Quantitation and distribution of metallic elements in sequestra of medication-related osteonecrosis of jaw (MRONJ) using inductively coupled plasma atomic emission spectroscopy and synchrotron radiation X-ray fluorescence analysis

Komiya, Ruri; Wada, Takahiro; Tsushima, Fumihiko; Sakamoto, Kei; Ikeda, Tohru; Yamaguchi, Akira; Harada, Hiroyuki; Uo, Motohiro

doi:10.1007/s00774-018-0975-3

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…A unique developmental process for enamel produces the most dense calcified tissue in the body: ~96% inorganic material (HA) and 4% organic material and water by weight [55][56][57][58]. In comparison, osseous tissue with the greatest mineral density is a nonvital sequestrum [131] and the abnormal bone of osteogenesis imperfecta (OI), i.e., brittle bone disease [132]. Medication-related oral necrosis of the jaw (MRONJ) results in exposed oral bone sequestra [131].…”

Section: Pathologic Perspectivesmentioning

confidence: 99%

“…In comparison, osseous tissue with the greatest mineral density is a nonvital sequestrum [131] and the abnormal bone of osteogenesis imperfecta (OI), i.e., brittle bone disease [132]. Medication-related oral necrosis of the jaw (MRONJ) results in exposed oral bone sequestra [131]. Under the influence of resorption-suppressing medications, e.g., bisphosphonates and denosumab, large sections of oral bone may die and hypermineralize to form a sequestrum particularly in areas of osseous infection [128].…”

Section: Pathologic Perspectivesmentioning

confidence: 99%

“…Accelerated mineral deposition to form enamel, bone sequestrum, and OI bone may involve substantial incorporation of trace elements (Sr, Zn, and Cu) which affects mechanical properties [133]. However, hypermineralized sequestra [131] and OI bone [132,134] are still at least 50% mineralized collagen so they are not nearly as hard or resorption resistant as enamel. Indeed, enamel is a unique genetic tissue that has no peer among other mineralized tissues relative to density, strength, rigidity, and hardness [38,[55][56][57][58].…”

Section: Pathologic Perspectivesmentioning

confidence: 99%

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Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

Roberts

Mangum

Schneider

2022

Curr Osteoporos Rep

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Purpose of the Review Compare pathophysiology for infectious and noninfectious demineralization disease relative to mineral maintenance, physiologic fluoride levels, and mechanical degradation. Recent Findings Environmental acidity, biomechanics, and intercrystalline percolation of endemic fluoride regulate resistance to demineralization relative to osteopenia, noncarious cervical lesions, and dental caries. Summary Demineralization is the most prevalent chronic disease in the world: osteoporosis (OP) >10%, dental caries ~100%. OP is severely debilitating while caries is potentially fatal. Mineralized tissues have a common physiology: cell-mediated apposition, protein matrix, fluid logistics (blood, saliva), intercrystalline ion percolation, cyclic demineralization/remineralization, and acid-based degradation (microbes, clastic cells). Etiology of demineralization involves fluid percolation, metabolism, homeostasis, biomechanics, mechanical wear (attrition or abrasion), and biofilm-related infections. Bone mineral density measurement assesses skeletal mass. Attrition, abrasion, erosion, and abfraction are diagnosed visually, but invisible subsurface caries <400μm cannot be detected. Controlling demineralization at all levels is an important horizon for cost-effective wellness worldwide.

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Section: Pathologic Perspectivesmentioning

confidence: 99%

Section: Pathologic Perspectivesmentioning

confidence: 99%

Section: Pathologic Perspectivesmentioning

confidence: 99%

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Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

Roberts

Mangum

Schneider

2022

Curr Osteoporos Rep

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“…Any irregularity along an enamel surface (fracture, chip, crack, or bonded attachment) may retain plaque and be cariogenic. In addition, plaque adhering to exposed oral bone sequestra inflame the surrounding mucosa [46,[90][91][92]. From a physiologic perspective, WSLs are localized pathologic processes (caries) that may or may not be active [83].…”

Section: Detection and Assessment Of White Spotsmentioning

confidence: 99%

Pathophysiology of Demineralization, Part II: Enamel White Spots, Cavitated Caries, and Bone Infection

Roberts

Mangum

Schneider

2022

Curr Osteoporos Rep

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Purpose of Review Compare noninfectious (part I) to infectious (part II) demineralization of bones and teeth. Evaluate similarities and differences in the expression of hard tissue degradation for the two most common chronic demineralization diseases: osteoporosis and dental caries. Recent Findings The physiology of demineralization is similar for the sterile skeleton compared to the septic dentition. Superimposing the pathologic variable of infection reveals a unique pathophysiology for dental caries. Summary Mineralized tissues are compromised by microdamage, demineralization, and infection. Osseous tissues remodel (turnover) to maintain structural integrity, but the heavily loaded dentition does not turnover so it is ultimately at risk of collapse. A carious tooth is a potential vector for periapical infection that may be life-threatening. Insipient caries is initiated as a subsurface decalcification in enamel that is not detectable until a depth of ~400μm when it becomes visible as a white spot. Reliable detection and remineralization of invisible caries would advance cost-effective wellness worldwide.

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“…Antiresorptive agents, such as bisphosphonate and denosumab, are widely used as the first‐line therapies for patients with osteoporosis or metastatic bone tumours 1 . However, medication‐related osteonecrosis of the jaw (MRONJ) is a serious adverse effect of those antiresorptive agents 2 …”

Section: Introductionmentioning

confidence: 99%

Bone single‐photon emission computed tomography‐CT peak standardized uptake value for chronic osteomyelitis, osteoradionecrosis and medication‐related osteonecrosis of the jaw

Minami

Ogura

2020

J Med Imag Rad Onc

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Introduction Recently, standardized uptake value (SUV) has been applied for the evaluation of SPECT‐CT. This study was performed to investigate the bone SPECT‐CT peak SUV for chronic osteomyelitis, osteoradionecrosis and medication‐related osteonecrosis of the jaw (MRONJ). Methods Sixty‐five patients with jaw lesions (12 chronic osteomyelitis, 12 osteoradionecrosis and 41 MRONJ) underwent SPECT‐CT after injection of technetium‐99m hydroxymethylene diphosphonate. The peak SUV was compared for the chronic osteomyelitis with osteoradionecrosis and MRONJ using GI‐BONE software. Statistical analyses for the peak SUV were performed by one‐way repeated measures analysis of variance with Tukey's HSD test. A P‐value lower than 0.05 was considered as statistically significant. Results Peak SUV for chronic osteomyelitis (15.6 ± 4.4) was significantly higher than those for osteoradionecrosis (6.7 ± 2.1, P = 0.000) and MRONJ (10.7 ± 6.1, P = 0.019). Conclusion The SPECT‐CT peak SUV using GI‐BONE software can be useful for the evaluation of jaw lesions, such as chronic osteomyelitis, osteoradionecrosis and MRONJ.

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Quantitation and distribution of metallic elements in sequestra of medication-related osteonecrosis of jaw (MRONJ) using inductively coupled plasma atomic emission spectroscopy and synchrotron radiation X-ray fluorescence analysis

Cited by 6 publications

References 22 publications

Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

Pathophysiology of Demineralization, Part I: Attrition, Erosion, Abfraction, and Noncarious Cervical Lesions

Pathophysiology of Demineralization, Part II: Enamel White Spots, Cavitated Caries, and Bone Infection

Bone single‐photon emission computed tomography‐CT peak standardized uptake value for chronic osteomyelitis, osteoradionecrosis and medication‐related osteonecrosis of the jaw

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