This document provides information about osteomyelitis and osteoradionecrosis of the jaws. It defines osteomyelitis as an inflammatory condition of bone that begins as an infection of the medullary cavity and spreads to involve the surrounding bone and periosteum. Predisposing factors include trauma, radiation damage, and systemic diseases. Imaging techniques useful for diagnosis include conventional radiographs, radionuclide scans, CT, and MRI. Treatment involves antibiotics, surgery to drain abscesses or remove dead bone (sequestra), and reconstruction if large portions of bone need to be resected.
Classification of Impaction and Methods & Techniques of Third molar/Manidibular impaction removal,Flap designs of impaction removal techniques and more
Classification of Impaction and Methods & Techniques of Third molar/Manidibular impaction removal,Flap designs of impaction removal techniques and more
Splinting is one of the oldest forms of aids to periodontal therapy. By redistribution of forces on the affected teeth the splint minimizes the effects caused by loss of support. Splinting teeth to each other allows weakened teeth to be supported by neighbouring teeth. This presentation reviews the rationale, techniques, advantages and ill effects of stabilization of teeth by splinting as an aid to periodontal therapy. With the acceptance and clinical predictability of adhesive procedures, the use of conservative bonding techniques to splint teeth offers a useful alternative to more invasive restorative procedures. Loss of tooth-supporting structures results in tooth mobility. Increased tooth mobility adversely affects function, aesthetics, and the patient’s comfort. Splints are used to overcome all these problems. When faced with the dilemma of how to manage periodontally compromised teeth, splinting of mobile teeth to stronger adjacent teeth is a viable option. This prolongs the life expectancy of loose teeth, gives stability for the periodontium to reattach, and improves comfort, function and aesthetics.
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine
Al-Azhar University. The Pathogenesis of infection in oro-facial region due to odontogenic origin is a common clinical issue. bacterial invasion to deeper tissues usually a spread from diseased dental pulp. Recent evidences indicated a multi-microbial nature. The spread of infection is governed by the thickness of the investing bone and the anatomical relation of the tooth root to the attached muscle. Infection could spread from one facial space to another, and the condition may be aggravated to life threatening situations.
Arthrocentesis of the temporomandibular jointAhmed Adawy
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine, Al-Azhar University. Arthrocentesis of the temporomandibular joint refers to lavage of the upper joint space, hydraulic pressure and manipulation to release adhesions of the “anchored disc phenomenon” and improve motion. The technique of arthrocentesis is discussed together with the indications and contraindications of the procedure. Further, the presentation includes modifications of the standard technique.
Splinting is one of the oldest forms of aids to periodontal therapy. By redistribution of forces on the affected teeth the splint minimizes the effects caused by loss of support. Splinting teeth to each other allows weakened teeth to be supported by neighbouring teeth. This presentation reviews the rationale, techniques, advantages and ill effects of stabilization of teeth by splinting as an aid to periodontal therapy. With the acceptance and clinical predictability of adhesive procedures, the use of conservative bonding techniques to splint teeth offers a useful alternative to more invasive restorative procedures. Loss of tooth-supporting structures results in tooth mobility. Increased tooth mobility adversely affects function, aesthetics, and the patient’s comfort. Splints are used to overcome all these problems. When faced with the dilemma of how to manage periodontally compromised teeth, splinting of mobile teeth to stronger adjacent teeth is a viable option. This prolongs the life expectancy of loose teeth, gives stability for the periodontium to reattach, and improves comfort, function and aesthetics.
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine
Al-Azhar University. The Pathogenesis of infection in oro-facial region due to odontogenic origin is a common clinical issue. bacterial invasion to deeper tissues usually a spread from diseased dental pulp. Recent evidences indicated a multi-microbial nature. The spread of infection is governed by the thickness of the investing bone and the anatomical relation of the tooth root to the attached muscle. Infection could spread from one facial space to another, and the condition may be aggravated to life threatening situations.
Arthrocentesis of the temporomandibular jointAhmed Adawy
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine, Al-Azhar University. Arthrocentesis of the temporomandibular joint refers to lavage of the upper joint space, hydraulic pressure and manipulation to release adhesions of the “anchored disc phenomenon” and improve motion. The technique of arthrocentesis is discussed together with the indications and contraindications of the procedure. Further, the presentation includes modifications of the standard technique.
Classification of peri-implant diseases and condition, implant failures causes, Peri-implant mucositis and its management, Peri-implantitis and its classification, clinical features, Treatment (Surgical and Non-surgical) And management. Implant success rate and conclusion.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
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the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. INTRODUCTION
• The word “osteomyelitis” originates from the ancient Greek words
osteon (bone) and muelinos (marrow)
• Inflammation process of the entire bone including the cortex and the
periosteum , recognizing that the pathological process is rarely
confined to the endosteum.
3. DEFINATION
•Osteomyelitis is considered as an inflammatory condition of bone
that usually begins as an infection of the medullary cavity, rapidly
involves the haversian systems and quickly extends to periosteum of
that area.
5. Osteomyelitis is initiated by a -
Contiguous focus of infection (jaw)
Hematogenous spread (children)
Osteomyelitis of mandible > maxilla
6. PATHOGENESIS
Acute inflammation following infection
⇃
Hyperemia
⇃
Capillary permeability ↑and infiltration of granulocytes
⇃
Tissue necrosis
⇃
Destruction of bacteria, vascular thrombosis & Pus forms
⇃
Intramedullary pressure ↑ as pus accumulates -> anesthesia
compression
⇃
Vascular collapse, venous stasis and ischemia
⇃
7. Pus accumulates with Stripping of
periosteum
⇃
vascular supply reduced
⇃
periosteum penetration and mucosal
fistulas
⇃
chronic Inflammation - >granulation
tissue & lysis of bone
⇃
separation of necrotic bone (sequestra)
⇃
sheath of new bone
(involucrum)cloaca
8. MICROBIOLOGY OF OSTEOMYELITIS
Osteomyeiltis of jaws now is recognised as a disease caused primarily
by-
-alpha hemolytic streptococci
-Peptostreptococcus
-Porphyromanas
-Fusobacterium
-Prevotella sp.
9.
10.
11. IMAGING TECHNIQUES
TYPES OF IMAGING-
• Conventional Radiographs
• Radionuclide imaging(Scintigraphy)
• Computed tomography
• Magnetic resonance imaging
12. Conventional Radiographs(H.M.Worth-1969)
Moth-eaten appearance
Enlargement of medullary spaces
Destruction and replacement
with granulation tissue.
Islands
Sequestra, with evidence of a
trabecular pattern and
marrow spaces.
A sheath of new bone
(involucrum) often is found,
separated from the sequestra
by a zone of radiolucency.
14. •
CONVENTIONAL RADIOGRAPHY
TECHNETIUM BONE SCANS
67Ga or IIIIn WBC scan
MRI or CT in selected cases (drainable abcess,
do MRI , sequestrum ,use CT
Positive Negative
Osteomyelitis (osteomyelitis highly suspected)
Positive Negative
Osteomyelitis (osteomyelitis highly suspected)
Positive Negative
(osteomyelitis Osteomyelitis
Highly suspected)
Positive negative
Osteomyelitis (Stop)
Aliabadi P Nikpoor J:Imaging osteomyelitis ,Arthritis Rheum 37:617,1994
15. ACUTE SUPPURATIVE OSTEOMYELITIS
• Acute intramedullary osteomyelitis
• Characterized by:
(1) deep, intense pain,
(2) high intermittent fever,
(3) paresthesia of the lower lip, and
(4) a clearly identifiable cause
(5)minimal swelling
(6)fistulas are not present.
16. Imaging
Conventional radiographs – not of much use
Radionuclide scan – positive
Lab investigations –
Generally negative
Slight leukocytosis.
Treatment
Immediate antibiotic therapy
Identification and correction of immunocompromising conditions.
17. SUB ACUTE SUPPURATIVE OSTEOMYELITIES
10 to 14 days after onset of Acute Suppurative osteomyelitis.
Clinical features –
Deep pain , malaise, fever and anorexia
Teeth begin to loosen (sensitive to percussion)
Pus exudes around the gingival sulcus and through mucosal
Fetid odor
Firm cellulitis of the cheek,
Expansion of the bone from increased periosteal activity,
Abscess formation.
Trismus is not always present
Regional lymphadenopathy
The patient's temperature may reach 1010 to 1020 F and the patient
often is dehydrated.
18. CHRONIC OSTEOMYELITIS
SUBTYPES
PRIMARY SECONDARY
In secondary chronic osteomyelitis,
the type observed in incompletely
treated acute osteomyelitis, the clinical
findings usually are limited to fistulas,
induration of soft tissues, and a
thickened or “wooden” character to
the affected area with pain and
tenderness on palpation..
19. • Conventional radiographs –
– Bone changes – 4 to 14 days
– Full extent of bone dissolution - 3 weeks
– 30-60% bone destruction is necessary
Moth-eaten appearance Island pattern
21. TREATMENT MODALITIES
PRINCIPLES OF TREATMENT :
(1) Evaluation and correction of host defenses,
(2) Gram staining and culture and sensitivity testing,
(3) Imaging to rule out bone tumors,
(4) Empirical administration of Gram stain-guided antibiotics,
(5) Removal of loose teeth and sequestra.
(6) Prescription of culture-guided antibiotic therapy, repeated cultures
(7) Possible placement of irrigation drains/ PMMC antibiotic beads
(8) Sequestrectomy, debridement, decortication, resection, or reconstruction
23. [B] Surgical management
1. Extraction of offending teeth
2. Incision and drainage
3. Sequestrectomy
4. Saucerisation
5. Decortication
6. Resection and Reconstruction
7. Post operative care
24. CONSERVATIVE MANAGEMENT
-Antibiotic Treatment-
Regime 1: hospitalized/medically compromised patient IV is
- Aqueous penicillin 2million U IV + metronidazole 500mg 6hrly
when improved for 48-72 hrs switch to
-Penicillin V 500mg 4hrly + metro 500mg 6hrly orally, for additional
4-6 weeks
OR
-Clindamycin 600-900mg 6hrly IV then
-Clindamycin 300-450mg 6hrly orally
OR
-Cefoxitin(Mefoxin) 1g 8hrly IV Or 2g 4hrly IM Or IV until no
symptoms then switch to
-Cephalexin (keflex) 500mg 6hrly orally, for 2-4 weeks
25. FOR PENICILLIN ALLERGIC PATIENTS:
• Clindamycin
• Cefoxitin
OR
• Ampicillin /sulbactam 1.5-3g IV 6hrly
when improved for 48-72 hrs switch to
• Amoxacillin/clavulanic acid (Augmentin) 875/125 mg Orally bid for
additional 4-6 weeks
Regime 2: For out patient treatment
Penicillin V 2g + metronidazole 0.5g 8hrly orally for 2-4 weeks after
last sequestrum removed & patients without symptoms
26. CLOSED WOUND IRRIGATION-SUCTION
• Technique—
• Tubes-3-4mm in diameter
– 6-10 inches in length
– Neosporin irrigant
• Advantages –
– High dose of antibiotic
(locally), no side effects
• Disadvantages –
– Labor intensive , Time consuming
27. Antibiotic Impregnated Beads
• TECHNIQUE
• Tobramycin or gentamicin in PMMA.
• Indications –
– chronically infected bone associated
with fractures
– refractory to systemic antibiotics.
• Advantages –
– deliver high concentrations of antibiotics
– low systemic concentrations thus low
toxicity
28. Hyperbaric oxygen therapy
• Involves intermittent , usually daily inhalation of 100% humidified
oxygen under pressure greater than 1 absolute ATP
• Each session , or dive is 90 minutes in length.
• Treatment given :-
• 5 days per week twice daily for 30.
• 60 or more dives at 2.4 ATA for 90 minutes while breathing.
29. SEQUESTRECTOMY
Removal of sequestrum (dead nerotic bone).
Fate of sequestra-
It may get infected and form a chronic infective
focus
May remain dormant with no changes in it.
May get revascularized and healing takes place
May get resorbed completely.
Antibiotics will not be able to penetrate into it
(avascular)
30. SAUCERIZATION
Removal of bony hollow cavity/ dead space
After removal of Sequestrum
A hollow cavity/dead space occurs
A large clot form in the cavity
The clot will most likely to get infected
So the margins of the bone which lodge the sequestra are
trimmed down
This create a saucer shaped defect instead of a deep
hollow cavity.
This saucer shaped defect can’t accumulate a large clot
31. DECORTICATION
• Removal of chronically infected cortex of bone. The lateral and
inferior border cortex is removed 1-2 cm beyond the affected area,
providing access to medullary cavity
• Cancellous bone is removed till the uninvolved area. (bleeding
points)
• .
32. RESECTION AND RECONSTRUCTION
• All the above procedures are not effective completely eliminating
the infective process.
• Once the part of the jaw is resected, it may be reconstructed using
autologous bone graft or reconstruction plates.
33. IINFANTILE OSTEOMYELITIS
- Seen a few weeks after birth and usually involves maxilla
• Occur via hematogenous route or from perinatal trauma of the oral
mucosa from the obstetrician’s finger or the mucosa suction bulb used
to clear the airway immediately after birth.
• Infections involving the maxillary sinus and infected human have also
been implicated as sources of infant infection.
34. Clinical findings-
Extraorally-
Periorbital cellulitis
Irritability and malaise,which are followed by hyperpyrexia,
anorexia and dehydration.
Convulsions and vomiting may occur.
Intra-orally-
Maxilla on the affected side is swollen both bucally and
palatally, especially in the molar region.
• Fluctuance is often present and fistulas may exist in the
alveolar mucosa.
• Leucocytosis is generally present.
35. Treatment-
– Intravenous antibiotics
– drainage of all abscesses.
– Sequestrectomy – conservative approach (danger of
damage to tooth buds)
– Antibiotics should be continued orally for 2 to 4 weeks
after all signs of infection have subsided.
– Supportive
36. NON SUPPURATIVE OSTEOMYELITIS
CHRONIC SCLEROSING OSTEOMYELITIS-
Focal Diffuse
• Other names- Sclerosing osteitis
Multiple enostosis
Local bone sclerosis
Ossifying osteomyelitis
Sclerosing cementoma
Giantiform cementoma
Sclerotic cemental masses of jaws.
•
37. Chronic focal sclerosing osteomyelitis
It It is an unusual reaction of bone to infection, occurring in instances of
extremely high tissue resistance or in cases of a low grade infection.
• Young persons below 20yrs
• Tooth most commonly involved is first molar
• Treatment consists of endodontic
therapy or extraction of involved
tooth following which the bony lesion
may remodel or remain distinct.
38. Chronic diffuse sclerosing
osteomyelitis
Shows a proliferative reaction of bone to low grade infection.
Here the portal of entry of infection is mainly through the
periodontium.
More common in females.
• Is of insidious in nature,
• On occasion results in mild suppuration and formation of fistulas to
establish drainage.
• In such cases patient might complain of vague pain and a bad taste .
39. • Treatment –
– Removal of the source of infection,
– Repeated culture and sensitivity testing,
– High doses of antibiotics for prolonged periods,
– Wound irrigation, antibiotic impregnated beads, and
debridement.
– Decortication or resection, and reconstrucrion
– HBO therapy
40. GARRE’S OSTEOMYELITIS / PERIOSTEITIS OSSIFICANS
• First described by Carl Garre in 1893 as a focal gross thickening of the
periosteum of long bones, with peripheral reactive bone formation
resulting from mild irritation or infection.
• A localized, hard, non-tender swelling over the mandible.
seen primarily in children and young adults.
• It is commonly associated with a carious molar, usually the first molar
and a history .of past toothache.
41. OSTEOMYELITIS DUE TO NON PYOGENIC ORGANISMS
ACTINOMYCOTIC OSTEOMYELITIS:
- It is a chronic infection manifests both with granulomatous and
suppurative features involving soft tissues and bone of cervicofacial
region.
- It is caused by Actinomycosis israelii.
- Actinomycosis is of endogenous origin.
Pathogenesis : Organisms gain entry into soft tissue
When established, infection spreads and typically appears on
cutaneous rather than mucosal surface.
42. Actinomycotic osteomyelitis of jaws are rare but may present as :-
• A periosteitis as a result of the involvement of the adjacent soft
tissues.
• An Actinomycotic osteomyelitis in which the mandible is thickened,
‘Woody hard’ swelling .
• Eventually sequestration of the bone occurs.
• A chronic infection of a fracture of the jaw bone and produce a
chronic fistula.
• Diagnosis is by microscopic examination of the pus.
Sulphur granules are present.
43. TUBERCULOUS OSTEOMYELITIS
• Mycobacterium tuberculosis is usually brought about
by hematogenous spread.
• Etiopathogensis :- “ Mycobacterium tuberculosis”
• Three possible methods of inoculation of bacteria into bone-
1)Direct inoculation of bacilli into oral mucosa through an ulcer or break
in the continuity of the mucosa
2) Spread to bone via an extraction of socket or an infected fracture line.
3) Hematogenous or lymphatic spread from primary focus elsewhere in
body
44. Surgical treatment:-
• Positive for AFB : Patient started Antikochs regimen. After
6 to 8 weeks the lesion is reviewed both clinically and
radioghphically to evaluate the need for surgical
debridement.
• Negative for AFB : -- Complete excisional biopsy and
debridement of tissue is done. Then tissue is sent for
histopatholical studies.
• Long term follow up
46. INTRODUCTION
• It is a chronic, nonhealing wound caused by hypoxia,
hypocellularity, and hypovascularity of irradiated tissue.
47. DEFINATIONS
• Marx –
”An area greater than 1cm of exposed area of bone in a field of
irradiation that has failed to show any evidence of healing for atleast
6 months.”
• Hutchinson-
• “An area of exposed bone (mandible) present for longer than 2
months in a previously irradiated field,in the absence of recurrent
tumour.
48. INCIDENCE
• Incidence of involvement of mandible ranges from 2-3%.
• Extraction of tooth causes ORN- 60-89% of cases
• Time period b/w RT and development of ORN has been
reported as a mean of 7.5 – 20 yrs.
49.
50. Radiation to the jaws in excess of 50 Gy/hr
Progressive obliterative arteritis
Aseptic necrosis of bone
Bony tissues become hypovascular,
hypocellular, and hypoxic
Breakdown occurs from minor injury to the tissue
(as the tissues cannot maintain normal cellular
turnover and collagen synthesis)
Kills bone cells
PATHOPHYSIOLOGY
51. Small high radiation particles TUMOUR CELLS/NORMAL CELLS
Cellular water
undergo radiolysis
H2O H+ +OH-
INTERACTS
DISRUPTS DNA
52. Radiation effect at various level-
• CELLULAR LEVEL-
The cell may undergo one of the following changes
a) cell may die
b) it may repair its DNA to survive with impaired function
c) may repair DNA damage and function normally.
• TISSUE LEVEL – Changes are seen as endothelial death, hyalinisation
and thrombosis of vessels. Fibrosis of marrow takes place. Mucosa
and skin undergoes fibrosis due to marked decrease in cellularity and
vascularity of connective tissue.
• ORGAN LEVEL – It is seen as a composite tissue which is hypoxic,
hypocellular and hypovascular when compare to normal surrounding
tissue. This is refered as 3 ‘H’ principle of osteradionecrosis.
53. Types of ORN
1. Type I: Develops shortly after radiation; is due to synergistic
effects of surgical trauma and radiation closely coupled in time.
2. Type II: Develops years after radiation and follows a traumatic
event; rarely occurs before 2 years after treatment; most
commonly occurs after 6 years; due to progressive endarteritis
and vascular occlusion of the nutrient vessels in the bone. .
3. Type III: (Spontaneous ORN) Occurs spontaneously without a
preceding traumatic event; usually occurs between 6 months and
3 years after radiation. ; due to immediate cellular damage and
death due to radiation treatment. This occurs when the radiation
dose exceeds 7000 Rads or the fraction doses are greater than
200 Rads per day.
54. CLINICAL FEATURES
• Early ORN may be asymptomatic even though the its main features
of exposed devitalised bone through ulcerated mucosa or skin can
be seen clearly.
• Pain is a common symptom and some patients have presented with
intractable pain.
• Other associated symptoms include dysaesthesia, halitosis,
dysgeusia, and food impaction in the area of exposed sequestra.
• In severe cases, patients can present with fistulation from the oral
mucosa or skin, complete devitalisation of bone, and pathological
fractures
55. MANAGEMENT
• Initial treatment is directed at controlling frank infection.
– Administration of parenteral antibiotics and fluids.
– Gentle irrigation of the soft tissue margins is useful in removing
debris and reducing inflammation
– Culture for sensitivity testing (fistulas present)
– Supportive treatment– good diet
• Conservative treatment -
– Indicated initially
– Irrigation of the exposed bone, mechanical debridement,
medicated pack
– Repeated until sequestration occurs or bone is penetrated by
granulation tissue.
56. • Ultrasound Therapy -- Neovascularity and Neocellularity
• Bone resection
– not candidates for extensive treatment
• HBO therapy
– l00%
– 2.4 absolute atmospheres pressure
– 90minute sessions (dives)
– 5 days a week totaling 30 or more sessions
57. Marx-University of Miami Protocol
Stage I
30 HBO sessions.
If softening of the exposed bone results the wound is debrided
and 10 more HBO sessions are provided.
Stage II
Noncontinuity resection of exposed bone (bleeding margins)
followed by 10 HBO sessions.
If the tissue heals completely with no exposed bone the patient is
considered a stage II responder.
Stage III
Continuity resection and 10 postoperative sessions of HBO
reconstruction after 3 months.
58. Hyperbaric oxygen is effective in treatment of osteomyelitis because:
• Hyperbaric oxygen enhances lysosomal degradation.
• The oxygen free radicals are formed which are toxic to anaerobic
pathogens.
• The elevated partial pressure of oxygen created, inactivate the
exotoxins released by the pathogens.
• The tissue oxygen level is elevated which enhances the healing.
• It helps in neoangiogenesis by encouraging endothelial proliferation.
59. Bisphosphonate-Related Osteradionecrosis of
jaws(BRONJ)
• What is BRONJ?
Bisphosphonate Related Osteonecrosis of the Jaw (BRONJ) can be
described as an area of bone in the jaw that has died and been
exposed in the mouth for more than 8 weeks in a person taking any
bisphosphonate
61. ACCORDING TO AAOMS
STAGING
CLASSIFICATION
CLINICAL MANIFESTATIONS TREATMENT
STAGE 1 Exposed bone, small oral ulcerations
without acute symptoms.
Rinse with 0.12%
Chlorhexidine and checkup
STAGE 2A Exposed bone necrosis or small oral
fistula without bone necrosis.
Symptoms controlled with medical
treatment
Rinse with 0.12%
Chlorhexidine,Antibiotics and
analgesics to be started
STAGE 2B Exposed bone necrosis or small oral
fistula without bone necrosis,but with
symptoms not controlled with medical
treatment
Rinse with 0.12%
Chlorhexidine,Antibiotics and
analgesics and surgery
STAGE 3 Jaw fractures ,skin fistula,osteolysis
extending till inferior border
Rinse with 0.12%
Chlorhexidine,Antibiotics and
analgesics and extensive
surgery with resection of bone
62. New protocols for prevention and treatment of
osteoradionecrosis
• Pentoxifylline is a methylxanthine derivative that 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.
63. REFERENCESr
• Oral and Maxillofacial infections,Topazian
• Peterson’s Oral and Maxillofacial surgery
• Shafers Textbook of oral pathology