Destructive membranous periodontal disease (ligneous periodontitis): a case report and 3 years follow-up

Baykul, Timuçin; Bozkurt, Yeşim Akaydin

doi:10.1038/sj.bdj.4811739

Cited by 27 publications

(23 citation statements)

References 5 publications

(17 reference statements)

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“…[31][32][33] However, the capacity to dissolve deposited fibrin in a timely manner is equally essential to maintaining health as the capacity to convert fibrinogen to fibrin. This is well illustrated by the progressive inflammation-associated, fibrindependent multiorgan pathology and impaired tissue regenerative capacity that is observed in humans and mice deficient in the key fibrinolytic protease zymogen plasminogen 27,29,30,[34][35][36][37][38][39][40][41][42] and by studies in humans and animals showing that extravascular fibrin deposition exacerbates the morbidity of a wide range of chronic human diseases, including tissue fibrosis, muscular dystrophy, rheumatoid arthritis, and multiple sclerosis, in large part through its ability to cause persistent inflammation. [43][44][45][46][47][48][49] Previous studies have suggested important roles of uPAR in cell adhesion, cell migration, cell proliferation, cell differentiation, and cell survival (Smith and Marshall 2 ; Blasi and Carmeliet 3 ; supplemental .…”

Section: Discussionmentioning

confidence: 99%

Selective abrogation of the uPA-uPAR interaction in vivo reveals a novel role in suppression of fibrin-associated inflammation

Connolly

Choi

Gårdsvoll

et al. 2010

Blood

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The urokinase plasminogen activator receptor (uPAR) has emerged as a potential regulator of cell adhesion, cell migration, proliferation, differentiation, and cell survival in multiple physiologic and pathologic contexts. The urokinase plasminogen activator (uPA) was the first identified ligand for uPAR, but elucidation of the specific functions of the uPA-uPAR interaction in vivo has been difficult because uPA has important physiologic functions that are independent of binding to uPAR and because uPAR engages multiple ligands. Here, we developed a new mouse strain (Plau GFDhu/GFDhu ) in which the interaction between endogenous uPA and uPAR is selectively abrogated, whereas other functions of both the protease and its receptor are retained. Specifically, we introduced 4 amino acid substitutions into the growth factor domain (

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Section: Discussionmentioning

confidence: 99%

Selective abrogation of the uPA-uPAR interaction in vivo reveals a novel role in suppression of fibrin-associated inflammation

Connolly

Choi

Gårdsvoll

et al. 2010

Blood

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“…[1][2][3][4][5] Because of its potent proinflammatory properties, the rate of deposition and removal of extravascular fibrin must be carefully coordinated. This is illustrated by the inflammation-associated multiorgan pathology and impaired tissue regenerative capacity of humans and mice deficient in the key fibrinolytic protease zymogen, plasminogen, [6][7][8][9][10][11][12][13][14][15][16][17] as well as by the capacity of extravascular fibrin to exacerbate the morbidity of a range of chronic human diseases, including multiple sclerosis, tissue fibrosis, muscular dystrophy, and rheumatoid arthritis. [18][19][20][21][22][23][24] Plasminogen is a serine protease zymogen present in plasma and extravascular fluids that is converted to the active protease plasmin by endoproteolytic cleavage by the closely related trypsin-like serine proteases urokinase plasminogen activator (uPA) and tissue plasminogen activator (tPA).…”

Section: Introductionmentioning

confidence: 99%

A CCR2 macrophage endocytic pathway mediates extravascular fibrin clearance in vivo

Motley

Madsen

Jürgensen

et al. 2016

Blood

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Key Points• Fibrin is cleared from extravascular space via endocytosis and lysosomal degradation by a CCR2-positive subset of inflammatory macrophages.• This novel endocytic fibrin degradation pathway is mechanistically coupled to extracellular fibrin degradation pathways.Extravascular fibrin deposition accompanies many human diseases and causes chronic inflammation and organ damage, unless removed in a timely manner. Here, we used intravital microscopy to investigate how fibrin is removed from extravascular space. Fibrin placed into the dermis of mice underwent cellular endocytosis and lysosomal targeting, revealing a novel intracellular pathway for extravascular fibrin degradation. A C-C chemokine receptor type 2 (CCR2)-positive macrophage subpopulation constituted the majority of fibrin-uptaking cells. Consequently, cellular fibrin uptake was diminished by elimination of CCR2-expressing cells. The CCR2-positive macrophage subtype was different from collagen-internalizing M2-like macrophages. Cellular fibrin uptake was strictly dependent on plasminogen and plasminogen activator. Surprisingly, however, fibrin endocytosis was unimpeded by the absence of the fibrin(ogen) receptors, aMb2 and ICAM-1, the myeloid cell integrin-binding site on fibrin or the endocytic collagen receptor, the mannose receptor. The study identifies a novel fibrin endocytic pathway engaged in extravascular fibrin clearance and shows that interstitial fibrin and collagen are cleared by different subsets of macrophages employing distinct molecular pathways. (Blood. 2016;127(9):1085-1096

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“…1 Rapor edilen cerrahi veya periodontal tedavilerde başarı sağ-lanamamıştır ancak bazı vakalarda diş kaybı sonrası lezyonların durağanlaştığı veya kaybolduğu gözlem-lenmiştir. [13][14][15][16][17]19 Baltacıoğlu ve ark. LP"li 2 vakayı bildirmişlerdir.…”

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“…6 Hipoplazminojen eksikliğinde oluşan dişeti büyümeleri ve alveol kemik kayıpları; "Amiloidoz Ülseratif Gingival Hiperplazi" , "Destrüktif Membranöz Periodontal Hastalık" veya "Lignöz Periodontitis"" olarak adlandırılır. 13,14 Dişetindeki lezyonlar LP ile ilgilidir ve diş kaybı ile birlikte kaybolmaktadır. 13,14 Etyolojisi tam olarak açık olmasa da LP, otoimmün reaksiyonlardan, travmadan, hipersensitivite reaksiyonlarından, genetik hastalıklardan ve bakteriyel veya viral enfeksiyonlardan sonra gelişebilir.…”

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Li̇gnöz Peri̇odonti̇ti̇s : Olgu Sunumu

Aytekin¹,

Hatipoğlu²,

Özgöz³

et al. 2015

Atatürk Üniversitesi Diş Hekimliği Fakültesi Dergisi

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Aim: Ligneous periodontitis is an infectious disease characterized by the inflammation of the supporting periodontal tissues, resulting in attachment and alveolar bone loss with plasminogen deficiency. This case report shows the treatment and follow-up of patient who have ligneous periodontitis.Case Report: Fifteen years old boy who had ligneous periodontitis applied to our periodontology clinic. Clinical and radiographic evaluation revealed severe periodontal breakdown around all teeth. Intraoral soft tissues were characterized by gingival reddening and swelling and the patient complained of periodic discharge of pus from the periodontal pockets, mobility, and severe pain. The probing depths were more than 7 mm %58 percent probing areas and there were radiolucent lesions around the teeth in panoramic radiograph.Full-mouth subgingival scaling and root planing under local anesthesia was performed and the pocket wall is gently retracted with a periodontal curette in an attempt to initiate drainage through the pocket entrance. Systemic amoxicillin and clavulanic acid applied for antibiotic therapy.Result: The goal of treatment was to create a clinical condition that is conducive to retaining as many teeth as possible for as long as possible but alveolar bone loss around the teeth was too severe. Systemic disorders such as plasminogen deficiency increase a patient's susceptibility to destructive periodontitis and have impacts on periodontal disease progression and severity.

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Destructive membranous periodontal disease (ligneous periodontitis): a case report and 3 years follow-up

Cited by 27 publications

References 5 publications

Selective abrogation of the uPA-uPAR interaction in vivo reveals a novel role in suppression of fibrin-associated inflammation

Selective abrogation of the uPA-uPAR interaction in vivo reveals a novel role in suppression of fibrin-associated inflammation

A CCR2 macrophage endocytic pathway mediates extravascular fibrin clearance in vivo

Li̇gnöz Peri̇odonti̇ti̇s : Olgu Sunumu

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