Abstract
BackgroundMultiple myeloma (MM) constitutes approximately 10% of hematological malignancies. Bisphosphonates have established themselves in solid organ metastasis and multiple myeloma lytic bone lesions by inhibiting osteoclast activation. Medication-related osteonecrosis of the jaw (MRONJ) emerges as an important complication. Investigating host-based factors, and developing personal risk factors gain importance in the development mechanism of MRONJ. We aimed to reveal the different genotype polymorphisms, and clinical effects of eNOS in patients with a diagnosis of MRONJ in MM patients.MethodsMedical records and blood samples were collected from 60 MRONJ patients with MM and 60 healthy controls. Inclusion criteria was having an exposed maxillofacial bone for more than eight weeks, a history of bisphosphonates, and no history of radiation therapy for the jaws. eNOS G894T and intron 4 VNTR were calculated by polymerase chain reaction and/or restriction fragment length polymorphism.ResultseNOS G894T and VNTR genotypes and alleles were compared statistically with the healthy control group. There was no significant difference between the two groups. In comparison between G894T and clinical parameters, aphthous stomatitis was more common in TT genotype, while DMFT > 3 was more common in TG-GG genotype (p = 0.035, 0.023).ConclusionseNOS induces osteogenesis in bone metabolism, with its regulatory effects on bone remodeling and also NO induced angiogenesis takes place indirectly with its protective effect on endothelial functions. We see that these polymorphisms affecting the entire process of bone remodeling and angiogenesis, especially mucosal damage, which is the triggering factor of MRONJ pathology, have been revealed in the MM patient group. Considering the MRONJ initiating factors, it is necessary to emphasize the importance of our study results. It should be seen as an important step for new studies towards MRONJ and its treatment.
Highlights
Multiple myeloma (MM) constitutes approximately 10% of hematological malignancies
There was no significant difference between the two groups in terms of G894T GG, GT and TT genotypes, and G and T alleles (p = 0.201, 0.954, 0.851, 1.000)
There was no significant difference between the two groups in terms of VNTR BB, BA and AA genotypes, and B and A alleles (p = 0.844, 0.496, 0.344, 1.000) (Table 2)
Summary
Multiple myeloma (MM) constitutes approximately 10% of hematological malignancies. Bisphosphonates have established themselves in solid organ metastasis and multiple myeloma lytic bone lesions by inhibiting osteoclast activation. Metastatic bone lesions can be encountered in many solid malignancies In this patient group, cancer cells that metastasize to bone stimulate osteoclasts via the cytokines they produce and cause bone destruction [5]. Lytic bone lesions in multiple myeloma occur by a similar mechanism. They cause bone destruction by secreting osteoclast stimulants such as nuclear-KB ligand (RANKL) receptor activator as well as molecules that inhibit osteoblastic activity such as dickkopf-1 (DKK) [5, 6]. Bisphosphonates have established themselves in solid organ metastasis, and multiple myeloma lytic bone lesions by inhibiting osteoclast activation [5,6,7]. Decreased osteoclast activity decreases bone remodeling and is used to prevent osteoporosis by increasing bone density [5,6,7]
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