ENDO-PERIODONTAL INTERRELATIONS
- INTRODUCTION:
The relationship between the endodontium and the periodontium is close; these two anatomical structures are actually in contact through the apical foramen and the lateral and/or accessory canals. The communication pathways between the periodontium and the endodontium explain the secondary effects of periodontal disease on the dental pulp, and also, conversely, those of pulp pathology on the periodontal tissues.
- ENDO-PERIODONTAL COMMUNICATION PATHWAYS:
According to CHAKER: There is a connective and vascular continuity between the pulp and the periodontium, called the “endo-periodontal continuum”.
The main communication routes are:
- dentinal tubules (JAC)
- side and accessory channels
- the inter-radicular space
- and finally, the apical zone
Non-physiological (pathological) communication pathways:
- These are iatrogenic root perforations during endodontic or prosthetic procedures.
- And vertical root fractures.
- DEFINITION::
According to Simon: endo-periodontal lesions include all cases or
an endodontic lesion communicates with a periodontal lesion and vice versa. The combination of the two lesions results in true endo-periodontal damage.
- CLASSIFICATION OF ENDO-PERIODONTAL LESIONS:
- WEINE classification (1976):
- CL1: clinical and radiological symptoms simulate periodontal disease, which are in fact due to pulp necrosis
- CL2: tooth suffering from endodontic and periodontal lesions which have joined together
- CL3: tooth not presenting an endodontic lesion, but requiring treatment
endodontic and root amputation to allow healing of a periodontal lesion.
- CL4: tooth showing symptoms of pulp or periapical disease and which in fact suffers from periodontal disease.
Periodontology Course – 4th year Dr. S. BENSAIDI
- BENDER AND SELTZER (Simon and Glickman) classification
- Cl I: Pure endodontic lesions
- Cl II: Primary endodontic lesions with secondary periodontal involvement
- Cl III: Pure periodontal lesions
- Cl IV: Primary periodontal lesions with secondary endodontic complications
- Cl V: Associated lesions (non-interfering in their topography).
- Cl VI: Combined lesions known as true endo-periodontal lesions
- Classification of MACHTOU AND COHEN 1988:
- endodontic lesion mimicking a periodontal lesion;
- periodontal lesion mimicking an endodontic lesion;
- true endo-periodontal lesion.
- PATHOLOGICAL INTERRELATIONS BETWEEN ENDODONTIUM AND PERIODONTAL:
- INFLUENCE OF PERIODONTAL DISEASE ON THE PULP:
- Gingivitis: The early stages of PD related to bacterial biofilm have no influence on pulp health. As long as the cementum remains intact, inflammation does not cross this barrier and pulp health remains preserved.
- Periodontitis: The progressive destruction of the tooth’s attachment system, brings the root surfaces and the contents of the periodontal pockets into direct contact.
Microorganisms from dental plaque, bacterial toxins and certain substances resulting from inflammation of the periodontium can infiltrate the cementum barrier and penetrate the dentinal tubules to reach the pulp.
Inflammation can also affect the pulp through the apex or accessory canals. This is the most obvious aspect of endo-periodontal pathology described under the term retro pulpitis.
Pulp necrosis appears when the disease process affecting the periodontium reaches a terminal stage, that is, when the bacterial plaque reaches the main apical foramina (Langeland et al., 1974).
- Occlusal Trauma: Increased functional demands can lead to an alteration or rupture of the apical vascular-nervous bundle, inducing necrobiosis of the pulp and pulp calcifications.
- INFLUENCE OF PULP PATHOLOGY ON THE PERIODONTIC:
If pulp inflammation has various causes: physical, chemical, mechanical, and bacterial, only the latter can cause periodontitis.
We can roughly classify pulp pathological conditions into:
- Pulp degeneration:
Sign of pulp aging and can be found in certain teeth whose function is absent, it can also be the result of occlusal trauma, or of iatrogenic origin (orthodontic, prosthetic), excessive force on the pulp leading to an alteration of its vascularization.
Pulp degeneration remains confined to the pulp and has no impact on the periodontium.
- Irreversible pulpitis:
The venous and lymphatic pulp system transports the products of cellular catabolism to the periodontium, however the quantity of irritants is insufficient to induce significant destruction of periodontal tissues.
The consequences on the periodontium of an inflammation of the pulp (pulpitis) are limited to
- a widening of the periodontal ligament
- rupture of the lamina dura
- or a small, clear periapical radio image.
It is important to note that pulpitis does not cause significant destruction of periodontal tissue.
- Septic pulp necrosis:
Microorganisms find favorable conditions for their growth and release various substances (enzymes, metabolites, antigens, etc.) which reach the periodontium by entering through the canals and foramina that connect the pulp to the periodontium.
Once in the periodontium, they induce alterations of an inflammatory nature resulting in:
- Destruction of periodontal tissue fibers
- Resorption of adjacent alveolar bone.
- Resorption of the hard tissues of the tooth may also be observed.
- acute periapical lesion (APL):
The quantitative and/or qualitative increase in the toxicity of infectious agents and the weakening of the host’s defenses leads to rapid, extensive and painful tissue destruction: periapical abscess
This abscess seeks to drain its purulent contents through a fistulous path; in general, two routes of exteriorization are possible:
- Desmodontal fistula: The fistula tract develops along the desmodontal space (path of least resistance) and puts the periapical lesion and the existing SGD or pocket in direct communication.
- Extraosseous fistula: A periapical abscess may also perforate the cortical bone near the apex, lifting soft tissues, including the periosteum covering the bone,
and drain into the sulcus or through the mucosa.
- Chronic periapical lesion (CPL):
When the periapical infection evolves quietly, the host’s defense against the swarming of germs can then be achieved by the formation of a granuloma; This chronic periapical inflammatory lesion is characterized by the presence
of richly vascularized granulation tissue that is infiltrated, to a variable degree, by inflammatory cells surrounded by collagen-rich connective tissue contiguous to the alveolar bone
Left to its own devices, it can remain stationary or increase in volume. Occasionally, a cystic transformation can occur and cause more extensive bone destruction.
- THE RECIPROCAL INFLUENCES OF ENDO-PERIODONTAL THERAPIES:
- Effects of periodontal therapy on the pulp:
- After scaling and root planing; Patients frequently complain of increased sensitivity of their teeth to thermal, osmotic and mechanical stimuli,
Symptoms peak in intensity during the first few weeks following treatment and then gradually fade.
- Root planing exposes the dentin tubules and lateral canals blocked by cementum, and results in the formation of a layer of reaction dentin that protects the pulp. This dentin is located opposite the treated root zone if the planing is limited to the cementum; however, if it is deep, the dentin reaction is more significant, leading to pulpal distress, hyperemia and dentin hypersensitivity.
- Application of citric acid after superficial or deep planing causes demineralization of peritubular dentin
Some authors even observe the appearance of abscesses and localized pulp necrosis.
- Impact of endodontic therapy on the periodontium:
Infectious products can reach the periodontium through the apex or accessory canals located at the level of lacunae in the canal filling, or through perforations or fractures during canal preparation, and can cause
the appearance of periodontal lesions.
Inflammatory periodontal lesions can also result from irritation, both mechanical and chemical, during coronal or root canal preparation.
- DIFFERENTIAL DIAGNOSIS OF ENDO-PERIODONTAL LESIONS:
- Diagnostic approach:
The diagnosis of endo-periodontal lesions allows:
- To determine the origin and chronology of the lesions;
- To adapt the appropriate treatment(s);
- To avoid unnecessary or even harmful therapies;
- And finally to reduce healing failures.
For a lesion to be qualified as true endo-periodontal, two criteria are necessary:
- The tooth involved in the lesion must have lost its pulp vitality
- The periodontal attachment system must be broken
It is therefore necessary to jointly assess periodontal and pulpal damage.
- Periodontal probing:
The gentle introduction of a graduated periodontal probe into the gingival sulcus and then its movement parallel to the tooth, from near to far, allows the clinician
to understand the morphology of the defect;
- Pulp vitality tests:
- Pulp vitality is a very important criterion for diagnosis.
- If it does not appear compromised, shift further attention to the periodontal side.
Thermal tests:
- Cold: The simplest way is to use a cooling spray on a cotton ball which will be applied to the vestibular surface after drying the tooth
- Warm: By a piece of heated gutta or by hot water placed with a syringe on a tooth isolated by the placement of an operating field (dam).
Electrical test: Carried out using a “pulp tester”.
Drilling test (cavity test): Usually when the tooth is decayed.
- The pain :
The presence of pain usually indicates endodontic involvement, especially if the pain is severe.
Usually, pain is absent if the periodontal pathology is chronic.
- edema :
*in case of pulp lesion: it appears in the vestibular sulcus.
*in case of periodontal lesion: it is found more coronally.
-in periodontal pathology, it is rare to observe facial edema closing the eye or affecting other parts of the face.
- Radiography:
Diagnosis cannot be based on X-ray examination alone.
The quality of the images must allow the presence of caries, bone trabeculation, continuity of the desmodontal space to be assessed and it is essential in the presence of a fistula to objectify the path using a gutta-percha cone on a retroalveolar radiograph.
Bone loss of endodontic origin is limited apically to a larger surface area, whereas bone loss of periodontal origin, affecting several surfaces, is larger coronally.
Radiography can demonstrate an endodontic lesion at the apex of a tooth and an intraosseous periodontal lesion, clearly separated by a bony bridge.
- Differential diagnosis between periapical abscess and periodontal abscess:
- TREATMENT OF ENDO-PERIODONTAL LESIONS:
The treatment of endo-periodontal lesions requires, jointly, the use of therapeutic means available in endodontics and periodontics.
Most authors recommend starting treatment with the endodontic phase , justifying their choice by the potential for regeneration of endodontic lesions.
If there is loss of periodontal attachment and the presence of true pockets, endodontic treatment must be accompanied by periodontal curettage and root planing in order to jointly eliminate the periodontal component. This is the case for periodontal lesions with secondary endodontic involvement, and for combined endo-periodontal lesions.
When surgical treatment is indicated, it is important to wait several months for the endodontic result before intervening.
Generally, endodontic treatment should be performed during the initial preparation phase, but should only be undertaken when the teeth are deemed periodontally salvageable.
Surgical treatment of endoperiodontal lesions can be classified into:
- Subtraction surgery: when a root must be amputated.
- Root amputation
- Hemisection
- Apical resection
- Additive surgery: filling cases
- Inductive (regenerative) surgery: use of guided tissue regeneration membranes.
- CONCLUSION:
The odontium and the periodontium are two inseparable entities.
The disruption of the balance of one cannot, under any circumstances, be without consequences for the other. Every practitioner must bear in mind, during any treatment, the different relationships that exist between the two specialties.
ENDO-PERIODONTAL INTERRELATIONS
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