Perio-endo Interface Flashcards
How are the periodontium and pulp connected
Natural
Pathological and iatrogenic
Natural communication
Dental tubules- may be exposed due to developmental defects (gap between cementum and enamel causes exposed dentine), disease process, surgical, periodontal procedures, traumatic injuries
Apical foramen- main route of communication, pulpal inflammation can caus a localised inflammatory reaction in the periodontium with or without bone/root resorption; can also be exposed due to severe loss of attachment
Lateral/accessory canals- 30-40% have lateral canals, majority are apically, contain connective tissue and blood vessels and connect circulatory system of pulp to periodontium, not all extend to the full width of dentine.
E.g. furcal canals- in furcations (can be in floor of the pulp chamber, or in other parts of the canals)
If there is radiolucency in furcations-can be a risk of exposing furcal canals- to necrotic/infectious products from the pulp down to the canals
Sensitivity test is needed- if pulp responds or not (if necrotic, no response)
Remember, multirooted teeth- sensitivity test can be inaccurate
Microbes present in teeth with chronic/asymptomatic periradicular periodontitis and chronic periodontitis
P. Gingivalis
Fusobacterium
P. Intermedia
Treponema denticola
AAA
Eikenella
Pathological/iatrogenic pathways of communication of pulp and periodontium
Developmental malformations
Resorptive lesions
Perforations
Cracks
Mucosal fenestrations
Developmental malformations
Palatogingival grooves-upper central and lateral incisors
If epithelial attachment is breached, groove becomes contaminated -becomes self sustaining infrabony pocket
Loss of attachment quickly extends to apical foramen and can lead to pulpal necrosis
Treatment - difficult as instrumentation and RSD does not works as infection is in the actual groove itself
The groove should be removed with a groove and use regenerative techniques
Resorptive lesions
2 requirements
-an injury
-a stimulus
3 types
External- can be associated with increased PPD and BOP
Internal- increased PPD, BOP,
Inflammatory cervical- starts where junctional epithelium attaches to the root surface and microbes in gingival sulcus stimulate and sustain resorptive process, always associated with increased PPD, BOP and gingival swelling
Perforation
Either pathological by caries/resorption or iatrogenic by procedural errors
May present as perio abscess-pain, swelling, pus through PDL
Closer the perforation to gingival sulcus is- increased likelihood of apical migration of gingival epithelium
Perforation prognosis depends on-
Location- if mind to apical third: better prognosis as it is sealable/bounded by bone (not if perio disease)
Time
Ability to seal perforation
Chance of building new attachment
Accessibility of the reaming RCS
Root fractures
Horizontal-if outwit alveolar bone/near crestal edge-there will be pocket formation
If in coronal third sudden deepening of PPD
Vertical fracture - common in endo teeth. It will lead to microbial colonization of crack space to periodontal inflammation to breakdown of connective tissue and alveolar bone
Diagnosis-take parallax radiographs, J shaped radiolucency. Deep narrow pocket, pain on biting, abscess
Definitive diagnosis -surgical exploration
Mucosal fenestrations
It is a pathological conditions characterized by the perforation of the alveolar bone plate and overlying mucosa by the root of the tooth
Generally asymptomatic but can be plaque retentive factors, lead to caries due to exposed root dentine or further periodontal destruction and have acces to RCS
Can be due to root prominence, developmental anomalies, periodontal disease, biotype, ortho movement etc
Treatment -first- RCT, then surgery and connective tissue graft to repair the damage
Can periodontal disease/treatment affect the pulp?
If there is a blood supply through the foramen and it is intact, the pulp can actually withstand any insults from periodontal disease
Pulpal necrosis was only seen where perio disease was so advanced that microbes reached the apical foramen
RSD and scaling can remove cementum and expose dentinal tubules
Polishing is more of a problem- due to heat generated causing irreversible pulpitis pulp necrosis
Heat produced depends on: speed, torque, amount of force-all causing odontoblast death
Evidence shows that pulp can be affected when subgingival plaque can access the apical foramen
Can endo disease/treatment affect periodontium?
We need open canals, a patent route to the periodontium, infected RCS, enough of virulent microbes to provoke periodontal response
But no studies demonstrated this
Lateral canals could be a route to periodontium and cause perio disease
What can influence the treatment options/prognosis for endo (think perio)
Timing of diagnosis and amount of perio support remaining
What do we need to do before diagnosis
Clinical examination
Palpation percussion, pocket depths, probing, mobility
If sinus/pus draining from PDL
Is there is- need to palpate to see if discharging, put GP in and X ray
Investigation/special tests- to distinguish if perio or endo
Gives indirect information about pulp status
If perio only- tooth will response to sensitivity testing
Use at least two tests
Perio endo lesion
Characterised by CAL, bone loss, periradicular pathology
For diagnosis -examination, history, sensitivity tests, radiographs (PA)
If perio endo lesion is present- can be treated or XLA?
Treatment depends if in aesthetic zone, why to keep it, XLA can lead to bone loss, biotype, future implants etc
Endo treatment first, then perio!!!
Root resection
Indications - root fracture, perforation root caries, root resorption, severe perio disease, grade II,III furcation
Contraindications -medical/physical issues, fused roots
Most frequent complications -caries in furcation areas, root fracture
