osteoradionecrosis
DESCRIPTION
ORN in detailTRANSCRIPT
![Page 1: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/1.jpg)
OSTEORADIONECROSIS
Dr. LAKSHMI NARAYANA MALABAR CANCER CENTRE
![Page 2: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/2.jpg)
Osteoradionecrosis (ORN), also known as post radiation osteonecrosis (PRON).
It was first described by Regaud 1920.
A serious, debilitating and deforming potential complication of radiation therapy
![Page 3: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/3.jpg)
![Page 4: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/4.jpg)
RADIATION INJURY An early and late phase.
Early radiation injury is secondary to depletion of frequently dividing cells (Labile cells)
Late radiation injury occurs in those tissues that proliferate slowly or not at all (Stable cells)
![Page 5: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/5.jpg)
PATHOPHYSIOLOGY OF OSTEORADIONECROSIS
Meyer in 1970 –
Triad of radiation, trauma, and infection
- development of osteoradionecrosis.
Irradiated bone +
Traumatic event +
Ingress of microorganisms =
Osteoradionecrosis
![Page 6: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/6.jpg)
Failure to demonstrate bacterial invasion in compromised bone,
Occurrence with no definable traumatic event, Poor response to treatment with antibiotic therapy .
..... Forced to think in another way
![Page 7: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/7.jpg)
PATHOPHYSIOLOGY OF OSTEORADIONECROSIS
Marx 1983 …...
Osteoradionecrosis - cumulative tissue damage
induced by radiation rather than trauma or bacterial invasion of bone.
Complex metabolic and tissue homeostatic
deficiency seen in hypocellular, hypovascular, and
hypoxic tissue.
Three "H" principle.
![Page 8: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/8.jpg)
THREE "H" PRINCIPLE
Radiation damaged cells not replaced by cells of the same type
Results in less cellular, more extracellular elements – collagen.
Fibrotic and poorly vascularized tissue – absent healing ability.
Breakdown becos – absent cellular turnover
Spontaneous breakdown.
![Page 9: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/9.jpg)
Role of trauma
collagen lysis and induced cellular death. This creates a wound with an oxygen
requirementand a demand for the basic elements of tissue repair
that are beyond the capabilities of the local tissue toprovide.
![Page 10: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/10.jpg)
EFFECTS OF RADIATION ON BONE
Depletion of osteoblasts - Increased osteoclastic resorption of bone
Reduced bone rebuilding potential + Progressive endarteritis - reduction of blood flow
through the Haversian and Volkmann’s canals = OSTEOPOROSIS
OSTEONECROSIS
![Page 11: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/11.jpg)
ULTIMATE EFFECT
Radiation
Hypoxic – Hypovascular - Hypocellular tissue
Tissue breakdown - Cellular death and collagen lysis exceed synthesis and cellular replication
Progression to non-healing wound - Energy, oxygen, and metabolic demands clearly exceed the supply
![Page 12: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/12.jpg)
RADIATION-INDUCEDFIBROATROPHIC THEORY
key event in the progression of ORN is the activation and dysregulation of fibroblastic activity that leads to atrophic tissue within a previously irradiated area.
![Page 13: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/13.jpg)
Three distinct phases are seen: prefibrotic phase in which changes in
endothelial cells predominate,with the acute inflammatory response.
constitutive organised phase in which abnormal fibroblastic activity predominates, and there is disorganisation of the extracellular matrix
late fibroatrophic phase, 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
![Page 14: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/14.jpg)
endothelial cells are injured cells produce chemotactic cytokines that
trigger an acute inflammatory response vascular thrombosis local ischaemia and tissue loss. seepage of various cytokines that cause
fibroblasts to become myofibroblasts. unusually high rates of proliferation,
secretion of abnormal products of the extracellular matrix, and a reduced ability to degrade such components.
![Page 15: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/15.jpg)
![Page 16: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/16.jpg)
MICRORADIOGRAPHIC ANALYSIS
Of bone in ORN suggests four possible mechanismsof bony destruction:
progressive resorption of osteoclasts mediated by macrophages that are unaccompanied by osteogenesis;
periosteocytic lysis, pathognomic of ORN; Extensive demineralisation that is secondary to
external stimuli such as saliva and bacterial products; and
accelerated aging of bone
![Page 17: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/17.jpg)
OSTEORADIONECROSIS
In the head and neck region Commonest site is mandible. Also reported in maxilla, temporal bone, sphenoid
and base of skull.
![Page 18: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/18.jpg)
WHY MANDIBLE AT AN INCREASED RISK?
Generally a bone – with more tenuous blood supply and more mechanically stress - more susceptible to the development of osteoradionecrosis.
The craniofacial skeleton receives its blood supply in three distinct manners:
1. vessels that enter the bone via direct muscular attachments, 2. periosteal perforators, and 3. intramedullary vessels
![Page 19: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/19.jpg)
WHY MANDIBLE AT AN INCREASED RISK?
Mandible - different dominant pattern of blood supply according to various anatomical regions in the bone itself.
The posterior segment of the mandible (condyle process and neck, coronoid, angle, and upper ramus) - redundant blood supply from the surrounding musculature, either from direct muscular attachments or through muscular perforators penetrating the periosteum.
Because of this redundancy, the posterior segment is typically less susceptible to radiation induced ischemia.
![Page 20: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/20.jpg)
The anterior segment of the mandible - no prominent nutrient vessel supply through the muscular attachments.
Injection studies in the mandible - primary nutrient source
for the body, parasymphyseal, and symphyseal regions is through an intramedullary source, the inferior alveolar artery.
In a study by Bras, et. al., radiation induced obliteration of the inferior alveolar artery was consistently found in osteoradionecrosis of mandible and was felt to be a dominant factor in the onset of the disease.
Bras J, DeJonge HKT, VanMerkestyen JPR. Osteoradionecrosis of the Mandible: Pathogenesis. American Journal of Otolaryngology. 11: pgs 244 - 250. 1990.
![Page 21: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/21.jpg)
INCIDENCE OF OSTEORADIONECROSIS
The overall incidence of ORN in pooled studies among radiation patients has dramatically declined.
11.8% (391 of 3,312 patients) before 1968
5.4% (602 of 11,077 patients) from 1968 to 1992 due to more efficient techniques in radiation
therapy.
Clayman L. Management of dental extractions in irradiated jaws: A protocol without hyperbaric oxygen therapy. J Oral Maxillofac Surg 1997;55:275–281.
![Page 22: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/22.jpg)
INCIDENCE OF OSTEORADIONECROSIS
Since 1997, lower incidence of 3.0%.
Michael J. Wahl, D.D.S. Osteoradionecrosis prevention myths. Int. J. Radiation Oncology Biol. Phys., Vol. 64, No. 3, pp. 661–669, 2006
![Page 23: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/23.jpg)
OVERALL INCIDENCE OF ORN IN RADIATION PATIENTS SINCE 1997-
CONTD
Patients (n) ORN cases (n) Study
151 3 Ang et al., 2001 (3)636 14 Babik et al., 2000 (4)1 0 Berg et al., 2000 (5)334 5 Bernier et al., 2004 (6)116 2 Brizel et al., 1998 (7)8 0 Carl and Ikner, 1998 (8)107 1 Chaux-Bodard et al., 2004 (9)35 4 Chavez and Adkinson, 2001 (10)1,758 61 Cheng et al., 2006 (11)413 10 Cooper et al., 2004 (12)24 0 David et al., 2001 (13)918 9 Dische et al., 1997 (14)
![Page 24: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/24.jpg)
OVERALL INCIDENCE OF ORN IN RADIATION PATIENTS SINCE 1997- CONTD
Patients (n) ORN cases (n) Study
759 17 Fu et al., 2000 (15)83 1 Gwozdz et al., 1997 (16)47 0 Lambert et al., 1997 (17)100 10 Lozza et al., 1997 (18)1,495 27 Mendenhall, 2004 (19)1 1 Németh et al., 2000 (20)81 4 Oh et al., 2004 (21)830 68 Reuther et al., 2003 (22)268 27 Studer et al., 2004 (23)1,194 11 Sulaiman et al., 2003 (24)193 9 Toljanic et al., 1998 (25)44 4 Tong et al., 1999 (26)36 2 Vudiniabola et al., 1999 (27)
9,632 290 3.0%
![Page 25: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/25.jpg)
TYPES OF OSTEORADIONECROSIS SPONTANEOUS ORN (39%) – degradative function
exceeds new bone production.
TRAUMA INDUCED ORN (61%) – reparative capacity of bone is insufficient to overcome an insult.
Bone injury can occur through direct trauma - 1. tooth extraction [84%], 2. related cancer surgery or biopsy [12%], 3. denture irritation [1%]) or 4. by exposure of the oral cavity to the environment secondary to overlying soft tissue necrosis.
Remy H Blanchaert, Jr, MD, DDS, Osteoradionecrosis of the Mandible
eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Head
And Neck Oncology
![Page 26: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/26.jpg)
CLASSIFICATION OF OSTEORADIONECROSIS
By Marx(1983)
Type I – Develops shortly after radiation, Due to synergistic effects of surgical trauma and radiation injury.
Type II – Develops years after radiation and follows a trauma Rarely occurs before 2 year after treatment & commonly occurs after 6 years. Due to progressive endarteritis and vascular effusion.
![Page 27: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/27.jpg)
Type III
Occurs spontaneously without a preceding a traumatic event.
Usually occurs between 6 months and 3 years after radiation.
Due to immediate cellular damage and death due to radiation
treatment.
![Page 28: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/28.jpg)
Stage I – Resolved healed osteonecrosis (A) – No pathologic fracture (B) – Pathologic fracture Stage II – Chronic persistent and non-progressive osteonecrosis (A) – No pathologic fracture (B) – Pathologic fracture Stage III – Active progressive osteonecrosis (A) – No pathologic fracture (B) – Pathologic fracture
![Page 29: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/29.jpg)
grade I, ORN confined to alveolar bone; grade II, ORN limited to the alveolar bone and/or
mandible above the level of inferior alveolar canal;
grade III, ORN involving the mandible below the level of inferior alveolar canal and ORN with a skin fistula and/or pathologic fracture.
Notani K, Yamazaki Y, Kitada H, Sakakibara N, Fukuda H, Omori K, Nakamura M. Management of mandibular osteroradionecrosis corresponding to the severity of osteoradionecrosis and the method of radiotherapy. Head Neck 2003: 25: 181–
186.
![Page 30: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/30.jpg)
Contributing factors of osteoradionecrosis
Radiation factors Tumor factors Dental factors Others
![Page 31: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/31.jpg)
![Page 32: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/32.jpg)
RADIATION FACTORS
Mechanism of radiation delivery – impact on the development and severity of necrosis.
Brachytherapy implants have the greatest relative risk in combination with external beam exposures of 6500 cGy
(12 - 15 times).
Sanger JR, Matloub HS, Yousif NJ, Larson DL. Management of Osteoradionecrosis of the Mandible. Clinics in Plastic Surgery.
20(3): pg 520. 1993.
![Page 33: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/33.jpg)
TUMOR FACTORS Statistically significant incidence of osteoradionecrosis
with 1. more advanced tumors (stage III or IV) 2. recurrent tumors 3. tumors involving the tongue, retromolar trigone, and floor of mouth, and 4. tumors invading bone
Kuluth EV, Jain PR, Stutchell RN, Frich JC. A Study of Factors Contributing to the Development of Osteoradionecrosis of the
Jaws. The Journal of Prosthetic Dentistry. 59 (2): pg 200. 1988.
![Page 34: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/34.jpg)
INCIDENCE OF ORN ACCORDING TO ANATOMIC SITE OF THE TUMOR
![Page 35: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/35.jpg)
DENTAL FACTORS Presence of carious and periodontally compromised teeth
in the irradiated mandible - associated with osteoradionecrosis.
The current school of thought - grossly carious, periodontally "hopeless," or those teeth deemed to have poor prognosis for retention beyond twelve months should be removed prior to the initiation of radiation therapy - this avoids dental manipulations in the post irradiation period.
Clayman L. Management of Dental Extractions in Irradiated Jaws: A Protocol Without Hyperbaric
Oxygen Therapy. Journal of Oral and Maxillofacial Surgery. 55: pg 275. 1997.
![Page 36: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/36.jpg)
DENTAL FACTORS
The post surgical healing time prior to starting radiation treatment -under debate.
Marx and Johnson - compared the incidence of osteoradionecrosis in pre-treatment tooth removal patients to the timing of the surgical insult.
From their collected data, most of the osteoradionecrosis developed - in those patents in which treatment was begun within the first two weeks post extraction.
No cases of osteoradionecrosis, when the tissue was allowed to heal for 21 days or more.
Marx RE, Johnson RP. Studies in the Radiobiology of Osteoradionecrosis and Their Clinical Significance. Oral Surgery Oral Medicine Oral Pathology. 64 (4):
pg 384. 1987.
![Page 37: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/37.jpg)
![Page 38: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/38.jpg)
![Page 39: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/39.jpg)
SIGNS AND SYMPTOMS Pain Swelling Trismus Halitosis Food impaction in the area of the lesion Exposed bone Pathologic fracture Oro-cutaneous fistula
![Page 40: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/40.jpg)
SYMPTOMATOLOGY OF PATIENTS WITH ORN
E. Ang, C. Black, J. Irish, D.H. Brown, P. Gullane, B. O’Sullivan and P.C. Neligan ,Reconstructive options in the treatment of osteoradionecrosis of the
craniomaxillofacial skeleton, British Journal of Plastic Surgery (2003), 56, 92–99
![Page 41: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/41.jpg)
EVALUATION OF OSTEORADIONECROSIS
A high index of suspicion that this presentation may be recurrent, or persistent, or even metastatic malignancy.
Deep biopsy of the lesion is helpful
Review of the pertinent radiation therapy records including the ports of radiation therapy, the total dose, dose per fraction, and timing of therapy.
A through dental examination - in those patients with remaining dentition.
![Page 42: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/42.jpg)
IMAGING STUDIES
Plain radiography of the mandible - depicts areas of local decalcification or sclerosis.
The formation of sequestra or involucra occur late or not at all in irradiated bone because of the severely compromised blood supply.
![Page 43: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/43.jpg)
PATHOLOGIC FRACTURE
![Page 44: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/44.jpg)
MANAGEMENT OF OSTEORADIONECROSIS
Initial treatment – control of infection if present.
Gentle irrigation of the soft tissue margins - removes debris and reduces inflammation.
Supportive treatment with fluids and a liquid or semi liquid diet high in proteins and vitamins.
![Page 45: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/45.jpg)
MANAGEMENT OF OSTEORADIONECROSIS
Pain may be controlled with narcotic analgesics, bupivacaine or alcohol nerve blocks, nerve avulsion or rhizotomy.
![Page 46: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/46.jpg)
An area of irradiated bone and mucosa that breaks down, whatever the cause, has a
much greater oxygen and metabolic demand than it had prior to being wounded.
![Page 47: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/47.jpg)
HYPERBARIC OXYGEN THERAPY
HBO is an adjuvant to surgery rather than an independent therapy.
It was first recommended by Valenzuela (1887) as a treatment for bacterial infections.
Reports of the benefits of HBO in osteoradionecrosis were first reported in the 1970’s by Mainous, Hart and Boyne.
![Page 48: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/48.jpg)
HYPERBARIC OXYGEN THERAPY
The basic mechanism of hyperbaric oxygen therapy is endothelial cell proliferation resulting in neovascularisation and collagen synthesis.
It consists of exposing a patient to intermittent short term 100% oxygen inhalation at a pressure greater than 1 atmosphere.
![Page 49: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/49.jpg)
HYPERBARIC OXYGEN THERAPY Marx (1983) presented a new concept in osteoradionecrosis
management - Marx HBO / surgical protocol.
The compromised bone and soft tissues are improved and revascularised with HBO and then if necessary, the necrotic bone is surgically removed.
The patient’s response or lack of response to HBO is the main
indicator for surgery.
The primary thrust is to distinguish dead bone from merely compromised bone and to surgically resect all dead bone.
![Page 50: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/50.jpg)
Three treatment stages of advancing clinical severity.
All patients who meet the definition of osteoradionecrosis (exposed bone present for six months or longer with no healing), begin stage I treatment.
If the disease does not resolve, Stage II treatment is begun.
Three exceptions representing advanced disease: patients with pathologic fractures, fistulas or radiographic evidence of osteolysis to the inferior border begin directly with stage III treatment and usually require discontinuity resection.
![Page 51: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/51.jpg)
STAGE I
Perform 30 HBO dives (1 dive per day, Monday-Friday) to 2.4 atmospheres for 90 minutes in a multiplace chamber or 2.0 ATA for 120 min in a monoplace chamber .
Reassess the patient to evaluate decreased bone exposure, granulation tissue covering exposed bone, resorption of nonviable bone, and absence of inflammation.
For patients who respond favorably, continue treatment to a total of 40 dives.
For patients who are not responsive, advance to stage II.
![Page 52: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/52.jpg)
STAGE 2 Perform transoral sequestrectomy with primary wound closure
followed by continued HBO to a total of 40 dives.
If wound dehiscence occurs, advance patients to stage III.
![Page 53: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/53.jpg)
STAGE 3
Patients who present with orocutaneous fistula, pathologic fracture, or resorption to the inferior border of the mandible advance to stage III immediately after the initial 30 dives.
Perform transcutaneous mandibular resection, wound closure, and mandibular fixation with an external fixator or maxillomandibular fixation, followed by an additional 10 postoperative HBO dives.
![Page 54: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/54.jpg)
STAGE 3 R Perform mandibular reconstruction 10 weeks after
successful resolution of mandibular ORN.
Reconstruction of the mandible in these patients consisted of either autogenous particulate bone and marrow within a custom-made stainless steel metal crib or autogenous particulate bone and marrow within a freeze-dried allogenic bone framework .
Complete 10 additional postoperative HBO dives.
![Page 55: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/55.jpg)
With adherence to this protocol, Marx noted resolution of all cases of osteoradionecrosis within one of the stages.
More specifically, 15% resolved in stage I, 15% resolved during stage II, and the remainder (70%) resolved in stage III.
RESULTS
![Page 56: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/56.jpg)
CONTRAINDICATIONS FOR HBO THERAPY
1. Untreated pneumothorax - (Absolute contraindication)
2. Pregnancy3. Emphysema4. Upper respiratory tract infection5. Uncontrollable fever6. Optic neuritis7. Ear problems
![Page 57: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/57.jpg)
![Page 58: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/58.jpg)
![Page 59: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/59.jpg)
![Page 60: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/60.jpg)
![Page 61: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/61.jpg)
![Page 62: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/62.jpg)
Role of Pentoxyphylline in osteoradionecrosis
Pentoxyphylline (Trental) is a member of the methylxanthine class of drugs as are caffeine and theophylline.
exerts an anti-TNF effect, increases erythrocyte flexibility, dilates
blood vessels, inhibits inflammatory reactions in vivo, inhibits proliferation of human dermal fibroblasts and the production of extracellular matrix, and increases collagenase activity in vitro.
The overall effect - blood more liquid and enable the red blood cells to travel deeper into tissues.
This enables better oxygen delivery to tissues and improved microcirculation.
![Page 63: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/63.jpg)
DELANIAN S, DEPONDT J, LEFAIX JL: MAJOR HEALING OF REFRACTORY MANDIBLE OSTEORADIONECROSIS AFTER
TREATMENT COMBINING PENTOXIFYLLINE AND TOCOPHEROL: A PHASE II TRIAL. HEAD NECK 27:114, 2005
Between June 1995 and January 2002, 18 patients were given a daily oral combination of 800 mg of PTX and 1000 IU of vitamin E for 6 to 24 months.
In addition, the last eight patients who were the worst cases were given 1600 mg/day clodronate 5 days a week.
RESULTS: Sixteen (89%) of 18 patients achieved complete recovery. The remaining two patients exhibited a 75% response at 6 months.
![Page 64: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/64.jpg)
![Page 65: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/65.jpg)
![Page 66: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/66.jpg)
PREVENTION OF OSTEORADIONECROSIS Prior to radiation therapy- Dental consultation - To
achieve optimal oral health.
Sleeper (1950) and Meyer (1958) - recommendations before irradiation is started.
1. The mouth should be made as clean as possible by scaling and irrigation.
2. All infections of soft tissues should be eliminated.
3. All infected and non-vital teeth should be extracted. All teeth in the line of irradiation, good or bad, also should be extracted.
![Page 67: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/67.jpg)
PREVENTION OF OSTEORADIONECROSIS
4. All teeth periodontally involved should be extracted.
5. If the parotid and submandibular glands are to receive heavy irradiation, all teeth should be extracted.
6. If the mouth shows much neglect throughout, all teeth should be extracted.
7. The use of antibiotic prophylaxis b4 extraction, though common practise, has not been validated in any study. However, prophylaxis could be incorporated into the protocol if desired.
![Page 68: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/68.jpg)
PREVENTION OF OSTEORADIONECROSIS
8. The patient should be thoroughly instructed in the maintenance of absolute hygienic care of the mouth.
9. Fluoride therapy should be used to prevent irradiation caries of any remaining teeth.
10. No radiotherapy should be attempted for 7-10 days following extractions in the mandible or for 3-6 days in the maxilla. If possible the radiation should start only 21 days after the tooth extractions.
![Page 69: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/69.jpg)
ORN AFTER PRERADIATION EXTRACTION AND POSTRADIATION
EXTRACTION Since 1986, the incidence of ORN after preradiation
extraction (3.0 –3.2%; 23 of 711–756 patients) was approximately the same as the incidence of ORN after postradiation extraction (3.1–3.5%; 16 of 461–508 patients) in pooled studies
Osteoradionecrosis can also occur in edentulous patients or spontaneously, and preradiation extractions cannot prevent these.
Michael J. Wahl, D.D.S. Osteoradionecrosis Prevention Myths
Int. J.Radiation Oncology Biol. Phys., Vol. 64, No. 3, pp. 661–669, 2006
![Page 70: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/70.jpg)
DELAY RADIATION THERAPY?
“Because the risk of ORN is approximately the same with postradiation as with preradiation extractions, it might be more important not to delay radiation therapy than to wait for preradiation extraction sites to heal”.
Michael J. Wahl, D.D.S. Osteoradionecrosis Prevention Myths
Int. J.Radiation Oncology Biol. Phys., Vol. 64, No. 3, pp. 661–669, 2006
![Page 71: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/71.jpg)
INT. J. RADIATION ONCOLOGY BIOL. PHYS., VOL. 64, NO. 3, PP. 661–669, 2006
![Page 72: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/72.jpg)
Instructions after radiotherapy of the jaws1. Strict oral hygiene.
2. If future work on the teeth or an operation - patients must inform the physician or dentist that their jaws have been previously irradiated.
3. Preferably no further extractions. If a tooth in the area of irradiation becomes caries - extraction must be done as atraumatically as possible under a course of antibiotics both preoperatively and postoperatively.
4. Dentures should not be used in the irradiated arch for one year after therapy.
![Page 73: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/73.jpg)
OSTEORADIONECROSIS OF THE TEMPORAL BONE
Following the treatment of nasopharyngeal carcinoma by external-beam radiotherapy.
Ramsden et al classified osteoradionecrosis of the temporal bone as either local or diffuse.
The local type is characterized by the presence of a bone sequestrum that is confined to the external auditory canal.
Patients usually present with chronic, offensive otorrhea and occasionally otalgia.
![Page 74: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/74.jpg)
OSTEORADIONECROSIS OF THE TEMPORAL BONE
In the diffuse type - widespread ischemic osteonecrosis of the skull base and adjacent structures.
These patients have usually received higher doses of external irradiation to the temporal bone.
Severe otalgia and pulsatile, offensive otorrhea are common. Cranial nerve palsies might also be present.
Diffuse osteoradionecrosis is associated with a recognized
incidence of local or regional complications, such as suppurative labyrinthitis, trismus, meningitis, cerebrospinal fluid leakage, and internal carotid aneurysm.
![Page 75: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/75.jpg)
MANAGEMENT OF OSTEORADIONECROSIS IN THE TEMPORAL BONE
Controversial.
For localized osteoradionecrosis - Conservative treatment with frequent aural toileting and topical antibiotics.
Rudge described complete success with the use of hyperbaric oxygen therapy specifically for osteoradionecrosis of the temporal bone.
![Page 76: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/76.jpg)
MANAGEMENT OF OSTEORADIONECROSIS IN THE TEMPORAL BONE
Other alternatives, such as modified radical mastoidectomy, have been performed in selected cases with good initial results, but no long-term follow up is available to validate this choice of treatment.
Temporal bone resection for diffuse osteoradionecrosis is reported to be an effective treatment.
![Page 77: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/77.jpg)
BISPHOSPHONATE RELATED OSTEONECROSIS OF THE JAW
First recognized in 2003 as a complication of bisphosphonate therapy
Higher frequency in the mandible (63%) than in the maxilla (38%)
Etiology is unclear and is the subject of current research and investigation.
![Page 78: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/78.jpg)
BISPHOSPHONATE RELATED OSTEONECROSIS OF THE JAW
True incidence is difficult to estimate.
Depending on recent retrospective reports could be <1%-9% of cancer patients receiving bisphosphonates.
Seen in cancer patients with multiple antineoplastic medications as well as bisphosphonates.
Multiple myeloma, breast cancer and prostate cancer are the primary neoplasms affected.
![Page 79: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/79.jpg)
BISPHOSPHONATE RELATED OSTEONECROSIS OF THE JAW
Current management is empiric. A conservative approach is recommended - includes
antibiotics, oral rinses, pain control, and limited debridement.
The roles of surgical treatment and hyperbaric oxygen therapy are still under investigation.
![Page 80: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/80.jpg)
CONCLUSION
The aim should be its prevention.
An understanding of the risk factors is important in preventing ORN after radiation therapy.
![Page 81: Osteoradionecrosis](https://reader036.vdocument.in/reader036/viewer/2022070317/556e0b54d8b42aba5d8b4e24/html5/thumbnails/81.jpg)
THANK YOU