Resorption 1 - Intro + Internal - 2020 Flashcards
What is required for root resorption?
Continual stimulation
Breakdown of the natural barriers (cannot control but can be prevented)
A blood supply
What factors should be considered when managing patients with resoption?
Can’t control the breakdown of natural barriers if the resorption has started but the continual stimulation can be removed and the blood supply can be reduced.
What are the types of resorption?
Internal and external.
Internal can be surface, inflammatory or replacement
External can be surface, inflammatory, replacement, invasive, orthodontic, pressure, physiological, or idiopathic.
What is internal root resorption?
Internal resorption caused by removal of dentin by clastic cells. It begins at the root canal wall and progresses through dentin towards the cementum.
May also resorb cementum and perforate the external root surface
How common is internal root resorption?
Not very common and affects 1 in 1000 teeth.
Typically 1 tooth per patient
Very occasionally 2 adjacent teeth with trauma the likely factor
Which teeth commonly are affected by internal root resorption?
2% of luxated teeth
Cabrini et al showed that 28% occur following pulpotomy
Ahlberg et al showed that 55% occur after autotransplantation
What is internal resorption often confused with?
External invasive root resorption
What is the most common type of internal root resorption?
Internal inflammatory resorption
What are the less common types of internal root resorption?
Internal surface resorption is very rare and cannot be detected clinically or radiographically
Internal replacement resorption is also very rare and is not well known or understood. Can easily be confused with external invasive resorption
What are the features of internal SURFACE resorption?
Minor areas of resorption of the root canal wall
Not visible radiographically
Only noted histologically
Believed to be self limiting if the irritant is removed
May be a precursor to internal inflammatory resorption?
What are the possible causes of internal SURFACE resorption?
Trauma to the tooth
Necrosis + infection of the coronal pulp
External whitening/bleaching of the tooth
Aetiology is UNKNOWN in most cases.
What did the Seale et al study show about internal root resorption?
Dog teeth treated with 35% hydrogen peroxide applied once per week for 4 week experienced internal surface resorption and active dentinoclasts were seen.
What is the pathogenesis of internal root resorption?
Largely unknown
Needs a stimulus (as discussed)
Transient in nature
How is internal surface resorption diagnosed?
Can not diagnose clinically
Can not be diagnosed radiographically but progression to inflammatory can be monitored radiographically
How is internal surface resorption managed?
If resorption continues as seen radiographically it is like internal inflammatory resorption
Therefore do root canal treatment
What are the features of internal inflammatory resorption?
Usually described as a radiolucent “oval-shaped” increase of pulp space (not necessarily always oval shaped though)
It can occur anywhere along the length of the canal
What are the possible causes of internal inflammatory resorption?
Trauma to the tooth
Necrosis + infection of the coronal pulp
Caries + Perio disease.
Aetiology is not always known or obvious
What is the pathogenesis of internal inflammatory resorption?
Bacteria in the pulp -> Damage to odontoblast layer and predentine of the canal wall must be damaged -> Exposure of mineralised dentine to clastic cells
Anything that irritates the pulp can cause this to happen
How does the causative agent of internal root resorption affect the type of root resorption observed?
If the cause of pulpitis was not bacteria, the number of macrophage-like cells declined after 6 - 10 weeks and fibroblast-like cells and hard tissue started forming.
If the cause was bacteria more extensive resorption was observed
What are the histological features of teeth that have undergone internal inflammatory root resorption?
Bacteria detected in the dentinal tubules and the pulp space coronal to the resorptive defect where the pulp was necrotic
The clastic cells had strong tartrate resistant acid phosphatase activity and lack of odontoblasts.
Normal pulp tissue was not present (no odontoblasts and no predentin were present and instead the pulp was replaced by periodontal-like connective tissue)
Apical third of the canal had inflamed pulp.
What is the overall pathogenesis of internal inflammatory resorption?
Coronal to the resorptive defect = necrotic and infected pulp tissue
Within the resorptive defect = Grnaulation tissue with clastic cells
Apical to the resorption area = pulp will be irreversibly inflamed or replaced with periodontal like connective tissue unless resorption no longer active
Progression due to interaction between the bacteria
and the tissue remaining apically - until it necroses
The “bacterial front” gradually moves apically
through the root canal until all the pulp necroses
As occurs in all teeth with pulp disease
2 phases for this resorption: Active and inactive phase.
How is internal inflammatory resorption diagnosed?
Radiographic appearance. Radiolucent area within the tooth showing enlargement of the root canal space with or without periapical radiolucency.
What are the clinical features of internal inflammatory resorption?
Usually same as teeth with pulpless infected root canal systems
PA conditions can vary (chronic apical periodontitis, chronic apical abscess, acute apical periodontitis)
How is internal inflammatory resorption differentiated from external invasice resorption?
External invasive resorption is characterised by sub-gingival origin.
Radiolucent areas with poorly defined margins
Very vascular tissue that bleeds easily
Can resemble caries or internal root resorption.
How commonly is external inflammatory resorption misdiagnosed as internal resorption?
In a study by Dr Abbott 36% of extensive invasive resorption cases were referred to as internal resorption.
What are pink teeth most commonly caused by?
Most likely due to external invasive resorption not internal inflammatory resorption.
What is required for internal inflammatory resorption and allows us to confidently assume pink teeth are caused by external invasive resorption?
Internal inflammatory resorption needs necrotic and infected pulp tissue coronal to the resorbing area to stimulate the resorption
There is insufficient space for this in the crown of the tooth.
How is internal inflammatory resorption managed?
Remove the pulp (if present)
Thoroughly clean and prepare the root canal
Medicate the root canal system
How would the active and inactive phase of internal inflammatory resorption be affected by resorption?
Active phase: would be necrotic coronally, inflamed / connective tissue apically
Inactive phase: Canal will be pulpless
What is the aim of cleaning and preparing the root canal?
Aim to remove resorbing cells and blood supply
Copious irrigation especially with 1% NaOCl
What is the aim of medicating the root canal system?
Medicate the root canal system to inhibit and destroy the clastic cells and remaining bacteria
Which intra canal medicaments should be used for internal inflammatory resorption?
Corticosteroid - antibiotic compound
Ca(OH)2
Combination -> CS-AB paste + Ca(OH)2
What are the effects of corticosteroids and tetracyclines?
Corticosteroids: ANti-inflammatory, antiresorptive, promote healing and are biocompatible
Tertracyclines: Anti-microbial, anti-resorptive, reduce replacement resorption and ankylosis, and promote PDL healing
What are the antiresorptive effects of CS-AB pastes?
CS: Directly inhibit and prevent attachment of clastic cells
Tetracyclines: Directly inhibit collagenase and clastic cells
What are the steps of managing internal inflammatory resorption?
1) Remove the pulp (if any present)
2) Thoroughly clean and prepare the root canal
3) Initially use CS-AB paste for 4 weeks (reduce inflammation, inhibit clastic cells, and anti-bacterial action)
4) Then use Ca(OH)2: Use 2 or 3 times - for 4 weeks each time.
5) Root canal filling - GP and sealer (use a thermoplastic technique for GP or lateral condesnation apically and then warmp GP in resorption defect)
Why is Ca(OH)2 used?
Anti-bacterial
Dissolves necrotic tissue
Kills resorbing cells
Inactivates LPS
Encourages hard tissue repair (Esp if the resorptive lesion has perforated the root)
How often should RCT treatment of internal inflammatory resorption be treated?
Clinical and radiographic reviews are essential.
Initially 6 months after RCF is completed.
Then every 3 - 4 years for as long as possible.
What is the prognosis of internal inflammatory treatment?
Very few studies due to rare occurrence but generally considered to have good or excellent prognosis after root canal treatment if no perforation and if tooth not weakened too much through loss of tooth structure
What is the definition of root resorption?
Resorption is either a physiological or a pathological process which results in the loss of substance from the tissue
What causes internal inflammatory resorption?
Most commonly associated with trauma and caries + PD disease
What is the pathogenesis of internal inflammatory resorption?
Bacteria in the pulp
Odontoblast layer and predentine of the canal wall are damaged
Mineralised dentin gets exposed to clastic cells
Injurious event that is needed to cause this damage is not known but could be anything that irritates the pulp.
Coronal to the resorption defect is necrotic and infected pulp, within the resorptive defect is granulation tissue with clastic cells, and apical to the resorption defect is irreversibly inflamed pulp tissue replaced with periodontal like connective tissue. (If there is no longer resorption then the entire canal will be pulpless and infected)
Progression occurs due to interaction between the bacteria and the remaining apical tissue until it necroses
Bacterial front gradually moves apically through the root canal until all the pulp necroses
What are the active and inactive phase of internal inflammatory resorption?
During the active phase: The necrotic tissue and the granulation + clastic tissue moves throughout the root to the apex.
During the inactive phase: PA radiolucency will form enlarging the root canal space. The shape and size are variable. This may or may not have a PA radiolucency.
How can external invasive resorption be differentiated from internal inflammatory resorption?
External invasive resorption is often subgingival and can be felt with a probe whereas internal inflammatory resorption can only be seen on radiograph.
Radiolucent area in external invasive resorption often has poorly defined margins whereas internal inflammatory resorption has well defined margins.
External invasive resorption leads to lots of bleeding whereas theres no bleeding caused by internal inflammatory resorption.
External invasive resorption causes pink teeth not internal inflammatory resorption.
What does Ca(OH)2 do for internal inflammatory resorption?
Anti-bacterial
Dissolves necrotic tissue
Kills resorbing cells
Inactivates LPS
How is internal replacement resorption typically diagnosed?
Often through incidental finding on radiograph. (Irregular enlargement of pulp space, and presence of bone replacing pulp and dentin)
Can be differentiated from external invasive resorption via probing, tube-shift, and CBCT.
