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The Role of Host Inflammation and the Commensal Microbiota in the Pathogenesis of Medication-related Osteonecrosis of the Jaw.- [electronic resource]
The Role of Host Inflammation and the Commensal Microbiota in the Pathogenesis of Medicati...
The Role of Host Inflammation and the Commensal Microbiota in the Pathogenesis of Medication-related Osteonecrosis of the Jaw.- [electronic resource]

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자료유형  
 학위논문(국외)
자관 청구기호  
기본표목-개인명  
표제와 책임표시사항  
The Role of Host Inflammation and the Commensal Microbiota in the Pathogenesis of Medication-related Osteonecrosis of the Jaw. - [electronic resource] / Williams, Drake Winslow.
발행, 배포, 간사 사항  
발행, 배포, 간사 사항  
Ann Arbor : ProQuest Dissertations & Theses , 2019
    형태사항  
    1 online resource(100 p.)
    일반주기  
    Source: Dissertations Abstracts International, Volume: 80-12, Section: B.
    일반주기  
    Publisher info.: Dissertation/Thesis.
    일반주기  
    Advisor: Kim, Reuben H.
    학위논문주기  
    Thesis (Ph.D.)--University of California, Los Angeles, 2019.
    이용제한주기  
    This item must not be sold to any third party vendors.
    요약 등 주기  
    요약Bisphosphonates (BPs) and denosumab (Dmab) are anti-resorptive drugs that are clinically used to treat bone disorders like osteoporosis and bone metastases. A detrimental side effect of these drugs that uniquely occurs in the oral cavity is BP- and Dmab-related osteonecrosis of the jaw (collectively called medication-related osteonecrosis of the jaw, or MRONJ), clinically defined as exposed necrotic bone with unclosed overlaying oral mucosa for at least 8 weeks. Although the first report of ONJ by BPs appeared in 2003, the exact pathophysiology of MRONJ is still largely unknown. Our laboratory has been working to examine and elucidate the pathophysiology of MRONJ. Previously, we established mouse models for MRONJ utilizing bisphosphonate and 慣RANKL antibody and identified that woven bone formation and inhibition of bone resorption are hallmarks of murine MRONJ lesions. We also utilized semi-unbiased gene profiling to identify and validate the importance of IL36 signaling in MRONJ pathogenesis.MRONJ often occurs following a dental intervention such as a tooth extraction which is typically performed to eliminate localized periodontal or periapical inflammation. Periodontal disease is caused by polymicrobial infection and subsequent host immune response
    주제명부출표목-일반주제명  
    부출표목-단체명  
    기본자료저록  
    Dissertations Abstracts International. 80-12B.
    기본자료저록  
    Dissertation Abstract International
    전자적 위치 및 접속  
     원문정보보기

    MARC

     008200317s2019        ulk          s          00        eng
    ■001000015491765
    ■00520200217181411
    ■007cr
    ■020    ▼a9781392233672
    ■040    ▼d225006
    ■08204▼a617.6
    ■090    ▼a전자도서(박사논문)
    ■1001  ▼aWilliams,  Drake  Winslow.
    ■24514▼aThe  Role  of  Host  Inflammation  and  the  Commensal  Microbiota  in  the  Pathogenesis  of  Medication-related  Osteonecrosis  of  the  Jaw.▼h[electronic  resource]▼cWilliams,  Drake  Winslow.
    ■260    ▼a[S.l.]▼bUniversity  of  California,  Los  Angeles.  ▼c2019
    ■260  1▼aAnn  Arbor▼bProQuest  Dissertations  &  Theses▼c2019
    ■300    ▼a1  online  resource(100  p.)
    ■500    ▼aSource:  Dissertations  Abstracts  International,  Volume:  80-12,  Section:  B.
    ■500    ▼aPublisher  info.:  Dissertation/Thesis.
    ■500    ▼aAdvisor:  Kim,  Reuben  H.
    ■5021  ▼aThesis  (Ph.D.)--University  of  California,  Los  Angeles,  2019.
    ■506    ▼aThis  item  must  not  be  sold  to  any  third  party  vendors.
    ■520    ▼aBisphosphonates  (BPs)  and  denosumab  (Dmab)  are  anti-resorptive  drugs  that  are  clinically  used  to  treat  bone  disorders  like  osteoporosis  and  bone  metastases.  A  detrimental  side  effect  of  these  drugs  that  uniquely  occurs  in  the  oral  cavity  is  BP-  and  Dmab-related  osteonecrosis  of  the  jaw  (collectively  called  medication-related  osteonecrosis  of  the  jaw,  or  MRONJ),  clinically  defined  as  exposed  necrotic  bone  with  unclosed  overlaying  oral  mucosa  for  at  least  8  weeks.  Although  the  first  report  of  ONJ  by  BPs  appeared  in  2003,  the  exact  pathophysiology  of  MRONJ  is  still  largely  unknown.  Our  laboratory  has  been  working  to  examine  and  elucidate  the  pathophysiology  of  MRONJ.  Previously,  we  established  mouse  models  for  MRONJ  utilizing  bisphosphonate  and  慣RANKL  antibody  and  identified  that  woven  bone  formation  and  inhibition  of  bone  resorption  are  hallmarks  of  murine  MRONJ  lesions.  We  also  utilized  semi-unbiased  gene  profiling  to  identify  and  validate  the  importance  of  IL36  signaling  in  MRONJ  pathogenesis.MRONJ  often  occurs  following  a  dental  intervention  such  as  a  tooth  extraction  which  is  typically  performed  to  eliminate  localized  periodontal  or  periapical  inflammation.  Periodontal  disease  is  caused  by  polymicrobial  infection  and  subsequent  host  immune  response
    ■650  4▼aDentistry.
    ■71020▼aUniversity  of  California,  Los  Angeles▼bOral  Biology  0615.
    ■7730  ▼tDissertations  Abstracts  International▼g80-12B.
    ■773    ▼tDissertation  Abstract  International
    ■791    ▼aPh.D.
    ■792    ▼a2019
    ■793    ▼aEnglish
    ■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T15491765▼nKERIS

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