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bisphosphonate-associated osteonecrosis of the jaw/phosphatase
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Effects of metformin on the prevention of bisphosphonate-related osteonecrosis of the jaw-like lesions in rats
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Purpose: In this study, we aimed to investigate the effect of glucose metabolism on bone healing after tooth extraction in an osteoporosis rat model administered zoledronic acid (ZA) and dexamethasone (DX).
Bisphosphonate-induced osteonecrosis of the jaws, bone markers, and a hypothesized candidate gene.
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OBJECTIVE
To determine whether any abnormality in serum bone markers is related to bisphosphonate-induced osteonecrosis of the jaw.
METHODS
We obtained serum bone markers and other relevant endocrine assays on 7 patients with osteonecrosis of the jaws (ONJ). The assays were C-telopeptide,
Serum Markers of Bone Turnover and Angiogenesis in Patients With Bisphosphonate-Related Osteonecrosis of the Jaw After Discontinuation of Long-Term Intravenous Bisphosphonate Therapy.
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OBJECTIVE
To analyze serum markers of bone turnover, angiogenesis, endocrine function, and inflammation in patients with bisphosphonate-related osteonecrosis of the jaw (BRONJ) who discontinued long-term intravenous bisphosphonate (BP) therapy.
METHODS
Serum samples were obtained from 25 BRONJ
Normal serum bone markers in bisphosphonate-induced osteonecrosis of the jaws.
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We obtained serum bone markers and other relevant endocrine assays on 5 patients with osteonecrosis of the jaw (ONJ). The assays were C-telopeptide, N-telopeptide, bone-specific alkaline phosphatase, osteocalcin, intact parathyroid hormone, T3, T4, TSH, and Vitamin D 25 hydroxy. Diagnostic criteria
Preexisting Periapical Inflammatory Condition Exacerbates Tooth Extraction-induced Bisphosphonate-related Osteonecrosis of the Jaw Lesions in Mice.
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BACKGROUND
Surgical interventions such as tooth extraction increase the chances of developing osteonecrosis of the jaw in patients receiving bisphosphonates (BPs) for the treatment of bone-related diseases. Tooth extraction is often performed to eliminate preexisting pathological inflammatory
The effects of different doses of teriparatide on bisphosphonate-related osteonecrosis of the jaw in mice.
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Bisphosphonate-associated osteonecrosis of the jaw is linked to suppressed TGFβ1-signaling and increased Galectin-3 expression: a histological study on biopsies.
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BACKGROUND
Bisphosphonate associated osteonecrosis of the jaw (BRONJ) implies an impairment in oral hard- and soft tissue repair. An understanding of the signal transduction alterations involved can inform therapeutic strategies. Transforming growth factor β1 (TGFβ1) is a critical regulator of
Teriparatide and the treatment of bisphosphonate-related osteonecrosis of the jaw: a rat model.
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OBJECTIVE
The objectives of this study were to establish a bisphosphonate-related osteonecrosis of the jaw (BRONJ) rat model and to analyse the effects of teriparatide (TP) on this model.
METHODS
Sprague-Dawley rats were divided into three groups: I-zoledronic acid (ZA, n = 10); II-ZA and
Changes in serological bone turnover markers in bisphosphonate induced osteonecrosis of the jaws: A case control study.
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Establishment of an Animal Model of Bisphosphonate-Related Osteonecrosis of the Jaws in Spontaneously Diabetic Torii Rats.
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BACKGROUND
We evaluated the side effects of bisphosphonate (BP) on tooth extraction socket healing in spontaneously diabetic Torii (SDT) rats, an established model of non-obese type 2 diabetes mellitus, to develop an animal model of BP-related osteonecrosis of the jaws (BRONJ).
METHODS
Male
Expression of Msx-1 is suppressed in bisphosphonate associated osteonecrosis related jaw tissue-etiopathology considerations respecting jaw developmental biology-related unique features.
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BACKGROUND
Bone-destructive disease treatments include bisphosphonates and antibodies against the osteoclast differentiator, RANKL (aRANKL); however, osteonecrosis of the jaw (ONJ) is a frequent side-effect. Current models fail to explain the restriction of bisphosphonate (BP)-related and denosumab
Differential impairment of vascularization and angiogenesis in bisphosphonate-associated osteonecrosis of the jaw-related mucoperiosteal tissue.
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OBJECTIVE
Impaired vascularization in the etiopathology of aminobisphosphonate-associated osteonecrosis of the jaw (BONJ) is assumed, but evidence is lacking. This immunohistochemical study differentiated vascularization and angiogenesis in BONJ-adjacent mucoperiosteal tissue.
METHODS
Twenty BONJ
Bisphosphonate-associated osteonecrosis of the jaw: a key role of inflammation?
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Osteonecrosis of the jaw (ONJ) can be associated with nitrogen-containing bisphosphonates (NBPs) therapy. Various mechanisms of NBP-associated ONJ have been proposed and there is currently no consensus of the underlying pathogenesis. The detailed medical and dental histories of 30 ONJ patients
Experimental development of bisphosphonate-related osteonecrosis of the jaws in rodents.
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Osteonecrosis of the jaw (ONJ) following the use of bisphosphonates has become of increased interest in the scientific community, due in particular to its as-yet-unsolved pathogenesis. An experimental model of ONJ was induced in normal male rats [alendronate (ALN); 1 mg/Kg/day; n = 10] and matched
Prospective biomarker evaluation in patients with osteonecrosis of the jaw who received bisphosphonates.
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Bone biomarkers have been suggested for the risk assessment for osteonecrosis of the jaw, a serious complication associated with bisphosphonate (BP) use; however, no consensus has been reached. This study investigated the possible associations between bone biomarkers and the development of
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