Seminar 9A: Resorption prof Flashcards
1
Q
What is dental resorption?
A
Physiological or pathological process
Loss of dentine and or cementum by hard tissue resorbing cells
2
Q
How does the clinical presentation of physiological and progressive resorption differ ?
A
Both often asymptomatic BUT progressive can become symptomatic in advanced stages
3
Q
What is the major risk of late diagnosis of resorption ?
A
Tooth loss
4
Q
How is dentine protected from resorption ?
A
Non mineralised structure : pre dentine and odontoblasts
5
Q
How is cementum protected from resorption ?
A
Non mineralised layer: pre cementum
Cells: cementoblasts
6
Q
Other than cells and non mineralised layer what else protects dentine and cementum from resorption ?
A
- Anti invasion factor from pre dentine and pre cementum, cartilage and blood vessel walls
- Intact PDL
- Hyaline layer of hopewell smith
7
Q
How does intact PDL prevent resorption ?
A
Prevents multinucleated dentinoclast cells from attaching to dental hard tissues
8
Q
What is the hyaline layer of hopewell smith?
A
Highly mineralised intermediate cementum layer
It MAY originate from the HERS
9
Q
What type of resorption does the HLHS protect against ?
A
External root resorption
10
Q
What does the HLHS cover ?
A
Dentinal tubules
11
Q
What does the HLHS prevent happening ?
A
Root canal irritants from escaping and reaching the PDL
12
Q
What type of cells perform resorption?
A
Multinucleated giant cells or CLASTIC cells
13
Q
What is the first cellular process of the clast cells during resorption ?
A
Attachment of the clastic cell membrane to the hard tissue
14
Q
In the cytoplasm of clast cells what zone must be attached to the hard tissue?
A
Clear zone
15
Q
What type of border is formed between the hard tissue and clast cell?
A
Ruffled border
Increased surface area for cocktail of enzymes to be released from and create a low pH environment
16
Q
What cells resorb bone?
A
Osteoclasts
17
Q
What cells resorb dentine and cementum?
A
Dentinoclasts
18
Q
What are the differences between osteoclasts and dentinoclasts?
A
Dentinoclast: smaller, fewer nuclei and minimal clear zone
19
Q
What two factors must occur prior to resorption to taking place?
A
- Damage to the non mineralised components
- Disruption to the odontoblasts , fibroblasts and cementoblasts which would usually offer protection
This allows colonisation of the clast cells
20
Q
What activates clast cells following injury ?
A
Acute inflammation
21
Q
By what process allows for progressive resorption?
A
Chronic inflammation either pulp or PDL
22
Q
How can resorption be classified ?
A
Site
Aetiology
Pathogenesis
23
Q
What are the types of pulpal resorption by site aetiology and pathogenesis
A
Internal
-transient
-progressive (sustained by bacteria or products OR sustained by cytotoxic materials during pulp therapy
24
Q
What are the types of non pulpal resorption by site aetiology and pathogenesis?
A
External
-transient
-progressive external without persistent inflammation (replacement resorption)
-progressive external with persistent inflammation of PDL
-progressive associated with systemic diseases
-progressive idiopathic resorption
25
What are the subcategories for progressive external resorption caused be persistent localised inflammation of PDL?
Root canal infection
Pressure
Foreign material
Subgingival plaque
26
Internal resorption occurs due to damage to what ?
Pre dentine and odontoblast layer
27
What is internal resorption sustained by ?
Pulpal inflammation
28
What can cause internal resorption?
Trauma
Restorative procedures / materials
Orthodontics
29
How common is internal resorption?
Very rare (0.1-1.6%) of permanent teeth affected
30
What symptoms does transient internal resorption present with?
Unlikely to be symptomatic because the pulpal inflammation is not sustained
31
In progressive internal resorption what is the initial stimulus to cause pulpal inflammation?
Bacteria and or products or materials that leak thru dentinal tubules or cracks
32
In the early stages of progressive IR what happens to the coronal pulp?
Becomes inflamed and then necrotic
33
What provides the ongoing blood supply for the progressive IR?
The resorptive tissue and the pulp tissue apical to this
34
When does progressive IR cease?
Once the pulp has necrotised
35
What will affect the rate of progressive internal resorption?
The strength of the inflammatory stimulus
36
In some cases of progressive IR calcified tissue can found inside the inflamed resorptive defect - what is this called?
Internal replacement resorption or
Metaplastic resorption
37
What are the clinical signs of IR?
If pulp chamber affected can lead to a pink spot on the crown
38
Why does the crown appear pink in IR?
The vascularised resorptive tissue is undermining the coronal enamel
39
In cases of IR would you expect pulp tests to be positive or negative ?
Positive as vital pulp is required to sustain the resorption
40
In some cases of IR why would the pulp
Test be negative ?
If the coronal pulp is necrotic then this may give a false negative as apically there maybe vital tissue OR
if the internal resorption has ceased as the pulp is truly/fully necrotic
41
In what scenario would patients develop symptoms in IR?
If the necrotic pulp becomes infected
42
How does IR present radiographically ?
Well circumscribed
Symmetrical
Oval
Pulp chamber cannot be seen through the lesion
43
In a mesio-distal parallax view how does IR appear?
Remains the same
44
In what circumstances can you have PARLs in IR?
total pulp necrosis
Root wall perforation
45
In which circumstance can it be difficult to determine internal or external resorption ?
When an IR lesion has increased in size so much that it has breached the root wall
46
How soon after identifying IR should root canal be commenced and why?
As soon as detected
To prevent root perforation and lesion progression
47
What concentration of NaOCl should be used in IR cases?
5% to help dissolve the inflamed tissue
48
What else could you consider using to enhance the effect of NaOCl in IR cases?
Ultrasonics
49
What should be checked for in cases of internal resorption once the canal is located?
A perforation using a curved file attatched to an apex locator. Want to ensure hypo is not extruded through any perforation
50
What inter-visit medicament should be used in PIR cases and why?
CaOH
-prevents recolonisation by bacteria
-facilitates removal of any residual inflamed tissue in the resorptive lesion
51
If there is an extensive lesion in PIR how would this change the use of CaOH?
Long term dressing should be left to induce hard tissue genesis
52
In what PIR circumstances would you delay obturation?
When there is a large lesion you may want to wait until bone healing has occurred to avoid extrusion of root canal filling material
53
What obturation methods may you consider using in PIR cases ?
-Thermoplasticed GP
-Combination of vertical and lateral compaction to fill void
-surgical approach to explore the defect
54
When are you most commonly expected to see external resorption?
1. Severe dental trauma
2. apical periodontitis
3. ortho treatment
55
Which part of the root is most commonly affected by external resorption?
Apical ++
Lateral and cervical less common
56
In transient ER to what tissues/cells has there been injury to?
precementum
cementoblasts
57
What is another name of transient ER?
external surface resorption
58
In which traumatic injury cases are you more likely you to see transient ER?
Less traumatic trauma injuries as there was damage followed by repair
59
How does transient ER appear clinically?
usually asymp
60
How does transient ER appear radiographically?
Usually cannot see the small resorptive defects and they are lined by intact PDL
61
What treatment is required for transient ER?
None
62
What is the other name of progressive external resorption without persistent inflammation of periodontal tissue?
Replacement resorption
63
In what clinical circumstances would you most commonly see RR/PER?
Luxation injuries
Following re-implantation of avulsed teeth when there is been damage to at least 20% of the cementum and extensive damage to PDL
64
What two factors that would usually be secreted allows the osteoclasts to populate the denuded root surface in RR/PER?
Anti-invasion factor
Collagenase
65
Which two tissues can osteoclasts not differentiate between?
Bone and Cementum
66
In RR/PER what type of tissue is laid down following the osteoclastic activity?
Bone is laid down by osteoblasts-akin to bone remodelling
67
What is the difference between ankylosis and RR?
in ankylosis there has been no loss of cementum/dentine - fusion just happens
68
What is the clinical presentation of RR/PER?
asymp
69
What is a clinical sign of RR/PER and ankylosis?
-high pitched sound when the tooth is tapped
-no physiologic tooth movement
70
If a tooth is infraoccluded what may this be a sign of?
Ankylosis
RR/PER
71
How does RR/PER appear radiographically?
Mottling between bone and cementum
NO PDL space
72
How do you manage RR/PER?
Management is manly in the form of prevention-ensuring avulsed teeth are stored in an appropriate medium to preserve the vitality of the PDL
73
What is the pathogenesis behind PER with inflammation of PDL sustained by root canal infection ?
-Root canal infection is the most common cause of PER
-Seen in 87.3% of teeth with periradicular periodontitis likely because the cementum at the apical CEJ root thin/non existent to offer an protection against resorption
-The concentration of resorbing factors can overcome the resistance to resorption especially when the inflammation is confined to a small root area
74
In cases of dental trauma how does PER with inflammation of the PDL sustained by root canal infection arise?
-damage of PDL leading to resorption of cementum and expose underlying dentine
-if the pulp becomes necrotic and infected then microbial products can diffuse through the dentinal tubules to the periradicular tissues fuelling the inflammation
75
How would you manage cases of dental trauma leading to PER with inflammation of the PDL sustained by root canal infection?
Long term dressing with CaOH
76
What are the clinical signs and simps of PER with inflammation of the PDL sustained by root canal infection?
-symps of CAP
-in extensive cases mobility
-pulp tests -ve
77
What are the radiographic signs and clinical
symps of PER with inflammation of the PDL sustained by root canal infection?
Resorptive lesions present at any level of the root
-in cases of no luxation injuries then maybe a PARL with shortening of the root
-resorptive lesions are ill-defined, asymmetrical
-the outline of the root canal is unchanged and the lesions change with parralax
78
How would you manage PER with inflammation of the PDL sustained by root canal infection?
-Prevention: by carrying out timely RCT where there have been extensive luxation injuries
-L0ng term CaOH dressing as intervisit
79
What challenges are posed when obturating PER with inflammation of the PDL sustained by root canal infection?
Ensuring GP is not extruded
80
How does PER with inflammation of the PDL sustained by pressure arise?
-impacted teeth
-ortho
-occlusal trauma
-cysts/tumours
81
How is PER with inflammation of the PDL sustained by pressure mediated?
On a molecular basis
82
What is the management for PER with inflammation of the PDL sustained by pressure?
Removal of the source of pressure
83
How does PER with inflammation of the PDL sustained by pressure present clinically?
-Asymp
-vital pulp
-increased mobility /shortened roota
84
How does PER with inflammation of the PDL sustained by pressure present radiographically?
Intact PDL surrounding the resorptive defect
85
What procedures would you see PER with inflammation of the PDL sustained by foreign material arise?
Seen following
-connective tissue grafting
-bone grafting
-tissue regen
86
Why do you see PER with inflammation of the PDL sustained by foreign material following certain procedures?
Often root planing is carried out prior to grafting/regen and this damages the cementum so dentintinoclasts can attach to the cementum
87
In which two PER with inflammation of PDL categories present the same way clinically and radiographically?
Foreign material and SG plaque
88
What is another name for PER with inflammation of the PDL sustained by sub gingival plaque?
cervical resorption
89
How is PER with inflammation of the PDL sustained by sub gingival plaque initiated?
Damage to the cervical attachment apparatus (cementum/PDL) below epithelial attachment by:
orthodox
scaling
orthographic/DA surgery
internal bleaching
90
In cases of PER with inflammation of the PDL sustained by sub gingival plaque is the pulp usually invaded?
NO!
Due to protection offered by predentine
-The lesion spreads cervically but not into the pulp
91
In cases of PER with inflammation of the PDL sustained by sub gingival plaque when is the pulp invaded?
If the predestine layer has been damaged or mineralised
92
How does PER with inflammation of the PDL sustained by sub gingival plaque present clinically?
-Asymp initially then pulpitis in advanced stages
-may see a pink spot when the enamel is undermined
-non carious cavity can be detected subgingivally but supracrestal
-pulp is usually vital
93
How does PER with inflammation of the PDL sustained by sub gingival plaque present radiographically?
-Well circumscribed/mottled lesions present at any position cervically
-Outline of pulp intact
-Where lesion involves proximal surfaces there maybe angular bone loss
94
How do you manage PER with inflammation of the PDL sustained by sub gingival plaque?
-Surgical exposure and curettage of lesion to remove all the inflammation tissue
-Any undermined enamel/dentine should be spared to help retain the GIC restoration
95
What soln can be placed following surgical exposure and removal of the resorptive tissue in PER with inflammation of the PDL sustained by sub gingival plaque?
90% trichloroacetic acid
96
In cases of pulpal exposure following surgical removal in PER with inflammation if the PDL sustained by sub gingival plaque what should happen next?
immediate root canal treatment shaping and obturation and then restore the defect
-if not done immediately access rates are reduced significantly
97
Why would you complete the RCT first then place the GIC in PER with inflammation if the PDL sustained by sub gingival plaque?
The restoration may become dislodged
