Search Results (154)

Objectives: This study aimed to evaluate the radiographic characteristics of medication-related osteonecrosis of the jaw (MRONJ) by digital panoramic radiographs and to investigate the associations between radiographic findings and clinical, demographic, and treatment-related variables in patients receiving antiresorptive therapy. Methods: A retrospective analysis was performed on 55 patients receiving antiresorptive therapy, categorized into a tooth-extraction group (n = 20) and an MRONJ group (n = 35). Standardized panoramic radiographs obtained at baseline (T0) and during the 6-month follow-up (T1) were evaluated for lamina dura thickness, trabecular bone alteration, osteosclerosis, cancellous bone loss, sequestration, and periosteal response. Statistical analyses were conducted on associations involving drug type, administration route, therapy duration, smoking, diabetes, hypertension, gender, and serum C-terminal telopeptide (CTX) levels. Results: The incidence of sequestrum development and cancellous bone loss was considerably higher in the MRONJ group. Sequestration demonstrated significant associations with both the duration of antiresorptive therapy (>3 years) and intermediate-risk CTX levels. No significant correlations were found between CTX and other radiographic parameters. Lamina dura thickening, trabecular alterations, osteosclerosis, and periosteal reaction exhibited no differences across groups or in relation to smoking, diabetes, age, or gender; periosteal reaction was an uncommon and variable finding. Conclusions: Panoramic radiography provides clinically useful information in the evaluation of MRONJ, particularly for identifying sequestration and cancellous bone degradation. The formation of sequestrum appears to be the most indicative radiographic indicator, representing both the duration of treatment and biochemical risk. Full article

Osteoporosis is a prevalent skeletal disorder characterized by reduced bone mass and microarchitectural deterioration, leading to increased fracture risk, particularly in aging populations. Postmenopausal osteoporosis (PMOP) remains the most common primary form and results from abrupt estrogen deficiency after menopause, which disrupts bone remodeling by accelerating the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis, suppressing Wnt/β-catenin signaling, and promoting inflammatory cytokine production. In contrast, drug-induced osteoporosis (DIOP) encompasses a heterogeneous group of secondary bone disorders arising from pharmacologic exposures. Glucocorticoids suppress osteoblastogenesis, enhance osteoclast activity, and increase reactive oxygen species; long-term bisphosphonate therapy may oversuppress bone turnover, resulting in microdamage accumulation; denosumab withdrawal triggers a unique rebound surge in RANKL activity, often leading to rapid bone loss and multiple vertebral fractures. Medications including aromatase inhibitors, SSRIs, proton pump inhibitors, heparin, and antiepileptic drugs impair bone quality through diverse mechanisms. Standard antiresorptive agents remain first-line therapies, while anabolic agents such as teriparatide, abaloparatide, and romosozumab provide enhanced benefits in high-risk or drug-suppressed bone states. Transitional bisphosphonate therapy is essential when discontinuing denosumab, and individualized treatment plans—including drug holidays, lifestyle interventions, and monitoring vulnerable patients—are critical for optimizing outcomes. Emerging approaches such as small interfering RNA (siRNA)-based therapeutics, anti-sclerostin agents, digital monitoring technologies, and regenerative strategies show promise for future precision medicine management. Understanding the distinct and overlapping molecular mechanisms of osteoporosis is essential for improving fracture prevention and long-term skeletal health. Full article

With the intensification of global population aging, the co-morbidity rate of periodontitis and osteoporosis has significantly increased. The two are pathologically intertwined, forming a vicious cycle characterized by bone immunoregulatory dysfunction in the periodontal microenvironment, abnormal accumulation of reactive oxygen species (ROS), and disruption of bone homeostasis. Conventional mechanical debridement and anti-infective therapy can reduce the pathogen load, but in some patients, it remains challenging to achieve long-term stable control of inflammation and bone resorption. Furthermore, abnormal bone metabolism in the context of osteoporosis further weakens the osteogenic response during the repair phase, limiting the efficacy of these treatments. Bioinspired cell membrane-coated nanoparticles (CMNPs) have emerged as an innovative technological platform. By mimicking the biointerface properties of source cells—such as red blood cells, platelets, white blood cells, stem cells, and their exosomes—CMNPs enable targeted drug delivery, prolonged circulation within the body, and intelligent responses to pathological microenvironments. This review systematically explores how biomimetic design leverages the advantages of natural biological membranes to address challenges in therapeutic site enrichment and tissue penetration, in vivo circulation stability and effective exposure maintenance, and oxidative stress and immune microenvironment intervention, as well as functional regeneration supported by osteogenesis and angiogenesis. Additionally, we conducted an in-depth analysis of the key challenges encountered in translating preclinical research findings into clinical applications within this field, including issues such as the feasibility of large-scale production, batch-to-batch consistency, and long-term biosafety. This review lays a solid theoretical foundation for advancing the clinical translation of synergistic treatment strategies for periodontitis with osteoporosis and provides a clear research and development pathway. Full article

Background. Glucocorticoid-induced osteoporosis represents a well-known type of secondary osteoporosis (SOp). While the most prevalent sub-category includes corticotherapy, another important contributor is represented by Cushing’s syndrome. In this traditional landscape, adrenal incidentalomas do not involve a standard cause of SOp, since most of them are non-functioning adrenal tumours (NFATs). Yet, 30–40% of them are not entirely “non-functioning”, due to mild autonomous cortisol secretion (MACS). Despite not being a guideline-based diagnosis, a lower ACTH might point to various NFATs/MACS complications. Objective. This study aimed to determine the relationship between the bone health status of post-menopausal women with NFATs/MACS and their baseline morning ACTH level. The bone health indicators were DXA, FRAX, and bone remodelling markers. Methods. This was a retrospective, real-life, transversal study in adult females who were hospitalized in a single tertiary centre of endocrinology. They were all anti-osteoporotic drug-naïve. The subjects underwent CT and DXA scanning and a 1 mg dexamethasone suppression test (DST). Results. The cohort (sample size of N = 84 patients, 61.49 ± 7.86 years) had a type 2 diabetes rate of 18%, arterial hypertension rate of 75%, and a dyslipidemia rate of 78%. Median ACTH was 11.89 pg/mL. The prevalence of MACS was 30.95%. The mean largest tumour diameter (LTD) was 2.25 ± 0.99 cm. ACTH correlated with second-day cortisol after the 1 mg DST (r = −0.301, p = 0.024), and LTD (r = −0.434, p < 0.001). ROC analysis for the bone resorption marker CrossLaps showed an AUC of 0.647 (p = 0.05), with the highest Youden index for the cut-off at 0.32 ng/mL (sensitivity 87.50%, specificity 39.50%). Bone impairment (osteoporosis + osteopenia) was found in 65% of patients, with an osteoporotic fracture prevalence of 4.76%. The lowest mean T-score (−1.12 ± 1.00) showed osteopenia, and the median trabecular bone score pointed a partially degraded microarchitecture [median (interquartile interval): 1.320 (1.230, 1.392)]. FRAX and FRAXplus estimations correlated with bone mineral density (BMD) at all three central DXA sites, regardless of the ACTH cut-off. Patients with a low ACTH (<10 pg/mL) displayed similar bone/adrenal features when compared to those with normal ACTH, except forbut they had a higher MACS rate (45.45% versus 21.57%, p = 0.021) and a larger LTD (2.67 ± 0.98 versus 1.98 ± 0.92 cm, p = 0.003). Fracture estimation showed that only in patients with a low ACTH, the 10-year fracture risk for major osteoporotic fractures (MOF) adjusted for lumbar BMD was lower than the risk for MOF adjusted for diabetes (p = 0.036), and the 10-year hip fracture risk was lower when adjusted for lumbar BMD (p = 0.007). ACTH correlated with lumbar BMD (r = 0.591, p = 0.002) only in the group with an ACTH < 10 pg/mL, suggesting its potential usefulness as a bone biomarker in these cases. On the other hand, MACS-negative subjects with a low ACTH versus those with a normal ACTH showed higher CrossLaps (0.60 ± 0.27 versus 0.42 ± 0.21 ng/mL, p = 0.022), indicating an elevated bone resorption even in patients with tumours that are regarded as true non-secretors. Conclusions. A subgroup of patients diagnosed with NFATs/MACS might be prone to skeletal damage, and biomarkers such as ACTH (specifically, suppressed ACTH) might serve as a surrogate pointer to help refine this higher risk in daily practice. Further research to address other ACTH cut-offs will place ACTH assays in the overall bone status evaluation in these patients, most probably not as a single biomarker, but in addition to other assays. Full article

Background/Objectives: Medication-related osteonecrosis of the jaw (MRONJ) is a serious complication of antiresorptive and antiangiogenic drugs with no consensus on optimal treatment. This study aimed to evaluate the clinical outcomes of MRONJ patients managed at a tertiary referral center over a 15-year period. Methods: We conducted a retrospective cohort study of 130 patients diagnosed with MRONJ (per AAOMS criteria) at a single tertiary hospital between 2006 and 2021. Data on demographics, underlying disease, drug history, MRONJ stage, triggering events, and treatment (conservative vs. surgical) were collected from medical records. Treatment outcomes were categorized as complete resolution, stable disease, or progression. Univariate and multivariate logistic regression analyses were performed to identify predictors of resolution. Results: Most patients (84.6%) had an underlying malignancy. The primary causative agents were zoledronic acid (47.7%) and denosumab (30.0%), the most frequent site was the mandible (66.2%), and the main trigger was dental extraction (59.2%). Crude resolution rates were 20.3% for conservative management versus 83.6% for surgical management. Treatment was stage-driven, with surgery common in advanced stages. At 12 months, 43.1% of all patients achieved complete resolution, and 52.3% remained stable. Multivariate analysis confirmed surgical treatment as the only independent predictor of complete resolution (OR = 20.1, 95% CI: 8.1–50). Conclusions: In this cohort, conservative care was generally sufficient for Stage I disease, while surgical intervention was the strongest predictor of healing and provided reliable outcomes for advanced MRONJ. These findings support an individualized, stage-appropriate treatment strategy. Full article

The next frontier in postmenopausal osteoporosis management lies not in novel pharmacological agents, but in the systematic integration of mechanism-guided drug selection, fall prevention, and long-term adherence strategies into a unified patient-centered care model. This review is intended for clinicians and clinical researchers involved in the diagnosis, treatment, and long-term management of postmenopausal osteoporosis. We provide a mechanism-to-practice framework that explicitly maps each therapeutic class to the specific molecular pathway it targets: bisphosphonates inhibit osteoclast function downstream of RANKL activation; denosumab blocks RANKL directly at the cytokine level; romosozumab inhibits sclerostin to restore Wnt-mediated bone formation. This mechanistic foundation supports a risk-stratified treatment paradigm in which antiresorptives address accelerated remodeling in moderate-risk patients, while patients at very high fracture risk—characterized by severe bone deficit or recent fragility fractures—benefit from an anabolic-first approach followed by consolidation. Beyond drug selection, we examine the persistent treatment gap in which fewer than 20% of post-fracture patients receive therapy, arguing that fall prevention—responsible for >90% of hip fractures—and medication adherence deserve equal priority in clinical practice. We further analyze key controversies, including T-score- versus FRAX-based intervention thresholds, limitations of the trabecular bone score, cost-effectiveness constraints on anabolic-first sequencing, and evidence gaps in post-denosumab transition strategies. By synthesizing mechanistic insights, guideline recommendations, and critical appraisal of current limitations, this review offers not only an overview of existing knowledge but a coherent decision-support model aimed at improving fracture prevention through comprehensive, individualized care. Full article

Medication-related osteonecrosis of the jaw (MRONJ) is a severe adverse event triggered by antiresorptive and/or anti-angiogenic agents, characterized by bone destruction, sequestrum formation, and refractory mucosal defects. Effective mucosal healing can be a critical factor for MRONJ prevention and treatment. While endoplasmic reticulum stress (ER stress) has been implicated in tissue repair, its role in MRONJ-associated mucosal healing impairment remains undefined. This study investigated the effects of the anti-angiogenic drug sunitinib on oral mucosal healing and its underlying mechanisms. A mouse model of palatal mucosal defects was established, RNA-seq, transmission electron microscopy, and morphological analyses were used to assess how sunitinib affects ER function during mucosal repair. Using human oral keratinocytes (HOKs), we further elucidated the subcellular mechanisms through which sunitinib influences cell proliferation, migration, cell cycle progression, tight junctions, and apoptosis via techniques such as qPCR, Western blotting, immunofluorescence, and flow cytometry. Our findings demonstrated that sunitinib might induce significant alterations in the morphology of the ER and mitochondria. Both in vivo and in vitro experiments revealed that sunitinib persistently activates the GRP78 (BIP)/PERK/ATF4/CHOP axis in HOKs. This sustained ER stress can inhibit keratinocytes migration and proliferation, disrupt tight junctions, and trigger the intrinsic mitochondrial apoptotic pathway, ultimately leading to impaired oral mucosal healing and barrier dysfunction. Critically, pharmacological inhibition of ER stress was shown to restore keratinocytes’ function and promote effective mucosal healing. These results indicated that targeting sunitinib-induced persistent ER stress might represent a promising therapeutic strategy to prevent and treat oral mucosal toxicity associated with this drug. Full article

Osteoporosis is an aging-related disease characterized by low bone mineral density and deteriorated bone structure, resulting in an increased risk of fractures. Currently, most osteoporosis therapies target osteoclasts to inhibit bone resorption, while the three FDA-approved anabolic agents include parathyroid hormone, parathyroid hormone-related protein, and anti-sclerostin antibody that promote osteoblast function. However, long-term treatment with these agents is associated with potential adverse effects and decreased therapeutic efficacy. This has prompted exploration of novel therapeutic strategies, including microRNAs (miRNAs), which are emerging as promising candidates. miRNAs have been reported to play important roles in regulating pathways involved in bone formation and resorption. In addition to their direct roles in osteoblasts and osteoclasts, miRNAs also serve as key mediators of communication between these cells, which is essential for maintaining bone homeostasis. The complexity of osteoporosis requires versatile regulators such as miRNAs that can modulate multiple biological pathways. Recent studies have demonstrated the potential of miRNA-based therapy to restore bone homeostasis in osteoporotic models. However, further studies are needed to develop tissue-specific delivery systems and evaluate long-term safety to improve the therapeutic potential of miRNAs as new osteoporosis drugs. Full article

Tanshinone IIA (T-IIA), a fat-soluble diterpene quinone extracted from Salvia miltiorrhiza, is widely recognized for its multiple pharmacological properties, including anti-inflammatory, antioxidant, anti-fibrotic, and anti-tumor effects. Recent studies have highlighted its great potential in treating bone metabolic disorders, especially osteoporosis and bone damage repair. Bone health depends on the dynamic balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Disruption of this balance can lead to diseases such as osteoporosis, which is often diagnosed after a fracture, seriously affecting the quality of life and increasing the medical burden. Early identification of high-risk groups and appropriate treatment are essential for preventing fracture recurrence. Studies have shown that T-IIA can promote osteoblast differentiation and inhibit osteoclast activity, targeting key signaling pathways such as NF-κB, PI3K/Akt, and Wnt/β-catenin, all of which are closely related to bone metabolism. T-IIA has a dual role in regulating bone formation and bone resorption, making it a potential drug for the treatment of osteoporosis. In addition, T-IIA has neuroprotective, hepatic, renal, cardiac, and cerebral effects, which enhance its therapeutic effect. Despite the remarkable efficacy of T-IIA, its clinical application is limited due to poor solubility and low bioavailability. Recent advances in drug delivery systems, such as liposome formulations and nanocarriers, have improved their pharmacokinetics, increased absorption rate, and bioavailability. Combination therapy with growth factors or stem cells can further enhance its efficacy. Future studies should focus on optimizing the delivery system of T-IIA and exploring its combined application with other therapeutic strategies to expand its clinical application range. Full article

Icariin (ICA) is a bioactive flavonoid compound extracted from Epimedium plants. In recent years, it has attracted significant research interest in the field of bone tissue repair due to its pharmacological effects via multiple targets and pathways. Studies have shown that ICA promotes the osteogenic differentiation of mesenchymal stem cells (MSCs) and enhances bone matrix formation by regulating signaling pathways such as Akt and Wnt/β-catenin. It concurrently inhibits osteoclast activity to maintain the balance of bone remodeling, thereby simultaneously stimulating new bone regeneration and suppressing bone resorption. At the same time, ICA exerts potent anti-inflammatory and antioxidant effects and promotes angiogenesis, improving the local microenvironment of bone injury and significantly facilitating the regeneration of bone and cartilage tissues. Additionally, ICA exhibits notable protective effects in multiple organ systems including the cardiovascular, hepatic, renal, and nervous systems. Specifically, ICA reduces cardiomyocyte apoptosis and fibrosis to preserve cardiac function, improves hepatic metabolic function and alleviates oxidative stress, attenuates renal inflammation and fibrosis, and—through neuroprotective actions—reduces neuroinflammation and promotes neuronal survival. These multi-organ effects help optimize the systemic environment for bone healing. However, ICA faces significant pharmacokinetic challenges. It has low oral bioavailability (due to poor absorption and extensive first-pass metabolism) as well as a short half-life. Consequently, maintaining effective drug concentrations in vivo is difficult, which limits its therapeutic efficacy and impedes clinical translation. To fully realize its regenerative potential, advanced drug delivery strategies (e.g., nanocarrier-based delivery systems) are being explored to enhance ICA’s bioavailability and prolong its duration of action. Overall, ICA’s multi-modal actions on bone cells, the immune microenvironment, and systemic factors make it a promising multi-target agent for bone regeneration. Addressing its pharmacokinetic limitations through optimized delivery and conducting further clinical studies will be crucial to realize its full therapeutic potential. This review provides a comprehensive overview of recent advances and challenges in translating ICA’s benefits into orthopedic therapy. Full article

Osteoporosis and sarcopenia are two aspects of the geriatric syndrome that frequently occur together and affect one another in a condition referred to as osteosarcopenia. Preventive and treatment options for osteosarcopenia exist but are mainly focused on the treatment of osteoporosis, as there is still no FDA-approved treatment for sarcopenia. Drugs for osteoporosis include antiresorptive and anabolic drugs and hormonal replacement therapies and are prescribed based on age, BMD and other patient characteristics, which, however, do not include the possible co-existence of sarcopenia. As several studies and clinical trials have shown that the pharmacological treatment of osteoporosis can also affect muscle tissue, in either a positive or negative manner, sarcopenia should be another factor affecting the choice of treatment, especially when facing equal treatment options for osteoporosis. The aim of this review was to summarize our current knowledge on the effects of FDA-approved drugs for the treatment of osteoporosis on muscle quality, mass and function. A better understanding of the effects that certain drugs have on muscle tissue might in the future help us to simultaneously at least partially also address the wasting of muscle tissue and avoid further pharmacologically induced decline. Full article

Every year, millions of people worldwide suffer from bone tissue damage caused by bone trauma and surgical operations, as well as diseases such as osteoporosis, osteoarthritis, osteomyelitis, and periodontitis. Bone defect repair is one of the major challenges in the field of regenerative medicine. Although bone grafts are the gold standard for treating bone defects, factors such as donor sources and immune responses limit their application. Functionalized nanomaterials have become an effective means of treating bone diseases due to their good biocompatibility and osteoinductivity, anti-inflammatory, and antibacterial properties. Metal–organic frameworks (MOFs) are porous coordination polymers composed of metal ions and organic ligands, featuring unique physical properties, including a high surface area–volume ratio and porosity. In regenerative medicine, MOFs function as the functions of drug carriers, metal ion donors, nanozymes, and photosensitizers. When combined with other functional materials, they regulate cellular reactive oxygen species, macrophage phenotypic transformation, bone resorption, osteogenesis, and mineralization, providing a new paradigm for bone tissue engineering. This study reviews the classification of functionalized MOF composites in biomedicine and the application of their synthesis techniques in bone diseases. The unique in vivo and in vitro applications of MOFs in bone diseases, including osteoarthritis, osteoporosis, bone tumors, osteomyelitis, and periodontitis, are explored. Their properties include excellent drug loading and sustained release abilities, high antibacterial activity, and bone induction abilities. This review enables readers to better understand the cutting-edge progress of MOFs in bone regeneration applications, which is crucial for the design of and functional research on MOF-related nanomaterials. Full article

Osteoporosis is characterized by an imbalance between bone formation and resorption, leading to decreased bone mass and an increased fracture risk, mainly associated with aging. Current treatments include anti-resorptive and anabolic drugs. However, these often have side effects, leading many patients to seek natural biological alternatives. We have demonstrated previously that hops extract, rich in compounds with estrogenic activity classified as phytoestrogens, exerts osteogenic effects by promoting the osteoblastic differentiation of bone marrow stem cells (BMSCs) while inhibiting osteoclast activity in vitro. In our study, young male Sprague Dawley rats were randomized into two groups: one received hops extract (LPL, 1% w/v in drinking water) for two months, and the other drank water alone (C). The rats were euthanized, and their femurs were dissected and processed for static histomorphometry and bone biomechanics. Additionally, BMSCs were isolated from the humeri to evaluate their osteogenic potential. Our result demonstrated that LPL treatment enhanced the osteogenic potential of humeral BMSCs in ex vivo assays, upregulating osteogenic genes and downregulating pro-resorptive markers. These findings correlated with improved femoral bone microarchitecture and biomechanical parameters. In conclusion, a two-month treatment with LPL enhanced the osteogenic capacity of BMSCs, improving bone microarchitecture and biomechanical properties. These results suggest its potential as a natural alternative for promoting bone health. Full article

Background/Objectives: Medication-related osteonecrosis of the jaw (MRONJ) is a challenging condition often associated with bisphosphonate use, leading to impaired bone healing and difficult clinical management. Given the lack of predictable therapeutic options, this study investigated the effects of systemic ozone therapy on MRONJ healing. This study aimed to analyze the effects of systemic ozone therapy on oral hard and soft tissue healing in senescent rats with medication-related osteonecrosis of the jaw (MRONJ) induced by antiresorptive therapy. Methods: Twenty-eight senescent Wistar rats, aged eighteen months and weighing ~350 g, were used for this study. The animals were divided into four groups. The negative control (SAL) group received saline applications, while the control-treated (SAL+OZ) group received saline applications and ozone therapy (0.7 mg/kg). The MRONJ (ZOL) group received Zoledronate, an intravenous antiresorptive drug (100 μg/kg), and the MRONJ-treated (ZOL+OZ) group received zoledronate application and was treated with systemic ozone therapy (0.7 mg/kg). All rats underwent molar extraction in the third week of the experiment and were euthanized in the seventh week of the experiment. The mandibles were resected, reduced, and prepared for microtomographic analysis, histopathological/histometric analysis, and immunohistochemistry. Results: The ZOL group presented characteristics of vitreous, non-vital, and dense bone, poor vascularization, and high values of inflammation markers compatible with MRONJ. In contrast, the ZOL+OZ group exhibited improvement in alveolar bone and soft tissue healing, a decrease in nonvital bone area, and modulation of local inflammation. Conclusions: It can be concluded that Ozone therapy improved oral hard and soft tissue healing of MRONJ in senescent female rats subjected to antiresorptive drugs and might be considered for future clinical applications. Full article

Background: Medication-related osteonecrosis of the jaw (MRONJ) is drug-induced bone destruction that is exposed for a minimum of 6 to 8 weeks in patients who have not received head and neck radiotherapy and who have not been diagnosed with facial bone metastases. MRONJ treatment outcomes are unpredictable. Therefore, alternative treatment methods are being explored, such as blood-derived platelet-rich preparations enriched with growth factors, including advanced platelet-rich fibrin (A-PRF). The presence of growth factors may enhance healing and reduce post-procedure complications. There are no studies examining the effect of A-PRF on the healing of patients with MRONJ. The aim of this study was to retrospectively evaluate treatment outcomes of patients with MRONJ surgically treated without and with the use of A-PRF. Materials and methods: This retrospective study included 28 patients who suffered from osteomyelitis due to MRONJ and underwent surgical treatment between 2019 and 2024. The patients were divided into two groups: the first group received surgical treatment without A-PRF, and the second group received surgical treatment with the application of A-PRF. This study analyzed demographic and clinical data, as well as treatment outcomes. Results: The patients were aged from 43 to 82 years. The most common cause of MRONJ was the administration of zoledronic acid for oncological reasons (22 patients, 78.6%), given intravenously. In 20 patients (71.4%), the antiresorptive treatment lasted longer than three years. The obtained healing distribution was binomial (presence or absence of healing). Estimation of the probability of healing using the maximum likelihood method provided a result of approximately 64%. The probability of ten or more healed patients in the A-PRF group was 41%. A-PRF helps with a probability of 59%, and without A-PRF, it was lower. Concomitantly, the differences between the group with A-PRF and without A-PRF were not statistically significant. Conclusions: The patients with MRONJ should have regular check-ups with radiological examinations at least every six months to detect possible recurrence. Treatment for MRONJ is long and difficult. Treatment of non-advanced lesions, without additional risk factors (such as treatment with zoledronate intravenously for oncological purposes for 3 years), showed a better prognosis. Sometimes, in addition to surgery, it is necessary to consider alternative methods. A-PRF may enhance MRONJ healing. However, there is no evidence of a significant effect of A-PRF on the healing of MRONJ. Full article