Maxillofacial osteoradionecrosis

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Review Article Maxillofacial osteoradionecrosis Amit T. Suryawanshi, S. N. Santhosh Kumar, R. S. Dolas, Ruchi Khindria, Vivek Pawar, Manju Singh

ABSTRACT Department of Oral and Maxillofacial Surgery, DPU, Dr. D. Y. Patil Dental College and Hospital, Pimpri, Pune, Maharashtra, India

Address for correspondence: Dr. Amit Suryawanshi, E‑mail: amitsuryawanshi999 @gmail.com

Osteoradionecrosis is a severe and delayed radiation‑induced injury, characterized by bone tissue necrosis and failure to heal. Cases of osteoradionecrosis present to the clinician with features of pain, drainage, and fistulation of the mucosa or skin related to exposed bone in the previously irradiated area. The tumour size and location, radiation dose, occurrence of local trauma, dental extractions, infection, immune defects, and malnutrition are predisposing factors. A better understanding of risk factors leading to the development osteoradionecrosis and of the underlying pathophysiology may improve the ability of the clinician to prevent the occurrence and help improve the prognosis of this complication. Although the frequency of osteoradionecrosis has declined since the introduction of newer methods of radiotherapy, this review focuses on the etiology, pathophysiology, clinical features, radiological features, diagnosis, and treatment modalities including the newer modalities. KEY WORDS: Jaws, management, osteoradionecrosis, physiopathology, risk factors

Introduction

Historical perspective

T

In 1922, Regaud published the first report about osteoradionecrosis of jaws after radiotherapy.[4] In 1926, further description of osteoradionecrosis was given by Ewing under the name Radiation Osteitis.[5] In 1970, Meyer classified osteoradionecrosis as one special type of osteomyelitis. In 1975, Mainous advocated the use of hyperbaric oxygen therapy (HBO) for late radiation tissue injury. In 1983, Robert Marx proposed the hypoxic, hypocellular, and hypovascular theory as a new way of understanding the pathophysiology of osteoradionecrosis. In 1992, Harris introduced the use of Ultrasound as one of the modes to treat osteoradionecrosis.[6] In 1998, Marx gave the 30/10 protocol that was employed in the treatment of established osteoradionecrosis. In 2004, Delanian and Lefaix put forward a new theory named radiation‑induced fibrosis that accounts for the damage to normal tissues, including bone after radiotherapy.[7]

he global incidence of oral cancer is 5,00,000 cases per year with mortality of 2,70,000 cases per year. The incidence of oral cancer in India is 40% among all cancers and about 1,00,000 patients suffer from oral cancer in any year. Oral cancer is responsible for 7% of all cancer deaths in males and 3% in females.[1] The recent protocol for management of oral cancer includes multimodal therapy, such as surgery with radiotherapy and/or chemotherapy. Radiation therapy is one of the major treatment modalities for the management of oral malignancies. Like with any treatment modality, even radiation therapy is associated with various complications. A long‑term side effect of radiotherapy that is also the most serious is osteoradionecrosis.[2,3] Literature reveals many terminologies to represent the same disease, such as radiation osteitis, radio‑osteonecrosis, radiation osteomyelitis, osteomyelitis of irradiated bone, osteonecrosis, radio‑osteomyelitis, septic osteoradionecrosis, and post‑radiotherapy osteonecrosis.[4] This review focuses on the general information on maxillofacial osteoradionecrosis for general practitioners. Access this article online Quick Response Code:

Website: www.jdrr.org DOI: 10.4103/2348-3172.126171

Definitions In literature, osteoradionecrosis has been defined in many ways [Table 1].[8,9] However, the authors feel that the definition given by Wong, Wood, and McLean (1997)[8] is the most appropriate and complete: “A slow‑healing radiation‑induced ischemic necrosis of bone with associated soft tissue necrosis of variable extent occurring in the absence of local primary tumour necrosis, recurrence, or metastatic disease that may or may not: i. Be superinfected (and accompanied by fistulation or cellulitis) ii. End in pathologic fracture iii. Resolve without surgery, hyperbaric oxygen therapy or both.”

How to cite this article: Suryawanshi AT, Kumar SS, Dolas RS, Khindria R, Pawar V, Singh M. Maxillofacial osteoradionecrosis. J Dent Res Rev 2014;1:42-9.

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Classification and staging systems There have been several staging or scoring systems that have been proposed. These systems are based on response to HBO therapy, degree of bone damage, clinical–radiological findings, length of bone exposure through the overlying skin or mucosa, and treatment needed [Tables 2 and 3].[8-15]

Risk factors The existing articles in literature fail to give an exact etiology for osteoradionecrosis. The etiology of osteoradionecrosis is considered to be multifactorial. These factors may increase the risk of the patient for development of osteoradionecrosis. The factors are classified into four groups as shown in Table 4.[15-18]

Pathophysiology The pathophysiology of osteoradionecrosis is not very clear till date. However, literature reveals three theories that have been put forward since 1970, as mentioned in the following: • Meyer’s Radiation, trauma and infection theory[19] Table 1: Definitions of osteoradionecrosis Year

Author(s)

Definition

1983

Marx[8]

1983

BeumerIII, Harrison, Sanders and Kurrasch[9]

1986

Morton and Simpson[9]

1987

Marx and Johnson[9]

1987

Epstein, Rea, Wong, Spinelli and Stevenson‑Moore[9]

1989

Widmark, Sagne and Heikel[9]

1990

Koka, Deo, Lusinichi, Roland and Schwaab[9]

An area of exposed bone greater than 1 cm in a field of irradiation that had failed to show any evidence of healing for at least 6 months An exposure of bone of the maxilla or mandible within the radiation treatment volume persisting for more than 3 months or longer A loss of soft tissue integrity and exposure of radiation damaged bone An exposure of nonvital irradiated bone, which fails to heal without intervention An ulceration or necrosis of the mucous membrane (In the absence of recurrent or metastatic disease), with exposure of necrotic bone for more than 3 months A non healing mucous or cutaneous ulcer with denuded bone, lasting for more than 3 months A persistent ulceration with exposure of devitalised bone, cellulitis, fistula and a pathologic mandibular fracture. Patients tumour free at primary site Exposed and necrotic bone associated with ulcerated or necrotic surrounding soft tissue which persists for greater 3 months in an area that had been previously irradiated (not caused by tumor recurrence) A loss of viable bone resulting from radiation therapy A bone and soft tissue necrosis of 6 months duration excluding radiation‑induced periodontal breakdown

1992

1993 1995

Harris[9]

Mirante and Urken et al.[9] Van Merkesteyn, Bakker and Borgmeijer-Hoelen[9]

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• Marx’s Hypoxic, hypocellular, and hypovascular theory[20] • Delanian’s Radiation‑induced fibroatrophic theory.[21]

Meyer’s radiation, trauma, and infection theory In 1970, in an excellent monograph on infectious disease of the jaws, Meyer defined the classic triad of osteoradionecrosis as radiation, trauma, and infection [Figure 1].[19] Meyer portrayed that the trauma provided the portal for invasion by oral microbiological flora into the underlying irradiated bone. Meyer’s theory lasted for a decade and became the foundation for the popular use of antibiotics with surgery to treat osteoradionecrosis.[19]

Marx’s hypoxic, hypocellular, and hypovascular theory Robert E Marx in his landmark study noted that there was no injury before the onset of osteoradionecrosis in 35% of his cases. He also found that composite irradiated tissues were more hypoxic than those that had not been irradiated [Figure 2].[20] Marx concluded that “Osteoradionecrosis is not a primary infection Table 2: Classification systems of osteoradionecrosis Year

Authors

Basis for classification

1983

Coffin’s classification[10]

1983

Marx classification[8]

1983

Marx staging[8]

1986

Morton and simpson’s Classification[11]

1987

Epstein’s stages[10]

1995

Late effects of normal tissue/ Somatic objective management analytic (SOMA) scale[12] Clayman’s classification[13]

Based on the extent of involvement Minor and Major Based on time period between radiation therapy and occurrence of osteoradionecrosis Type I-III Based on the treatment modalities involved along with HBO therapy Stage I-III Based on the duration of occurrence of osteoradionecrosis Minor, Moderate and Major Based on the progress of the disease Stage I-III Based on subjective symptoms and objective signs of osteoradionecrosis Grade 1-4

1997 1998 2000

Radiation therapy oncology group scoring[12] Store and Boysen’s staging[11]

2002

Kagan and Schwartz’s staging[14]

2003

Notani et al’s Classification[12]

2009

National cancer institute common terminology criteria (version‑IV)[12]

Based on the presence/absence of soft tissue break down Type I and II Based on the severity of bone morbidity Grade 0-5 Based on the extent of involvement of soft and hard tissues Stage 0-3 Based on the clinical assessment and physical findings of osteoradionecrosis Stage I-III For mandibular osteoradionecrosis after clinical examination and orthopantogram Class I-III Based on clinical presentation of osteoradionecrosis Grade 1-5

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Table 3: Classification of osteoradionecrosis Year

Classification

Stages/ grades

Description

Management

2002

Kagan and Schwartz’s staging[15]

Stage I

Conservative management

Grade 1

Minimal soft tissue ulceration and limited exposed cortical bone Localized involvement of the mandibular cortex and underlying medullary bone Minimal soft tissue ulceration Presence of an oro‑cutaneous fistula and mild soft tissue necrosis Full thickness involvement of the bone, including the inferior border. Pathological fracture may also be present Asymptomatic

Grade 2

Symptomatic

Grade 3

Severe symptoms

Grade 4 Grade 5

Life‑threatening consequences Death

Medical intervention indicated (e.g., topical agents); limiting instrumental ADL Limiting self‑care ADL; elective operative intervention indicated Urgent intervention indicated

Stage II Stage II a Stage II b Stage III 2009

Bone toxicity according to the National Cancer Institute Common Terminology Criteria[12]

Conservative management or minor surgical procedures

Surgical intervention, including bone and/ or soft‑tissue replacement Clinical or diagnostic observations only; intervention not indicated

ADL: Activities of daily living

Table 4: Risk factors of osteoradionecrosis Type of risk factors

Risk factors

Description of risk factors

Patient related factors

Gender Age[16] Race[15] Site[15]

Male predominance (male:female=1.6:1) Common in elderly patients Common in whites (74%) The oral cavity and oropharynx comprised the vast majority of primary tumors leading to osteoradionecrosis of the jaws Squamous cell carcinoma is more prone to lead to the occurrence of osteoradionecrosis As the stage of carcinoma increases the risk for development of osteoradionecrosis increases Larger tumours were associated with higher incidence of osteoradionecrosis Patients undergoing adjuvant radiotherapy had more risk for developing osteoradionecrosis 3D‑CRT or IMRT, have reduced the risk of developing osteoradionecrosis Risk of developing osteoradionecrosis increases with higher RT doses Increases acute toxicity especially mucositis, but its effect on late toxicity is less clear Ablative surgical procedures increased risk of developing osteoradionecrosis after radiation Tobacco smoking as a risk factor for osteoradionecrosis Alcohol consumption during and after radiotherapy is one of the risk factors for developing osteoradionecrosis Poor oral hygiene increases the risk for development of osteoradionecrosis Steroid and anticoagulants use before or after radiation reduced the risk of osteoradionecrosis Positive association between presence of dental disease pre‑radiation therapy and osteoradionecrosis For every one point increase in BMI, osteoradionecrosis risk decreased by 27% Secondary infection in post‑radiotherapy phase correlated with severe mandibular osteoradionecrosis Dentoalveolar surgery in post‑radiotherapy phase is an established predisposing factor for the development of osteoradionecrosis Poor nutritional status increases the risk of osteoradionecrosis

Tumour‑related factors

Treatment‑related factors

Miscellaneous factors[15‑18]

[15]

Histopathology[17] Stage[18] Size[16,17] Radiotherapy setting[15,18] Radiotherapy modality[15,17] Radiotherapy dose[17,18] Chemotherapy[16,17] Surgery[17,18] Active smoking[15-18] Alcohol[16] Inadequate oral hygiene[17] Steroids and anticoagulants[15] Dental diseases[15] Body‑mass index[16] Secondary infection[17] Dental extraction[18] Nutritional status[15]

of irradiated bone, but a complex metabolic and homeostatic deficiency of tissue that is created by radiation‑induced cellular injury; micro‑organisms play only a contaminating role in osteoradionecrosis; and trauma may or may not be an initiating factor.”[20]

Delanian’s radiation‑induced fibroatrophic theory Radiation‑induced fibrosis is a new theory that accounts for the damage to normal tissues, including bone, after radiotherapy. 

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It was introduced in 2004 when recent advances in cellular and molecular biology explained the progression of microscopically observed osteoradionecrosis [Figure 3].[21] Three distinct phases are seen: • The initial prefibrotic phase in which changes in endothelial cells predominate together with the acute inflammatory response • The constitutive organised phase in which abnormal fibroblastic activity predominates, and there is disorganisation of the extracellular matrix Journal of Dental Research and Review ● Jan-Apr 2014 ● Vol. 1 ● Issue 1

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Journal of Dental Research and Review ● Jan-Apr 2014 ● Vol. 1 ● Issue 1

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• The late fibroatrophic phase, when attempted tissue remodelling occurs with the formation of fragile healed tissues that carry a serious inherent risk of late reactivated inflammation in the event of local injury.[10]

Microbiology Osteoradionecrosis was earlier attributed to secondary infection in the traumatized irradiated tissue following the nonhealing wounds and exposed bone. However, this was challenged by Robert Marx in 1983.[20] The detailed description of various microorganisms detected in osteoradionecrosis is given in Table 5.[8,22-27] Further studies on bacterial flora associated with osteoradionecrosis are required, which may contribute to a more precise use of antibiotics.

Clinical features The incidence of osteoradionecrosis varies from 0.95% to 35% as shown in Table 6.[28-36] The patient is usually asymptomatic. Pain and evidence of exposed bone are the most common chief complaints. Trismus, fetor oris, and elevated body temperature are usually present during the initial period although acute infection is usually not present. Other clinical features of osteoradionecrosis are swelling, nonresolving painful mucosal ulcer, dysgeusia, dysguesia, xerostomia, food impaction, malocclusion, telangiectasia, orocutaneous fistula, and missing hair follicles. The tissues surrounding the bone may be indurated. Surface texture changes such as cutaneous flaking and keratinisation may be present. Surface colour changes may also be seen. Pathologic fracture of the jaws may be evident in severe cases. Rarely, Deep cellulitis of face and neck may be present.[28]

difficult to differentiate from recurrent tumour if bone changes are not visible on CT.[28] PET scan is helpful to differentiate between osteoradionecrosis and recurrent tumour.[28] Radionuclide bone scanning with technetium methylene diphosphonate (99mTc‑MDP) can identify pathophysiologic Table 5: Microbiology of osteoradionecrosis Year

Author(s)

Microorganisms isolated

1983 2005

Marx Store and Olsen[22]

2005

Støre, Eribe and Olsen[22] Hansen, Wagner, Kirkpatrick and Kunkel[23] Nason and Chole[24]

Surface contaminants Polymicrobial bacterial infection‑rods, spirochetes and cocci. Rods were the predominant Porphyromonas gingivalis Actinomyces species Actinomyces species

2006

2007 2005

Aas, Paster, Stokes, Olsen and Dewhirst[25]

1988

Calhoun, Shapiro, Stiernberg, Calhoun and Mader[26]

2006

Kjetil Pedersen[27]

Radiological features The presence of osteoradionecrosis cannot always be diagnosed radiographically and often clinically obvious signs of exposed necrotic may not be accompanied by significant radiologic changes. Plain radiography shows an ill‑defined cortical destruction without sequestration. The periphery may be ill‑defined as in osteomyelitis. Bone pattern can be granular. Scattered regions of radiolucency may be seen, with or without central sequestra. The most common effect on surrounding bone is stimulation of sclerosis. Computed tomography plays an important role in diagnosis of osteoradionecrosis since it is hard tissue lesion. Anterior– posterior and supero–inferior extent of the osteolytic lesion is best judged with CT scans comparatively. Hence, from diagnostic purpose to the surgical intervention, CT is recommended as far as osteoradionecrosis is concerned.[29] MRI reveals development of new heterogeneous signal within the marrow of an irradiated area (intermediate or low T1 signal, intermediate or high T2 signal). Adjacent muscles may appear oedematous and show intense enhancement, which can be 

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[8]

50% of the oral and 80% of the intestinal indigenous bacterial flora consist of uncultured phylotypes Firmicutes Actinobacteria Proteobacteria Fusobacteria‑Fusobacterium nucleatum Spirochaetes Bacteroidetes Campylobacter gracilis Streptococcus intermedius Peptostreptococcus sp. oral clone FG014 Uncultured bacterium clone RL178 Prevotella spp Streptococcus sp. Bacteroides sp. Lactobacillus sp. Eubacterium sp. Klebsiella sp. Actinomyces Treponema spp Porphyromonas gingivalis

Table 6: Incidence of osteoradionecrosis Year

Author(s)

1972 1972 1974 1976 1980

Carl, Schaaf, Chen, and Tak Yee[28] Daley, Drane, and Mc Comb[29] Wang[30] Bedwinck[31] Murray, Herson, Daly, and Zimmerman[32] Constantino, Friedman and Steinberg[33] Epstein and van der Meij et al.[34] Clayman[35]

1995 1997 1997 2000 2003 2004 2006

Thorn, Sand Hansen, Specht and Bastholt[36] Vissink, Jansma, Spijkervet, Burlage and Coppes[37] Reuther, Schuster, Mende, and Kübler[38] Wahl[39]

Incidence (%) 4 22 17 14 19 5 to 15 5 to 15 Before 1968-11.8 After 1968‑5.4 5 to 15 2.6 to 22 1 to 37.5 3 to 3.5

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changes in bone earlier than conventional radiography because scan changes reflect osteoblastic activity and good blood flow.[28]

at sites of osteoradionecrosis, confirming that it is a hypovascular and hypoxic tissue with decreased metabolic rate.[28]

Infrared spectroscopy is a noninvasive method. This shows a reduction of the amount of deoxygenated haemoglobin

Histologic features

Table 7: Preventive management of osteoradionecrosis

The histological findings noted by Marx showed endothelial death, hyalinisation, and thrombosis of vessels with a fibrotic periosteum.[25]

Measures to be taken Preradiation protocol A thorough clinical and radiographic examination is recommended for patient scheduled for radiotherapy Teeth with poor prognosis should be removed Oral hygiene regimen should be started as soon as possible. This includes. Teeth brushing with soft brush with the frequency of four times daily Warm saline (NaCl and NaHC03) mouth wash daily especially after brushing Fluoride treatment either 0.4% stannous fluoride gel, 1% sodium fluoride or 1% acidulated fluorophosphate gel in a custom tray for 15 min twice daily Intraradiation protocol Weekly prophylaxis with fluoridated polishing paste Analgesics, dietary supplements, antifungal and antibiotics prescription Postradiation protocol Patients who have completed radiotherapy should not wear dentures for at least a year to maximize tissue healing Fluoride treatment and oral hygiene care should be continued. Artificial saliva may have to be prescribed Life‑long follow‑up

Diagnostic criteria In 1997, Wong, Wood, and McLean have given diagnostic criteria for osteoradionecrosis that seem to be agreed by the majority of the authors: • The affected site should have been previously irradiated • There should be absence of recurrent tumour on the affected site • Mucosal breakdown or failure to heal should occur, resulting in bone exposure • The overlying bone should be ‘dead’, usually due to a hypoxic necrosis • Cellulitis, fistulation, or pathologic fracture need not be present to be considered as osteoradionecrosis.[30] Osteoradionecrosis usually develops after 3-6 months having bone exposure at least for 3 months.[30]

Table 8: Precautions to be taken for dental extractions in osteoradionecrosis

Management

Precautions to be taken

The management of osteoradionecrosis is divided into two methods. 1. Preventive management 2. Therapeutic management.

Preradiotherapy dental extractions The policy followed in most institutions is to remove unrestorable teeth prior to radiotherapy The mandibular teeth in the bone to be radiated above 6,000 cGy are indicated for extraction The extractions should be carried out in a nontraumatic manner with minimal damaged to the surrounding tissues. Planned preradiotherapy extractions include alveoloplasty and primary closure with minimal periosteal elevation Antibiotic therapy is usually prescribed for 1 to 4 weeks The interval period between extraction and radiotherapy is extremely crucial Beumer III and Curtis and Maxymiw, Wood & Liu stated that at least two weeks interval is required in order not to delay the radiation therapy Marx and Johnson recommended an interval of three weeks before commencing radiotherapy, based on experimental studies that show osteoid takes 3 weeks to form Teeth with questionable prognosis should be carefully discussed with the patient Post‑radiotherapy dental extractions Extractions should be limited to one or two teeth at a time The techniques should be as Atraumatic and aseptic as possible Flaps should be raised conservatively to minimize displacement of mucoperiosteum Sharp projections of bone require· re‑contouring or minor alveoloplasty followed by primary closure Hyperbaric oxygen therapy can be considered as prophylaxis against ORN The prophylactic use of ultrasound as an alternative to hyperbaric oxygen is recommended by Reher and Harris Prophylactic antibiotics for extractions are required ORN: Osteoradionecrosis Journal of Dental Research and Review ● Jan-Apr 2014 ● Vol. 1 ● Issue 1

Preventive management The prevention of osteoradionecrosis begins as early as the head and neck malignancy is diagnosed. The patient should be reviewed by the multidisciplinary team consisting of Table 9: Therapeutic management of osteoradionecrosis Methods Nonsurgical management Pharmacological Antibiotic therapy Analgesics Antifungal therapy Antiviral therapy Newer agents: Pentoxyphilline, tocopherol, clodronate and combination therapy Nonpharmacological Local wound care Hyperbaric oxygen therapy Ultrasound therapy Electrotherapy Ozone therapy Surgical management Sequestrectomy Resection with continuity defect Reconstruction Rehabilitation 47 

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a dentist/oral and maxillofacial surgeon. The measures taken to prevent osteoradionecrosis, as per Donoff’s protocol, are mentioned in Table 7.[37] The precautions that are to be taken during dental extraction are summarized in Table 8.[38]

Therapeutic management The nonsurgical and surgical management with a note on recent medications are summarized in Table 9.[39]

Conclusion Osteoradionecrosis can be a cruel blow to patients and their families who have been enduring radiotherapy for the treatment of cancer. Prevention of osteoradionecrosis by regular follow‑up and early diagnosis should be the goal of every health care professional managing head and neck cancer patients. Improved radiotherapy protocols, multidisciplinary preventive care and reconstructive surgery can help to improve the quality of life of patients suffering from osteoradionecrosis.

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13. Meghji S. Bone remodelling. Br Dent J 1992;172:235-42. 14. Van Merkesteyn JP, Bakker DJ, Borgmeijer-Hoelen AM. Hyperbaric oxygen treatment of osteoradionecrosis of the mandible: experience in 29 patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;80:12-6. 15. Regaud C (1922a) Sur la necrose des os attenté par un processus cancereux et traites par les radiaions. Compt Rend Soc Biol 1992a;87:427. 16. Hutchinson IL, Colpe M, Delpy DT, Richardson CE, Harris M. The investigation of osteoradionecrosis of the mandible by near infrared spectroscopy. Br J Oral Maxillofac Surg 1990;28:150-4. 17. Tong AC, Leung AC, Cheng JC, Sham J. Incidence of complicated healing and osteoradionecrosis following tooth extraction in patients receiving radiotherapy for treatment of nasopharyngeal carcinoma. Aust Dent J 1999;44:187-94. 18. Oh HK, Chambers MS, Garden AS, Wong PF, Martin JW. Risk of osteoradionecrosis after extraction of impacted third molars in irradiated head and neck cancer patients. J Oral Maxillofac Surg 2004;62:139-44. 19. Meyer I. Infectious diseases of the jaws. J Oral Surg 1970;28:17-26. 20. Marx RE. Osteoradionecrosis: A new concept of its pathophysiology. J Oral Maxillofac Surg 1983a;41:283-8. 21. Delanian S, Lefaix JL. The radiation-induced fibroatrophic process: Therapeutic perspective via thantioxidant pathway. Radiother Oncol 2004;73:119-31. 22. Store G, Eribe ERK, Olsen I. DNA-DNA hybridization demonstrates multiple bacteria in osteoradionecrosis. Int J Oral Maxillofac Surg 2005;34:193-6. 23. Hansen T, Kunkel M, Weber A, James Kirkpatrick C.Osteonecrosis of the jaws in patients treated with bisphosphonates - histomorphologic analysis in comparison with infected osteoradionecrosis. J Oral Pathol Med 2006 Mar;35:155-60. 24. Nason R, Chole RA. Bacterial biofilms may explain chronicity in osteoradionecrosis of the temporal bone. Otol Neurotol 2007;28:1026-8. 25. Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE.Defining the normal bacterial flora of the oral cavity. J Clin Microbiol 2005;43:5721-32. 26. Calhoun KH, Shapiro RD, Stiernberg CM, Calhoun JH, Mader JT. Osteomyelitis of the mandible. Arch Otolaryngol Head Neck Surg. 1988;114:1157-62. 27. Aas JA, Reime L, Pedersen K, Eribe ER, Abesha-Belay E, Støre G, et al. Osteoradionecrosis contains a wide variety of cultivable and noncultivable bacteria. J Oral Microbiol 2010;2. doi: 10.3402/jom. v2i0.5072. 28. Chrcanovic BR, Reher P, Sousa AA, Harris M. Osteoradionecrosis of the jaws – a current overview – Part 1. Physiopathology and risk and predisposing factors. J Oral Maxillofac Surg 2010;14:3-16. 29. Al-Nawas B, Duschner H, Grötz KA. Early cellular alterations in bone after radiation therapy and its relation to osteoradionecrosis. J Oral Maxillofac Surg 2004;62:1045. 30. Wang, Schaaf, Chen. Dental extractions in irradiated head and neck patient: a retrospective analysis of Memorial Sloan-Kettering Cancer Center protocols, criteria and end results. J Oral Maxillofac Surg 1974;61:1123-31. 31. Bedwinck, Hutchinson IL. Complications of radiotherapy in the head and neck: an orofacial surgeon's view. In: Tobias JS, Thomas PRM (eds) Current radiation oncology. Arnold, London, 1976. pp 144-77. 32. Thorn JJ, Hansen HS, Specht L, Bastholt L. Osteoradionecrosis of the jaws: Clinical characteristics and relation to the field of irradiation. J Oral Maxillofac Surg 2000;58:1088-93. 33. Hutchison IL, Cope M, Delpy DT, Richardson CE, Harris M. The investigation of osteoradionecrosis of the mandible by near infrared spectroscopy. Br J Oral Maxillofac Surg 1995;28:150-4. 34. van der Meij, Beumer J 3rd, Harrison R, Sanders B, Kurrasch M. Preradiation dental extractions and the incidence of bone necrosis. Head Neck Surg 1997;5:514-21. 35. Harris M. The conservative management of osteoradionecrosis of the mandible with ultrasound therapy. Br J Oral Maxillofac Surg 1997;30:313-8. 36. Morrish RB Jr, Chan E, Silverman S Jr, Meyer J, Fu KK, Greenspan D. Osteonecrosis in patients irradiated for head and neck carcinoma. Cancer 1981;47:1980-3. 37. Tong AC, Leung AC, Cheng JC, Sham J. Incidence of complicated healing and osteoradionecrosis following tooth extraction in patients

Journal of Dental Research and Review ● Jan-Apr 2014 ● Vol. 1 ● Issue 1

[Downloaded free from http://www.jdrr.org on Wednesday, September 09, 2015, IP: 14.140.125.38] Suryawanshi, et al.: Maxillofacial osteoradionecrosis receiving radiotherapy for treatment of nasopharyngeal carcinoma. Aust Dent J 1999;44:187-94. 38. Ramli R, Ngeow WC, Rahman RA, Chai WL. Managing complications of radiation therapy in head and neck cancer patients: Part IV. Management of osteoradionecrosis. Singapore Dent J 2006;28:11-5.

39. Vanderpuye V, Goldson A. Osteoradionecrosis of the mandible. J Natl Med Assoc 2000;92:579-84. Source of Support: Nil, Conflict of Interest: None declared.

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