## 1 Introduction
### Medication-Related Osteonecrosis the Jaw (MRONJ)  
In 2003, [PERSON] reported a series of 36 patients presenting with painful bone exposure in the maxilla or mandible that were unresponsive to medical or surgical interventions. He then termed this clinical presentation as bisphosphonates-related osteonecrosis of the jaws (BRONJ) as all of these patients had receive intravenous bisphosphonates (Pamidronate (Aredia) or Zolderonate (Zometa) for the treatment of hypercalcemia secondary to multiple myeloma, metastatic breast carcinoma, and osteoporosis [21].  
In 2014, the term \"medication-related osteeonecrosis of the jaw\" (MRONJ) was introduced by American Association of Oral and Maxillofacial Surgeons (AAOMS) as it was proven that osteeonecrosis of the jaws was not limited to the use of bisphosphonates (BP) alone [22]. It may also develop in patients on antiresorptive and antiangiogenic medications such as denosumab and bevacizumab. These drugs are often used for the treatment of malignancy with bone metastasis or metabolic bone disease, primarily osteoporosis.  
The incidence of MRONJ in relation to denosumab was 1.8% versus zoledronate 1.3% in underlying malignancy and multiple myeloma [23], between 0.3% and 0.4% with bevacizumab [24], and 16% among patients who received combined therapy of bisphosphonates and antiangiogenesis [25].  
Based on the AAOMS 2014 position paper, MRONJ is defined as [22]  
1. Exposed bone or bone that can probed through an intraoral or extraoral fistula in the maxillofacial region that persisted for longer than 8 weeks;
2. Current or previous treatment with antiresorptive or antiangiogenic agents;
3. No history of radiation therapy to the jaws or obvious metastatic disease to the jaws. The incidence of MRONJ was shown to be as high as 18.3% [26]. The exact pathophysiology of MRONJ is yet to be fully understood. Much of the current understanding on the pathophysiology is based on experimental findings in animal studies and their appraisal in the context of the human condition [27]. Various hypotheses have been discussed in the literature, including bone-remodeling inhibition, lack of immune resiliency, soft tissue toxicity, inflammation or infection, and angiogenesis inhibition [28].  
[PERSON] et al. (2019) hypothesized that there is a possibility that antiresorptive and anti-angiogenic drugs share a common pathogenetic mechanism. These drugs inhibit angiogenesis by interfering with endothelial cell proliferation and survival, leading to loss of blood vessels and avascular necrosis [29].  
To date, no single treatment protocol has been proven to manage MRONJ with predictable outcomes [30]. Treatment strategies are guided by clinical staging ranging from conservative measures such as antimicrobial therapy and 0.12% chlorhexidine mouthwash during the initial stages to surgical debridement in advanced stages. Different therapeutic approaches have been used with variable success rate, including ozone therapy, hyperbaric oxygen therapy, teriparatide laser, pentoxiflline, andtocopherol, all of which aim to improve healing [30; 31; 32].  
In this paper, we aim to present our treatment strategy and outcomes of incorporating the use of L-PRF as a surgical adjunct in treatment of ORN and MRONJ.