Apikale benresorpsjoner, tilheling av fistler og apikale forandringer
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Apikale benresorpsjoner, tilheling av fistler og apikale forandringer
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 • Nivåer – – – – Klinikk Røntgen Histologi Biologiske mekanismer • Dentinresorpsjon – Mest aktuell • Andre osteolytiske prosesser: cyster, tumorer 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 1 Hvordan oppstår odonto/osteoklaster? • Osteoclasts formation requires the presence of RANK ligand (receptor activator of nuclear factor κβ) and MCSF (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/osteoklaster? • • • • 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 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. 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). www.drstoute.com/procedures/path1.htm ameloblastoma http://en.wikipedia.org/wiki/Osteoclast; 2007-06-21 2 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? 3 Where are the microbes? AP PDL Nordahl, Mjør, Haapasalo, Ørstavik Infected dentin? Side connections? P No cells available to start digesting Surface repair resorption Ankylosis ---- Inflammatory root resorption Microtrauma? Etter Haapasalo 2004 Behandling av intern resorpsjon Elisabeth Samuelsen 4 Elisabeth Samuelsen Fuss et al. 2003 Heithersay 2004 5 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 Heithersay 2004 Heithersay 2004 Heithersay 2004 Fig 9 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.) A low powered photograph shows the walling off of the pulp space by dentin separating it from the surrounding extensive resorptive process Fig 12 Heithersay 2004 Heithersay 2004 6 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 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 glassionomer cement. Adjunctive orthodontic extrusion may be employed in some advanced lesions. Heithersay 2004 Fig 18a Heithersay 2004 7 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 8 Endo memento 1998-03-03 14 år gammel pike Fraktur midtrot; lingualt dislokert; 12 (!) asensibel; 11,21(!),22,23 pos • ”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 Fraktur midtrot; lingualt dislokert; 12 (!) asensibel; 13,11,21(!),22,23 pos Kontroll 11 mndr; alle pos sens remplassert; fiksert labialt; 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. Rett etter fjernelse av fiksering; 13 til 23 nå pos senstest 1999-02-22 2009-09-16 Kontroll 14 år; alle pos sens test; ingen subj sympt. 2012-09-06 ”Stå stille, ikke bare gjør noe” 2012-09-06 2009-09-16 9 Transient AP Respons på subluksasjon Day 0 Respons på subluksasjon Boyd 1995 Day 0 1 month 1 month 4 months 10 months EPT høy terskel; CO2 kulde positiv; EPT tilbake etter 4 mndr 27 months 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 10 2009-09-30 2009-09-30 Tann 12 11 22 23 34 43 2009-09-30 T0 T+14d T+34d 0916 0930 1020 41 80 80 39 45 28 70 80 48 80 2009-09-30 10 % falske svar på EPT 2009-10-20 2009-10-20 2009-10-27 2009-10-27 11 2011-10-19 2010 La tilheling skje uforstyrret, men behandle infeksjonen før den ”setter seg” Prognostiske vurderinger Langtidseffekter av behandlingsbeslutninger Estetikk Problematisering: obliterasjon 11 Endodonti, kirurgi og protetikk etter traume 2009-2012 Endodonti, kirurgi og protetikk etter traume 2009-2012 Kroniske traumer/senfølger: Cervikal resorpsjon 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 Endodonti (nesten) alltid nødvendig ved cervikale resorpsjoner 12 Senfølger: transplantasjon/kjeveortopedi? Her er agenesi startpunkt for behandling; det kan også være traumer Ferdigbehandlet -> 1-års-kontroll, ingen data siden. 60% i funksjon etter 1,5 til 7 års observasjon, færre i denne kategorien Pike, 17 år. Agenesi 15,14,12,22,24,25 Kontinuerlig kjeveortopedi 4 år 2004: Autotranspl 45 til 13 og 34 til 22 Uformell endo-konsult oktober 2012, OPG juni 2012 Feb 2008 Ktr 2 år 2012. Passe fornøyd med estetikken. Anbefales gingivektomi og laminat på ”22”. -> spes-klinikk OPG Juni 2012 Jun 2012: Totalobliterasjon av ”22”; endodonti-konsultasjon 13 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 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 2004 09 15: til endodontisk 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 endodontisk behandling; 2 fistler: 2 måneder uten oppfølging 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 Harald Prestegaard, UiO 2005 01 12: Fistler lukket, tilheling apikalt, men 13M verre (infeksiøs rotresorpsjon), og stadig øm: ekstraheres Harald Prestegaard, UiO 14 Rotfylt tann vs implantat Rotfylt tann Implantat • Pro: • Pro: – Etter full tilheling, topp prognose – Bevarer alveolarprosess; enkel vei til god estetikk – Kan etterfølges av ny behandling • Con: 2006 03 21: Implantater 13 og 21, asymptomatisk med full tilheling 11. Rotfylt før permanent restaurering – Traumetenner mindre studert – Uforutsigbare senskader – Etter full tilheling, topp prognose – Kjente og begrensede komplikasjoner • Con: – Lang behandlingstid – Vanskeligere estetikk – irreversibelt Harald Prestegaard, UiO Endodonti vs implantat 100 80 60 Prosent 40 20 0 Endo Success Survival Impl Repair Synkope og fall mars 2004 Start endo sept 2004 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 Birte Nikolaisen: Nov 2004 periradicular periodontitis (p = 0.001), post placement (p = 0.013), and overfilling (p = 0.003). 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. Birte Nikolaisen Ingen blødning, asymptomatisk, kirurgi utsatt, ble ikke aktuelt 15 List opp vilkårene for tannresorpsjon • Dentin må eksponeres: Eksamensspørsmål – 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 Hva er typisk for intern rotresorpsjon? 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 • 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) – Isolerte – Multiple 16 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 Beskriv de 4 klassene for cervikal rotresorpsjon • 1 Hva er typisk for cervikal rotresorpsjon? • Klinisk – Gjerne asymptomatisk – Pink spot kan forekomme – Kan simulere karies I tannhalsen – 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 – ”Møllspist” dentin; ekstensjoner også aksialt i tannen – Kan omslutte pulpa; omrisset av den kan gjenkjennes • Histologisk – Invasjon av osteoid vev i resorpsjonsområdet PU.1 regulates cytokine-dependent proliferation and differentiation of granulocyte/macrophage progenitors – Lokalisert i samlet kavitet uten utløpere • 2 • Røntgenologisk A mononuclear phagocyte colony-stimulating factor (M-CSF) synthesized by mesenchymal cells 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). 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. 17