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Radiation-induced oral mucositis RIOM is a major dose-limiting toxicity in head and neck cancer patients. It is a challenge for radiation oncologists since it leads to cancer therapy interruption, poor local tumor control, and changes in dose fractionation.

In the United Sates, its economic cost was estimated to reach 17, This review will discuss RIOM definition, epidemiology, impact and side effects, pathogenesis, scoring scales, diagnosis, differential diagnosis, prevention, and treatment.

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This coincides with recruitment of various inflammatory cells and release of inflammatory cytokines, chemotactic mediators, and growth factors. RIOM can progress to an acute life-threatening stage as a result of severe physical obstruction of food and water intake with subsequent weight loss and septic complication due to lost protective epithelial and basement membrane barriers.

This leads to limitations of local tumor control due to cancer treatment interruption and alterations in radiation dose fractionation 4 — 7.

Studies suggested the stages of progression of RIOM as initial hyperemia and erythema during the preulcer phase, during which there is a release of various pro-inflammatory cytokines from epithelial, vascular, and connective tissue cells at the site of tissue injury. This is followed by the epithelial phase with various degrees of desquamation and basement membrane damage with loss of the protective barrier, which ends with the physical appearance of the ulceration.

The postulcerative phase varies depending on the extent of the tissue toxicity. A secondary infection with Gram-negative bacteria or yeast may occur, with microcoagulation of the vasculature that worsens the inflammation by the local ischemia with more necrotic tissue yield.

The final stage will be the healing phase and fibrosis 289. Pathobiology of oral mucositis OM The pathogenesis of each phase is illustrated. Republished with the permission of Dr. Differential diagnosis of radiation-induced oral mucositis. A Henke feber i hela new york, denture-related lesion, B aphthous ulcer, C oral mucositis, and D oral thrush. Many risk factors have been identified for RIOM. These risk factors include concomitant chemotherapy CTbad oral hygiene, below average nutritional stratus, lack of antibiotic use at early stage mucositis, and smoking They found that very young age, female gender, poor oral health and hygiene, decreased saliva secretion, low BMI, poor renal function with elevated serum creatinine level, smoking, and history of RIOM are risk factors predicting the development of RIOM in head and neck cancer patients Patient-linked factors leading to increased risk for oral mucositis OM RIOM treatment adds an economic cost that was estimated to increase up to 17, The major clinical consequences of RIOM include hospital admission or extended hospitalization for total parenteral nutrition, intravenous IV analgesia, and IV antibiotics.

The pathophysiology of RIOM is not fully understood. Recent studies proposed that the pathogenesis of RIOM is composed of four phases: At the inflammatory phase, the RT-induced tissue injury results in the release of inflammatory cytokines; e.

These mediators might increase the damage by increasing the vascular permeability, leading to more infiltration and recruitment of inflammatory "Henke feber i hela new york." Stem cells travel to the site Henke feber i hela new york the tissue injury with other innate immunity components, e.

On the other hand, there are some anti-inflammatory cytokines, such as IL and IL, that work to minimize the injury The epithelial phase is initiated within a week by the apoptotic and cytotoxic effects of RT on the proliferating basal cells.

This is why the recovery period is dependent on the rate of epithelial turnover, which could be enhanced by growth factors like epidermal growth factor and keratinocyte growth factor KGF After a week, the epithelial breakdown ends with the beginning of the ulceration. This occurs, when epithelial loss leads to disrupted basement membrane, formation of ulcer pseudomembrane, and inflammatory exudate. The ulceration stage is very painful, since the protective barrier that covers the nerve endings at the lamina propria is lost The resulting microcoagulation and neutropenic state facilitate the Gram-negative bacteria and yeast colonization with the production of secondary infection.

Signaling pathways involved in the development of mucositis This is followed by amplification of this signal The end result will be more tissue injury and stimulated apoptosis The basement membrane protective barrier is lost during the ulceration phase.

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This leads to Gram-negative and yeast secondary infection potential, which adds more pro-inflammatory reactions and complicates the already existing inflammation. The healing phase starts by matrix signaling to basal epithelial cells to migrate, proliferate, and differentiate The result will be more tissue injury and stimulated apoptosis. During the ulceration and loss of the protective barrier, secondary infection adds more pro-inflammatory reactions and complicates the already existing inflammation before the healing phase starts by matrix signaling to basal epithelial cells to migrate, proliferate, and differentiate.

A Initial phase, B primary damage phase, C signal amplification phase, and D ulcerative phase. There has been more than one grading scale for RIOM. Comparison of OM scoring scales 1421 — The OMI is considered internally consistent with high test—retest and interscorer reliability, and it shows solid validity OMAS records the objective assessment of OM depending on the scoring of the presence and size of the ulceration or pseudomembrane score 0—3: Apart from the early clinical signs and symptoms, CBC with differential is considered the baseline to help radiation oncologists to determine the most susceptible time for developing OM or oral infection.

Radiation oncologists can start the RT "Henke feber i hela new york" that there is no evidence of any periodontal disease. If at any point RIOM develops, oral lesion culture and antimicrobial therapy are recommended as soon as possible Since renal diseases are considered contributing factors for OM 15chemistry levels should be regularly monitored by the treating physician Oral assessment guide Differential diagnosis of RIOM 20 Although RIOM is considered a self-limited injury in some patients, it could be a lethal injury in moderately to severely ill patients, which could lead to Henke feber i hela new york admission with obligatory cessation of RT.

Patient losses are a common event Henke feber i hela new york these circumstances Maintaining good oral care is the main preventive measure for RIOM to minimize the risk for candidiasis or secondary bacterial infection, especially in hyperfractionated radiotherapy, combined CCRT regimens, or RT combined with a targeted agent due to increased mucositis severity 3.

We will summarize the most recent agents and measures to prevent RIOM. Criteria for each level of evidence Diet recommended for RIOM patients Nevertheless, in another study, the authors concluded that bmMSCs transplantation had no therapeutic benefits on RIOM in single-dose RT when compared to the therapeutic effect of mobilization of endogenous BM stem cells Radiation-induced oral mucositis RIOM the clinical trials that have been done until 2 a. We have documented 40 RIOM treatment and prevention clinical trials.

Clinical trials for RIOM as listed on http: Despite its high incidence, RIOM is a self-limited radiotherapy-induced normal tissue injury. It is a dose-limiting toxicity in most cases of head and neck cancer patients. However, in moderately to severely sick patients, it could be a lethal injury. Many preclinical and clinical studies have been conducted for the prevention and treatment of RIOM.

Currently, there are numerous prevention and treatment strategies for RIOM. However, there is no single agent or management regimen that has been agreed upon between caregivers that significantly improves RIOM to a clinically relevant and satisfactory standard.

RIOM treatment focuses on palliative measures and symptoms relief; e. Interestingly, mesenchymal stromal cells therapy for RIOM shows promise for potential therapeutic and clinically relevant benefits. However, more studies are still needed to confirm such therapeutic potential.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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English language editing was Henke feber i hela new york by Jenny Warrington. National Center for Biotechnology InformationU.

Journal List Front Oncol v. Published online May Author information Article notes Copyright and License information Disclaimer. This article was submitted to Radiation Oncology, a section of the journal Frontiers in Oncology. Received Jun 10; Accepted Apr The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract Radiation-induced oral mucositis RIOM is a major dose-limiting toxicity in head and neck cancer patients. Open Henke feber i hela new york a separate window. Significant predictors for RIOM. Table 2 Patient-linked factors leading to increased risk for oral mucositis OM Age Increased risk in very young age high cell turnover rate and old age slower healing rate Gender Trends to increased risk in females Oral health and hygiene Maintaining good oral hygiene and oral health lowers radiation-induced oral mucositis RIOM risk Salivary secretory function Decreased saliva leads to increased RIOM risk Genetic factors Potential for high RIOM risk in certain individuals still to be identified Body mass index Delayed healing and increased breakdown in malnourished individuals Renal function Increased mucotoxicity linked with high serum creatinine level poor renal function Smoking Delays the healing Previous cancer treatment History of mucositis due to previous cancer treatment increases the risk.

Table 3 Signaling pathways involved in the development of mucositis B-cells receptor signaling Cell cycle: Table 4 Comparison of OM scoring scales 1421 — Table 6 Oral assessment guide Prevention of RIOM Maintaining good oral care is the main preventive measure for RIOM to minimize the risk for candidiasis or Henke feber i hela new york bacterial infection, especially in hyperfractionated radiotherapy, combined CCRT regimens, or RT combined with a targeted agent due to increased mucositis severity 3.

Good oral hygiene has been found to be one of the most effective ways to lower the risk of RIOM and minimize its progression. Pre-existing oral pathology, e. It is recommended to do early oral examination before starting any mucosal toxic therapy for cancer patients.

To help minimize the oral side effects of antineoplastic therapy, it is recommended to eliminate any oral pathology before the beginning of RT.

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