5.endo perio lesion

Endo-perio continuum

Contents

0 Introduction0 Classification0 Etiology 0 Routes of communication0 Biologic effects of pulpal infection on periodontal

tissues0 Biologic effects of periodontal infection on dental pulp0 Differential diagnosis of pulpal and periodontal

infection0 Treatment considerations

Introduction

0 The fact that the periodontium is anatomically interrelated with the dental pulp by virtue of apical foramina and lateral canals creates pathways for exchange of noxious agents between the two tissue compartments when either or both of the tissues are diseased.

0 The simultaneous existence of pulpal problems and inflammatory periodontal disease can complicate diagnosis and treatment planning and affect the sequence of care to be performed.

Classification Oliet and Pollock, 1968

Based on treatment procedures

1. Lesions that require endodontic treatment procedures only

a) Any tooth with necrotic pulp and apical granulomatous tissue replacing periodontium and bone, with or without a sinus tract (Chronic Peri-apical abscess).

b) Chronic peri-apical abscess with a sinus tract draining through a section of the attachment apparatus in its entire length alongside the root.

c) Root fractures, longitudinal and horizontal

d) Root perforationsa) Pathologicb) Iatrogenic

e) Teeth with incomplete apical root development and inflamed or necrotic pulp, with or without periapical pathosis

f) Endodontic implantsg) Replants

a) Intentional or b) traumatic

h) Transplantsa) Autotransplants orb) Allotransplants

i) Teeth requiring hemisection or radisectomyj) Root submergence

2. Lesions that require periodontal treatment procedures only

a) Occlusal trauma causing reversible pulpitisb) Occlusal trauma plus gingival inflammation resulting

in pocket formation

a) Reversible but increased pulpal sensitivity caused by trauma or possibly by exposed dentinal tubules

b) Reversible but increased pulpal sensitivity caused by uncovering lateral or accessory canals exiting into the periodontium

c) Suprabony or infrabony pocket formation treated with overzealous root planing, leading to pulpal sensitivity

d) Extensive infrabony pocket formation, extending beyond the root apex and sometimes coupled with lateral or apical resorption, yet with pulp that responds within normal limits to clinical testing

3. Lesions that require combined endodontic-periodontic treatment procedures

a) Any lesion in group I that results in irreversible reactions in the attachment apparatus and requires periodontic treatment

b) Any lesion in group II that results in irreversible reactions in pulp tissue and also requires endodontic treatment

Classification

0The following classification system was developed by Simon, Glick and Frank in 1972:

1. Primary Endodontic Disease2. Primary Periodontal Disease3. Primary Endo w/ Secondary Perio 4. Primary Perio w/ Secondary Endo5. True Combined Lesions

Primary Endodontic Disease

0Typically, endodontic lesions resorb bone apically and laterally and destroy the attachment apparatus adjacent to a non-vital tooth

0It is possible for an acute exacerbation of a chronic peri-apical lesion on a tooth with a necrotic pulp to drain through the PDL into the gingival sulcus. This clinical presentation mimics the presence of a periodontal abscess, or a deep periodontal pocket.

Primary Endodontic Disease

0 When endodontic infection drains through the PDL, the pocket is very narrow and deep. In reality, it is a sinus tract of pulpal origin that opens through the PDL, and not breakdown due to periodontal disease.

0 A similar situation can occur where drainage from the apex of a molar tooth extends coronally into the furcation area. These cases resemble a “through-and-through” furcation defect of periodontal disease

Primary Endodontic Disease

0 For diagnosis - trace the sinus tract by inserting a gutta-percha cone and exposing radiographs to determine the origin of the lesion.

0 The sinus tract of endodontic origin is probed down to the tooth apex, where no increased probing depth would otherwise exist around the tooth.

Primary Endodontic Disease

0 Primary endodontic disease will heal following root canal treatment

0 The sinus tract extending into the gingival sulcus or the furcation area disappears at an early stage once the necrotic pulp has been removed and the root canals are well sealed.

Primary Endodontic Disease

Pre-op - periapical and furcal RL + a deep narrow perio defect

Primary Periodontal Disease

0 Caused by periodontal pathogens

0 It is the result of progression of chronic periodontitis apically along the root surface

0 Pulp tests yield a clinically normal pulpal reaction

Primary Periodontal Disease

0Frequently accumulation of plaque and calculus are seen throughout the dentition

0Periodontal pockets are wider, and are generalized

Primary Periodontal Disease

Pre-op: alveolar bone loss + a periapical lesion, a deep narrow pocket was traced on the mesial aspect of the root, the tooth tested vital

Primary Periodontal Disease

The tooth was extracted. Note the deep mesial radicular developmental groove

Primary Endo with Secondary Perio

0 This happens with time as suppurating primary endodontic disease remains untreated, it may become secondarily involved with periodontal breakdown

0 Plaque forms at the gingival margin of the sinus tract and leads to plaque-induced periodontitis in the area

Primary Endo with Secondary Perio0The pathway of

inflammation into the periodontium is through the apical foramen, accessory and lateral canals

Primary Endo with Secondary Perio

0The treatment and prognosis are now different than those of teeth simply having endo or perio disease

0The tooth requires both endodontic and periodontal treatments

0Root fractures and perforations may also present as primary endo with secondary periodontal involvement

Primary Endo with Secondary Perio

Pre-op: interradicular defect extends to the apex Post-op

Primary Perio with Secondary Endo

0 Apical progression of a periodontal pocket continues until the apical tissues are involved

0 The pulp may become necrotic as a result of infection entering via the apical foramen

Primary Perio with Secondary Endo

0The progression of periodontitis by way of lateral canal and apex to induce a secondary endodontic lesion

Primary Perio with Secondary Endo

0In single-rooted teeth the prognosis is usually poor, as the periodontal breakdown is very severe, necessitating extraction

0In molar teeth the prognosis may be better, since not all the roots may suffer the same loss of supporting periodontium. Root resection may be considered as a treatment alternative

Primary Perio with Secondary Endo

0 Even though unusual, the treatment of periodontal disease can also lead to secondary endodontic involvement. Lateral canals and dentinal tubules may be opened to the oral environment by scaling and root planing or surgical flap procedures

Primary Perio with Secondary Endo

At initial presentation shows evidence of horizontal bone loss as well as a periapical radiolucency. The crown was intact, but vitality tests were negative. The post-op radiograph shows that a lateral canal was exposed to the oral environment due to bone loss. That lateral canal could serve as a potential pathway for bacteria.

True Combined Disease

0True combined endo/perio disease occurs less frequently than other endo/perio problems

0It is formed when an endodontic disease progressing coronally joins with an infected periodontal pocket progressing apically

0The degree of attachment loss in this type of lesion is large.

True Combined Disease

0Concomitant endo-perio lesion is an additional classification that has been proposed to describe the presence of endo and perio disease as two separate and distinct entities

True Combined Disease

Radiograph shows separate progression of endodontic disease and periodontal disease. The tooth remained untreated and consequently the two lesions joined together

True Combined Disease

Radiograph shows bone loss in 2/3 of the root with calculus present and a separate periapical radiolucency. Clinical exam revealed coronal color change and pus exuding from the gingival crevice. Pulp vitality tests were negative

True Combined Disease

Etiology

0 Sundqvist et al, 1989; Baumgartner and Falkler, 1991 – 0 Eubatcerium sp0 Peptostreptococcus sp0 Fusobacterium sp0 Porphyromonas sp0 Prevotella sp0 Streptococcus sp0 Lactobaclillus sp0 Wolinella sp0 Actinomyces sp

Anatomic Considerations

0 There is an intimate relationship between the periodontium and pulpal tissues

0 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

I. Route of communicationApical foramina

Pulpal infection

Persistent infection in pulp

Secondary infection and breakdown of tissues in the periodontium

Continued bone loss and extension of lesion to external mucosal surface

Sinus tract formation

Retrograde periodontitis/Chronic peri-

radicular periodontitis/Chronic

radicular abscessIt represents the periodontal tissue breakdown from an apical to

cervical directionMost common example of pulpal disease leading to secondary

periodontal breakdown

Retrograde periodontitisPulp necrosis

Inflammatory bone resorption at the root apex

Severe periodontal diseaseInitiate or exacerbate changes in the pulp tissue

Orthograde periodontitisIt results from a sulcular infection

Orthograde periodontitis

0 Typically identified as a peri-apical radiolucency

II. Route of communicationLateral or accessory canals

Lateral/accessory canals

0 Found along the length of root canals.

0 Vertucci et al, 1974 - Maxillary II premolars – 59.5% have lateral canals out of which 0 Apical regions – 78.2% 0 Midroot level – 16.2%0 Cervial regions – 4%

Lateral/accessory canals

0 Gutman, 1978 – Permanent molar furcation region – 28.4% of permanent Ist molars – accessory canals in furcation areas.

0 Kirkhan, 1975 – out of 100 permanent teeth extracted as a result of severe periodontal disease, only 2 had accessory canals in the periodontal pocket.

0 Thus likelihood of primary periodontal infection reaching the dental pulp through accessory canals is rare.

III. Route of communicationDentinal tubules

Dentinal tubules

0 Torneck, 1998 - Dentinal tubules have tapered structure along the length from pulpo-dentin complex (PDC) to the dentinoenamel junction (DEJ) with diameter of –0 2.5 µm at PDC0 0.9 µm at DEJ

0 Shovelton, 1964 – bacterial colonization in tubules from infected root canals.

Dentinal tubules

0 Guiliana, 1997 – bacterial invasion into dentinal tubules from the periodontal pocket suggesting that dentinal tubules may allow pulpal irritation from chronic periodontal infection.

0 Exposed dentinal tubules in areas of denuded cementum may serve as communication pathways between the pulp and PDL

Additional Avenues of communication between Pulp & Periodontium

0 Developmental malformations – such as palatogingival grooves of maxillary incisors. These usually begin in the central fossa, cross the cingulum, and extend apically with varying distances

0 Perforations – these may result from extensive carious lesions, resorption, or from operator error

0 Vertical root fractures – these can produce deep periodontal pocketing and localized destruction of alveolar bone. The fracture site provides a portal of entry for irritants from the root canal to the PDL

Biologic effect of pulpal infection on periodontal

tissues

Biologic effect of pulpal infection on periodontal tissues

0 Untreated endodontic infection – risk factor for progression of periodontal disease.

Untreated endodontic infection

Biologic effects of periodontal infection on dental pulp

Biologic effects of periodontal infection on dental pulp

0 Bender and Seltzer, 1972; Pace et al, 2008 – effect of periodontal disease on dental pulp is controversial compared to effects of pulpal disease on the periodontium.

0 Rubach and Mitchell , 1965; Seltzer et al, 1967; Seltzer et al, 1963 – inflammation and localized pulpal necrosis have been observed next to lateral canals exposed by periodontal disease.

Biologic effects of periodontal infection on dental pulp

0 Czarnecki and Schilder, 1979; Mazur & Massler, 1964; Torabinejad and Kiger, 1985 – no correlation between periodontal disease and changes within the pulp.

Differential diagnosis of pulpal and periodontal

infection

Differential diagnosis

0 To establish a correct diagnosis and0 To initiate appropriate therapy.0 Challenging task.

If lesion is of

pulpal origin

Treated by

periodontal

therapy

Lesion will

not resolv

e

Differential diagnosis

If lesion is of

periodontal origin and a vital pulp

Treated by endodontic

therapy

Lesion will not resolve

Diagnosis is based on

0 Patient’s subjective symptoms0 Coronal integrity0 Radiographic appearance0 Tooth vitality and periodontal probing

Different Characteristics of Pulpal & Periodontal Lesions

 Primary Pulpal

Primary Periodontal

Independent Endodontic-Periodontic

Combined Endodontic-Periodontic

Patient symptom

Varies Mild discomfort Varies Varies

Coronal integrity

Compromised Intact Compromised Compromised

Radiographic lesions

PARL (Periapical radiolucency)

Crestal bone loss

Separate PARL and crestal lesions

Continuous bony lesions from alveolar crest to apex

Vitality Non-vital Vital Nonvital Non-vital

Periodontal probing

Narrow probing to apex

Generalized bone loss

Generalized bone loss

Generalized bone loss with narrow probing to apex

Patient’s subjective symptoms

0 During initial stage of pulpitis - patient complains of0 Sensitivity and pain exacerbated by stimuli such as –

0Temperature change,0Pressure and/or0biting

Reversible pulpitis

0 Symptoms of reversible pulpitis – resolve with time as a result of0 Closure of dentinal tubules, 0 clearance of microbial irritants and toxins, and0 reparative dentin formation

Irreversible pulpitis

Persistent inflammation

Irreversible pulpitis

Irreversible pulpitis

0 Sharp and untriggered pain0 Acute pain to thermal stimuli may subside after

several days as the pulp becomes necrotic, and the bacteria and their by-products migrate apically in the complex canal system.

As infection extends to and then past the

apical foramen or a lateral

periradicular canal

Tooth – sensitive to

bite pressure and

percussion

Elevation of tooth

Necrotic tooth

Peri-radicular abscess

Tooth feels

"high” on occlusion

0 Patients with irreversible pulpitis or chronic pulpal infection (i.e. necrosis) may be completely asymptomatic.

0 Thus diagnosis of primary pulpal infection is made with objective findings – such as 0 percussion, 0 palpation, 0 biting, 0 periodontal probing, and 0 vitality testing

Acute periradicular abscess

Periodontal abscess

1. Extreme pain to – Pressure, Bite, Percussion Palpation around the tooth apex if the infection penetrates the bony cortical plate

2. Edema and swelling

1. Cause less pain – because there is little or no elevation of the periosteum

2. Edema and swelling – confined to the cervical portion of the tooth

Visual Examination

0Extra-oral examination0Facial asymmetry0Swelling0Extra oral sinus tract

Extra-oral Swelling

Visual Examination

Extra oral sinus tracts associated with necrotic teeth

Visual Examination

Intra-oral examination0Swelling0Redness0Sinus tract

Acute apical abscess

Acute apical abscess

Visual Examination

A sinus tract traced with a gutta-percha cone

Visual Examination

Hard tissues0Caries0Large or defective restorations0Discolored/chipped teeth

Discoloration

Percussion Test

0A very significant test0Always compare suspect tooth with adjacent and

contralateral teeth0Tenderness indicates inflammation in the PDL0Cause of inflammation may be pulpal or

periodontal

Percussion Test

Vertical percussion Horizontal percussion

Percussion Test

Tooth Slooth

Used to assess cracked teeth and incomplete cuspal fractures

Palpation

Acute periradicular abscess

Periodontal abscess

3. Redness – apically if a pulpal abscess swells and elevates the surrounding tissues.

4. Usually probe normally increased mobility (depending on bone loss).

Patients describe the tooth as feeling longer or higher than the adjacent teeth. (González-Moles  & González, 2004)

3. Redness and a smooth appearance of the marginal gingival tissues – more common

4. Objective findings - bleeding on probing, suppuration, increased pocket depth, increased tooth mobility, lymphadenopathy occasionally (Herrera et al, 2000)

Periodontal Examination

Periodontal Examination

An isolated deep pocket may indicate a root fracture

Transillumination0 Helps to identify vertical crown fracture0 Produces light and dark shadows at fracture site

A crack will block and reflect the light when transilluminated

Acute periradicular abscess

Periodontal abscess

Drainage two sitesmost prevalent site - sinus tract develops when the area of swelling breaks through the mucoperiosteum and exits the mucosal tissue, either near or at some distance from the site of the infection.

Coronal IntegrityAcute periradicular abscess

Periodontal abscess

1. loss of coronal integrity, such as occurs with caries, failing restorations, extensive restorations and the existence of cracks or fractures that extend to the pulpal tissues

1. intact crown structure and absence of coronal defects

Radiographic appearance

0 coronal status, 0 crestal bone height and shape, 0 presence of periapical or lateral radiolucency, 0 bony trabeculation, 0 integrity of lamina dura, and 0 careful evaluation of the obturation status of the root

canal space if endodontic therapy has been previously attempted.

Radiographs

Characteristic J-shaped or halo lesion associated with fractured root

Vitality

0 Periodontal abscess - test vital to thermal testing unless the acute condition is a true combined lesion in which both endodontic and periodontal compartments become diseased

0 Teeth with both a periradicular infection and a periodontal abscess usually test nonvital.

0 Exceptions to this are either 0 extremely calcified canals, 0 extensively restored teeth, or 0 multirooted teeth in which some canals may be necrotic

as the result of either pulpal or periodontal disease. 0 Other canals may still retain vital tissue that respond to

thermal or electric pulp testing.

0 Thermal testing is usually the most reliable way of determining pulpal health or disease.

0 Patients with an irreversible pulpitis often report a lingering painful response to a thermal stimulus.

0 Keenan et al, 2005 - In later stages of pulpitis, heat exacerbates the symptom more than the cold, and the application of cold may even cause short-term pain relief.

0 Addy, 2005 - Although thermal testing can be informative as to the status of the pulp, a patient's response to thermal stimuli may be confused with hypersensitivity resulting from exposed dentin and patent dentinal tubules without pulpitis.

0 Therefore, thermal testing must be combined with other diagnostic criteria, as discussed previously, to distinguish between the lesions originating from pulpal or periodontal infection.

Thermal Tests

0Cold always used0Heat rarely used0Compare reaction with adjacent and

contralateral teeth0Refractory period of at least 10 minutes

before pulp can be retested accurately

Thermal Tests

Thermal Tests

Ice stick

CO2 Snow

Thermal Tests

0Isolate area with cotton rolls0Dry teeth to be tested0Ask patient to:

0 “Raise hand on feeling cold”0 “Lower hand when cold feeling goes away”

0Record:0 + or – sensitivity to cold0 Time until cold sensitivity was felt0 Time that cold sensitivity lingered

Thermal Tests

Classic Responses to Thermal (cold) Testing:0 Normal Pulp: Moderate transient pain0 Reversible Pulpitis: Sharp pain; subsides quickly0 Irreversible pulpitis: Pain lingers 0 Necrosis: No response(Note false positive and false negative responses common)

Electric Pulp Test

0A direct test of nerve elements of pulpal tissue0Vitality versus non-vitality only – not whether

vital pulp is normal or inflamed0In multi-rooted teeth, where one canal is vital –

tooth usually tests vital0False positives and false negatives may occur

Electric Pulp Test

False positive reading:0 Electrode contact with metal restoration or gingiva0 Patient anxiety0 Liquefaction necrosis0 Failure to isolate and dry teeth prior to testing

Electric Pulp Test

Electric Pulp Test

False negative reading:0 Patient is heavily premedicated0 Inadequate contact between electrode and enamel0 Recently traumatized tooth0 Recently erupted tooth with open apex0 Partial necrosis

Electric Pulp Testing

Treatment Decision-Making and Prognosis

0 Treatment decision-making and prognosis depend primarily on the diagnosis of the specific endodontic and/or periodontal disease

0 The main factors to consider are pulp vitality and type and extent of the periodontal defect

Treatment Decision-Making and Prognosis

0Diagnosis of Primary endo and Primary perio disease usually present no clinical difficulty. In primary endo the pulp is nonvital. In primary perio the pulp is vital

0However, the diagnosis of the combined endo/perio lesions could present a challege as they present clinically and radiographically very similar. The diagnosis is often tentative with a definitive diagnosis formulated following treatment

Treatment Decision-Making and Prognosis

0The prognosis and treatment of each endo/perio disease type varies

0Primary endo should only be treated by endodontic therapy and has a good prognosis

0Primary perio should only be treated by periodontal treatment. The prognosis depends on severity of the perio disease and patient response to treatment

Treatment Decision-Making and Prognosis

0Combined lesions should be treated with endodontic therapy first. Treatment should be evaluated in 2-3 months, and only then should periodontal treatment be considered. This sequence allows for sufficient time for initial tissue healing and better assessment of the periodontal condition to determine if the tooth needs SC/RP or surgical treatmen. Prognosis depends on the periodontal involvement and treatment

0Cases of True Combined disease usually have a more guarded prognosis