic in origin

Odontogenic lesions arise from remnants of odontogenesis (or the tooth-forming organ), either mesenchymal or ectodermal in origin.

Nonodontogenic lesions trace their origins to a variety of precursors and therefore are not as easily classified.

NON ODONTOGENIC LESIONS

Dentigerous Cyst Lateral Periodontal Cyst Odontogenic Keratocyst

ODONTOGENIC CYSTS

Central Giant Cell Granuloma. Nasopalatine Duct Cyst Simple Bone Cyst. Globulomaxillary Cyst Enostosis.

MALIGNANCIES

Carcinomas or sarcomas of various types are found in the jaws, rarely as primary but usually as metastatic lesions

Carcinoma : Generally found in older patients, involvement of the jaws (usually the mandible) is by metastasis from a primary lesion elsewhere

Carcinoma lesions of the jaw may also manifest pain and swelling, loosening of teeth or paresthesia, similar to endodontic pathosis

BIBLIOGRAPHYGrossman's Endodontic Practice Endodontics Fifth ed. – John I. Ingle The internet