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Resorpsjoner og
reaksjoner
Dag Ørstavik
UiO, IKO, Avd. endo 2013 http://www.uio-endo.no
Vevsreaksjoner som involverer ben og
dentin • Apikal periodontitt
– Akutte faser, abscess
– Kroniske aspekter
– Fistel
• Intern resorpsjon
• Ekstern resorpsjon
• Cervical resorpsjon
– Idiopatisk
– Multiple
• Andre osteolytiske prosesser:
cyster, tumorer
• Nivåer
– Klinikk
– Røntgen
– Histologi
– Biologiske
mekanismer
• Dentinresorpsjon
– Mest aktuell
Classification
• Local mechanical repair resorption (undetected)
• Transient root resorption
• Pressure resorption
• Infection-induced root resorption
– Internal resorption
– External inflammatory root resorption
• Cervical root resorption (incl Multiple cervical
resorptions)
• Replacement resorption (ankylosis)
Modified from Tronstad 2003
The resorptive process
• Denudation:
– Cementum
– Predentin
• Remodelling:
– Deposition
– Resorption
• Infectious/pathological
– Internal inflammatory
– External inflammatory
• Physiological/protective
– Pressure induced
– Surface repair
– Replacement/ankylosis
Menezes R, Garlet TP, Letra A, Bramante CM, Campanelli AP, Figueira Rde C, Sogayar MC, Granjeiro JM, Garlet
GP. Differential patterns of receptor activator of nuclear factor kappa B ligand/osteoprotegerin expression in human
periapical granulomas: possible association with progressive or stable nature of the lesions.
J Endod. 2008 Aug;34(8):932-8
Hvordan oppstår odonto/osteo-
klaster? • Osteoclasts formation requires the presence of RANK
ligand (receptor activator of nuclear factor κβ) and M-CSF (Macrophage colony-stimulating factor). These membrane bound proteins are produced by neighbouring stromal cells and osteoblasts; thus requiring direct contact between these cells and osteoclast precursors.
• M-CSF acts through its receptor on the osteoclast [precursor], c-fms (colony stimulating factor 1 receptor), a transmembrane tyrosine kinase-receptor, leading to secondary messenger activation of tyrosine kinase Src. Both of these molecules are necessary for osteoclastogenesis and are widely involved in the differentiation of monocyte/macrophage derived cells.
http://en.wikipedia.org/wiki/Osteoclast; 2007-06-21
Hvordan oppstår odonto/osteo-
klaster? • Osteoclasts formation requires the presence of RANK ligand (receptor activator of
nuclear factor κβ) and M-CSF (Macrophage colony-stimulating factor). These membrane bound proteins are produced by neighbouring stromal cells and osteoblasts; thus requiring direct contact between these cells and osteoclast precursors.
• M-CSF acts through its receptor on the osteoclast, c-fms (colony stimulating factor 1 receptor), a transmembrane tyrosine kinase-receptor, leading to secondary messenger activation of tyrosine kinase Src. Both of these molecules are necessary for osteoclastogenesis and are widely involved in the differentiation of monocyte/macrophage derived cells.
• RANKL is a member of the tumour necrosis family (TNF), and is essential in osteoclastogenesis. RANKL knockout mice exhibit a phenotype of osteopetrosis and defects of tooth eruption, along with an absence or deficiency of osteoclasts. RANKL activates NF-κβ (nuclear factor-κβ) and NFATc1 (nuclear factor of activated t cells, cytoplasmic, calcineurin-dependent 1) through RANK. NF-κβ activation is stimulated almost immediately after RANKL-RANK interaction occurs, and is not upregulated. NFATc1 stimulation, however, begins ~24-48 hours after binding occurs and its expression has been shown to be RANKL dependent.
• Osteoclast differentiation is inhibited by osteoprotegerin (OPG), which binds to RANKL thereby preventing interaction with RANK.
http://en.wikipedia.org/wiki/Osteoclast; 2007-06-21
Figure 2. Mode of action and biological effects of RANKL, RANK, and OPG on
bone metabolism and the immune system. (1) RANKL is expressed by
osteoblastic lineage cells (cell-bound RANKL) and activated T lymphocytes
(soluble RANKL). A truncated ectodomain form of RANKL is derived from the
cell-bound form after cleavage by the enzyme TACE. (2) All three RANKL
variants stimulate their specific receptor, RANK, which is located on
osteoclastic and dendritic cells and thus modulate various biological functions.
(3) OPG is secreted by osteoblastic lineage and other cells and acts as a
soluble receptor antagonist which neutralizes RANKL (black), and thus,
prevents RANKL-RANK interaction.4 OPG also blocks the pro-apoptotic
cytokine TRAIL (white).
Schoppet M, Preissner KT,
Hofbauer LC. RANK ligand and
osteoprotegerin: paracrine
regulators of bone metabolism
and vascular function. Arterioscler
Thromb Vasc Biol. 2002 Apr
1;22(4):549-53. Review.
http://en.wikipedia.org/wiki/Osteoclast; 2007-06-21
www.cda-adc.ca/.../graphics/russell_figures.htm
cuspid resorption
http://www.unige.ch/cyberdocuments/theses2002/MeiriS
D/images/image051.jpg
ankylose
Mavragani et al., 2000
Karies?
Nordahl,
Mjør,
Haapasalo,
Ørstavik
Where are the microbes?
AP
P
PDL
Etter Haapasalo 2004
Infected dentin? Side connections? No cells available to start digesting
Microtrauma?
----
Ankylosis
Surface repair
resorption
Inflammatory
root
resorption
Elisabeth Samuelsen
Behandling av intern resorpsjon
Elisabeth Samuelsen
Fuss et al. 2003
Heithersay 2004
Heithersay 2004
Histologic appearance
of an incisor tooth with
invasive resorption. An
intact layer of dentine
and predentine on the
pulpal aspect (*)
separates the pulp from
the resorbing tissue.
The resorption cavity is
filled with a mass of
fibrovascular tissue
with active
mononucleated and
multi nucleated classic
cells lining resportion
lacunae (arrows).
(Hematoxylin-eosin
stain; original
magnification x 40.).
(Courtesy of Dr John
McNamara.)
Heithersay 2004
Fig 9
Heithersay 2004
Heithersay 2004
Heithersay 2004
Histologic appearance of an extensive invasive cervical resorption with
radicular extensions. Masses of ectopic calcific tissue are evident both
within the fibrovascular tissue occupying the resorption cavity and on
resorbed dentin surfaces. In addition communicating channels can be
seen connecting with the periodontal ligament (large arrows). Other
channels can be seen within the inferior aspect of the radicular dentine
(small arrows). (Hematoxylin-eosin stain; original magnification x30.)
Fig 12
Heithersay 2004
A low
powered
photograph
shows the
walling off of
the pulp
space by
dentin
separating it
from the
surrounding
extensive
resorptive
process
Heithersay 2004
Mass of fibrovascular tissue infiltrated with inflammatory cells, located within
a large resorptive cavity that has a wide connection with the periodontal
tissue (large arrow). The dentin has been extensively replaced by bone-like
tissue. A small section of intact pulp can be seen on the superior aspect of
the section (small arrow). Hematoxylin-eosin stain; original magnification
x30.)
Heithersay 2004
Heithersay 2004
Heithersay 2004
Treatment
• non-surgical treatment involves topical
application of a 90% aqueous solution of
trichloracetic acid to the resorptive tissue,
curettage, endodontic treatment where
necessary, and restoration with glass-
ionomer cement. Adjunctive orthodontic
extrusion may be employed in some
advanced lesions.
Heithersay 2004
Fig 18a Heithersay 2004
Invasive Cervical Resorption
• Class 1 – Denotes a small invasive resorptive lesion near the cervical area with shallow penetration into dentine.
• Class 2 – Denotes a well-defined invasive resorptive lesion that has penetrated close to the coronal pulp chamber but shows little or no extension into the radicular dentine.
• Class 3 – Denotes a deeper invasion of dentine by resorbing tissue, not only involving the coronal dentine but also extending into the coronal third of the root.
• Class 4 – Denotes a large invasive resorptive process that has extended beyond the coronal third of the root.
Heithersay 2004
Heithersay 2004
Heithersay 2004
Endo memento
• ”Hvor er bakteriene?”
– Pulpa eksponert eller ikke
• ”Hvor lenge har de vært der?”
– Komplisert kronefraktur (infraksjoner)
– Utslåtte tenner: ikke bare periodontiet
• ”Hva er skaden på periodontiet?”
– Infeksiøs resorpsjon
– Cervikal resorpsjon – en senskade?
1998-03-03
14 år gammel
pike
Fraktur midtrot;
lingualt
dislokert;
12 (!) asensibel;
11,21(!),22,23
pos
1998-03-03
Fraktur midtrot;
lingualt dislokert;
12 (!) asensibel;
13,11,21(!),22,23 pos
remplassert;
fiksert labialt;
Rett etter
fjernelse av
fiksering;
13 til 23 nå
pos senstest
1998-03-16
Dental Trauma Guide
For root fractures where the coronal fragment have been avulsed
out of the socket please use the treatment guidelines for avulsion
otherwise proceed as described below.
Rinse exposed root surface with saline before repositioning.If
displaced, reposition the coronal segment of the tooth as soon as
possible.
Check that correct position has been reached radiographically.
Stabilize the tooth with a flexible splint for 4 weeks. If the root
fracture is near the cervical area of the tooth stabilization is
benificial for a longer period of time (up to 4 months).
Monitor healing for at least 1 year to determine pulpal status. If
pulp necrosis develops, then root canal treatment of the coronal
tooth segment to the fracture line is indicated.
2009-09-16 1999-02-22
Kontroll 11 mndr;
alle pos sens
2012-09-06
Kontroll 14 år;
alle pos sens test;
ingen subj sympt.
2009-09-16 2012-09-06 ”Stå stille, ikke bare gjør noe”
Day 0
Respons på subluksasjon
1 month
Day 0
Transient AP Respons på subluksasjon
Boyd 1995
1 month
4 months
10 months
27 months EPT høy terskel; CO2 kulde
positiv; EPT tilbake etter 4 mndr
The patient (female, 35 yrs) was in a bicycle accident
30.08.2009 and treated at the University Hospital. Teeth 33 to
41 and tooth 21 were extracted, and the maxilla was luxated
because of fracture. The patient was referred to the
Department of Prosthodontics for evaluation and treatment,
and then referred to the Department of Endodontics (Thomas
Myrhaug).
2009-09-16
+18 dager: 2009-09-16
2009-09-16
2009-09-30
2009-09-30
2009-09-30
2009-10-20
2009-09-30
2009-10-20
2009-09-30
T0 T+14d T+34d
Tann 0916 0930 1020
12 41
11 80 70 48
22 80 80 80
23 39
34 45
43 28
10 % falske svar på EPT
2009-10-27
2009-10-27
2010
2011-10-19
Endodonti, kirurgi og protetikk etter traume 2009-2012
La tilheling skje
uforstyrret,
men behandle
infeksjonen før
den ”setter seg”
Problematisering:
obliterasjon 11
Endodonti, kirurgi og protetikk etter traume 2009-2012
Prognostiske vurderinger Langtidseffekter av
behandlingsbeslutninger
Estetikk
The patient (female, 54 yrs) has had orthodontic treatment twice. The first time was when she
was 11-12 years and the second time 12 years ago (at 42). She complained to her dentist almost
a year after the first symptoms, now with signs of an acute periodontal infection. Radiographs
revealed an extensive resorptive process that had developed in her lower right canine.
C Herbjørnsen 2007
Kroniske traumer/senfølger: Cervikal resorpsjon
Endodonti (nesten) alltid nødvendig
ved cervikale resorpsjoner
Ferdigbehandlet -> 1-års-kontroll, ingen data siden.
60% i funksjon etter 1,5 til 7 års observasjon,
færre i denne kategorien
Uformell endo-konsult oktober 2012, OPG juni 2012
Senfølger: transplantasjon/kjeveortopedi? Her er agenesi startpunkt for behandling; det kan også være traumer
Feb 2008 Pike, 17 år. Agenesi 15,14,12,22,24,25
Kontinuerlig kjeveortopedi 4 år
2004: Autotranspl 45 til 13 og 34 til 22
OPG Juni 2012
Ktr 2 år 2012. Passe fornøyd med estetikken. Anbefales gingivektomi
og laminat på ”22”. -> spes-klinikk
Jun 2012: Totalobliterasjon av ”22”; endodonti-konsultasjon
Jun 2012: CBCT viser åpenbar benpatologi med overveiende sannsynlig pulpalt utspring; en apikal periodontitt med lateral lokalisasjon. Tverrsnittet viser totalobliterasjon av ”22”. Endodonti vanskelig eller umulig? Snittbilder: B Mork-Knutsen, IKO, UiO
21 år, kvinne
Fall fra sykkel
2004 07 22:
13 slått ut
[12 ikke til stede]
11, 21 slått ut
1 time etter fallet:
13, 11 remplassert,
21 tapt
2004 09 15: til endo-
dontisk behandling;
2 fistler
Harald Prestegaard, UiO
21 år, kvinne
Fall fra sykkel
2004 07 22:
13 slått ut
[12 ikke til stede]
11, 21 slått ut
1 time etter fallet:
13, 11 remplassert,
21 tapt
2004 09 15: til endo-
dontisk behandling;
2 fistler: 2 måneder
uten oppfølging
Harald Prestegaard, UiO
2004 09 15: Vanlig behandling med Ca(OH)2 etter irrigasjon NaOCl og CHX
Harald Prestegaard, UiO
2004 11 03: Fistler lukket, tilheling apikalt, men 13M? Infeksiøs resorpsjon?
Harald Prestegaard, UiO
2005 01 12: Fistler lukket, tilheling apikalt,
men 13M verre (infeksiøs rotresorpsjon), og stadig øm: ekstraheres
Harald Prestegaard, UiO
2006 03 21: Implantater 13 og 21, asymptomatisk med full tilheling 11.
Rotfylt før permanent restaurering
Harald Prestegaard, UiO
Rotfylt tann vs implantat
Rotfylt tann
• Pro:
– Etter full tilheling, topp
prognose
– Bevarer alveolarprosess;
enkel vei til god estetikk
– Kan etterfølges av ny
behandling
• Con:
– Traumetenner mindre
studert
– Uforutsigbare senskader
Implantat
• Pro:
– Etter full tilheling, topp
prognose
– Kjente og begrensede
komplikasjoner
• Con:
– Lang behandlingstid
– Vanskeligere estetikk
– irreversibelt
Endodonti vs implantat
0
20
40
60
80
100
Prosent
Endo Impl
Success Survival Repair Failure
Doyle SL, Hodges JS, Pesun IJ, Law AS, Bowles WR. Retrospective cross sectional comparison of initial nonsurgical
endodontic treatment and single-tooth implants. J Endod. 2006 Sep;32(9):822-7. NSRCT outcomes were affected by
periradicular periodontitis (p = 0.001), post placement (p = 0.013), and overfilling (p = 0.003).
Synkope og fall mars 2004
Start endo sept 2004
Birte Nikolaisen: Nov 2004
September 6th endodontic treatment of 11 and 21 was started. Both coronal and apical parts were instrumented and
dressed with Ultracal®. Teeth were reopened and inter-appointment dressing changed four times in the period from
September 6th to November 2nd due to pain and/or persistent bleeding from the canal.
Desember 2004, after MTA and
composite placement.
Ingen blødning, asymptomatisk,
kirurgi utsatt, ble ikke aktuelt
Birte Nikolaisen
Eksamensspørsmål
List opp vilkårene for
tannresorpsjon
• Dentin må eksponeres:
– Cementum eller predentin må være brutt
• Det må være bløtvev med blodtilførsel mot
dentin
– Fra pulpa
– Fra periodontiet
List opp årsaker til tannresorpsjon
• Fysiologisk/beskyttende
– Trykkindusert
– Overflatereparasjoner
– Vevsintegrasjon: Ankylose
• Infeksiøst/patologisk
– Intern resorpsjon
– Ekstern inflammatorisk
Hva er ”blunting” av røtter? Når
skjer det?
• Røttene (spesielt overkjevens
front) er forkortet og avrundet
• Forekommer etter aggressiv
kjeveortopedisk behandling
Klassifisér kliniske former av
rotresorpsjon
• Lokale resorpsjoner reparerer mikroskader i cement (ikke synlige klinisk el røntgenologisk)
• Forbigående rotresorpsjon (etter mindre traume)
• Trykkindusert rotresorpsjon (ortodonti, tannfrembrudd, tumorer)
• Infeksjonsindusert rotresorpsjon – Intern rotresorpsjon
– Ekstern inflammatorisk rotresorpsjon
• Erstatningsresorpsjon (ankylose)
• Cervikale resorpsjoner – Isolerte
– Multiple
Hva er typisk for intern
rotresorpsjon?
• Klinisk
– Gjerne asymptomatisk
– Uten tegn,
– Men kan være brutt
gjennom og gi
symptomer på
periodontitt eller
(sjelden) frakturere
• Røntgenologisk
– Jevn, nær sirkulær
– Sentrert ut fra pulpa
• Histologisk
– Nekrose koronalt, vitalt
apikalt (en stund)
Hva er typisk for ekstern
inflammatorisk rotresorpsjon?
• Klinisk
– Gjerne asymptomatisk
– Kan forløpe svært
hurtig
– Følger gjerne et
traume (intrusjon,
eksartikulasjon)
• Røntgenologisk
– Eksentriske opptak vil
vise at
periodontalspalten er
involvert
• Histologisk
– Nekrotisk infisert pulpa
– Ingen spesielle
kjennetegn i bløtvevet
Hva er typisk for cervikal
rotresorpsjon?
• Klinisk
– Gjerne asymptomatisk
– Pink spot kan
forekomme
– Kan simulere karies I
tannhalsen
• Røntgenologisk
– ”Møllspist” dentin;
ekstensjoner også
aksialt i tannen
– Kan omslutte pulpa;
omrisset av den kan
gjenkjennes
• Histologisk
– Invasjon av osteoid vev
i resorpsjonsområdet
Beskriv de 4 klassene for cervikal
rotresorpsjon
• 1 – Lokalisert i samlet kavitet uten utløpere
• 2 – Starter utbredelse sidelengs og apikalt
• 3 – Begynner å omslutte pulpa, tydelige spor i apikal
retning
• 4 – Omslutter pulpa, utløpere apikalt på begge sider av
rotkanalen
Crit Rev Oral Biol Med. 2004;15(2):64-81.
NEW MOLECULES IN THE TUMOR
NECROSIS FACTOR LIGAND AND
RECEPTOR SUPERFAMILIES WITH
IMPORTANCE FOR PHYSIOLOGICAL AND
PATHOLOGICAL BONE RESORPTION.
Lerner UH.
A mononuclear phagocyte
colony-stimulating factor
(M-CSF) synthesized by
mesenchymal cells
PU.1 regulates
cytokine-dependent
proliferation and
differentiation of
granulocyte/macrophage
progenitors
Receptor activator of nuclear
factor- B ligand (RANKL) is a
critical cytokine for osteoclast
differentiation and activation and
an essential regulator of
osteoblast-osteoclast cross-talks
(4). RANKL activates its receptor
RANK, which is located on
osteoclastic lineage cells, and this
interaction is prevented by
osteoprotegerin (OPG), which acts
as an endogenous receptor
antagonist and blocks the effects of
RANKL (4). While RANKL
enhances bone resorption and
bone loss and promotes
osteoporosis, OPG has opposite
effects (5).