Osteomyelitis is an inflammatory condition of bone that involves the medullary cavity and has a tendency to progress along this space and involve the adjacent cortex, periosteum, and soft tissue. It is commonly caused by odontogenic infections or trauma. Staphylococcus aureus accounts for 80% of jaw osteomyelitis cases. The infection initiates from a contiguous focus or hematogenous spread and causes inflammation, tissue necrosis, pus formation, and bone destruction if not properly treated. Without treatment, it can progress to chronic stages involving bone lysis, sequestrum formation, and involucrum development.
• Actinomyces species are classified as anaerobic, gram positive and filamentous bacteria.
• It is a chronic granulomatous suppurative and fibrosing disease caused by anaerobic or microaerophilic gram-positive nonacid fast, branched filamentous bacteria.
• Most of the species isolated from actinomycotic lesions have been identified as A. israelii, A. viscosus, A. odontolyticus, A.naeslundii or A. meyeri.
• These microorganisms have been identified in dental plaque, dental calculus, necrotic pulp, and tonsils.
• The usual pattern of this disease is one characterized chiefly by the formation of abscesses that tend to drain by the formation of sinus tracts.
• pus from the abscesses is examined on a clean glass slide, it shows the typical ‘sulfur granules’ or colonies of organisms, which appear in the suppurative material as tiny, yellow grains.
• Another infection that produces this type of sulfur granules is botryomycosis.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
• Actinomyces species are classified as anaerobic, gram positive and filamentous bacteria.
• It is a chronic granulomatous suppurative and fibrosing disease caused by anaerobic or microaerophilic gram-positive nonacid fast, branched filamentous bacteria.
• Most of the species isolated from actinomycotic lesions have been identified as A. israelii, A. viscosus, A. odontolyticus, A.naeslundii or A. meyeri.
• These microorganisms have been identified in dental plaque, dental calculus, necrotic pulp, and tonsils.
• The usual pattern of this disease is one characterized chiefly by the formation of abscesses that tend to drain by the formation of sinus tracts.
• pus from the abscesses is examined on a clean glass slide, it shows the typical ‘sulfur granules’ or colonies of organisms, which appear in the suppurative material as tiny, yellow grains.
• Another infection that produces this type of sulfur granules is botryomycosis.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
osteomyelitis of jaw bones / dental implant courses by Indian dental academy Indian dental academy
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OSTEOMYELITIS is an inflammation of medullary portion of bone marrow or cancellous bone.
MUCORMYCOSIS is a rare opportunistic fungal infection with high morbidity and mortality.
seminar is about the mechanism of action of the central and periphary acting analgesics. the pathway of pain and various analgesic and their properties
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
1. Osteomyelitis
"is often more than simply the presence of organisms in the
skeleton and often less than pain, swelling, and drainage.'‘
David Seligson Orthopedics in May 1994
4. Osteomyelitis of the jaws was once a frequently
encountered disease and was dreaded because of its
prolonged course and associated with disfigurement
and dysfunction due to loss of teeth and bone and
occasional facial scarring.
5. DEFINITION
Osteomyelitis is an inflammatory condition of
bone that involves the medullary cavity and has
a tendency to progress along this space and
involve the adjacent cortex, periosteum, and soft
tissue.
From:- topazian 4° edition chapter 10
6. Greek words
Osteon – Bone, muelinos – marrow
Infection of medullary portion of bone
7. introduction
Fairly common disease in maxillofacial clinics
Last 50 years – Profound change - Prevalence,
clinical course & management
Introduction of - “Pencillin”
Sophistication in medical & dental science
Availability of adequate treatment
Modern diagnostic imaging methods
8. Inflammation of medullary space – also caused
by
Traumatic injuries,
Radiation,
Chemicals etc.
Term “osteomyelitis”- confined to infection caused
by pyogenic organisms (Marx 1991)
9. Pre antibiotic era
Classical presentation - acute form followed by
chronic
Massive clinical symptoms – bone necrosis, neo-
osteogenesis, sequestrum formation, intra and
extra oral fistula formation and facial disfigurement
Entry of antibiotics –
Concealed acute phase
Elimination of infection
Sub acute & chronic forms more prominent
10. Jaw osteomyelitis – Differ from long bones
Presence of teeth
Connects - oral cavity to PDL membrane
Specific immunological & microbiological aspects
Classifications – based on
Clinical course
Pathological-anatomical and/or radiological features
Etiology
Pathogenesis
11. Some terms
Acute / Subacute osteomyelitis
Rarely seen
Duration – 1 month after onset of symptoms
Subacute – used interchangeably with acute
Chronic osteomyelitis
Suppurative
Nonsuppurative
13. Chronic nonsuppurative osteomyelitis
Heterogeneous group - chronic sclerosing,
proliferative periostitis, actinomycotic and radiation
induced types (Topazian 1994, 2002)
Lack – pus & fistula
Hudson (1993) and Burnier(1995) – “A condition of
prolonged refractory osteomyelitis due to
inadequate treatment, a compromised host,
increased virulence and antibiotic resistance of the
involved microorganisms”
14. SAPHO syndrome, Chronic Multifocal
Recurrent Osteomyelitis (CRMO)
Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis
S A P H O
Few case reports linking association
CRMO – characterized by periods exacerbations &
remissions
Noted in adults & children
15. Periostitis ossificans, (Garre’s osteomyelitis?)
Descriptive term for a condition, caused by several
entities
Periosteal inflammatory reaction to non specific stimuli
-----formation of new immature type of bone outside
the normal cortical layer
Garre’s osteomyelitis - most confusing & misinterpreted
term, (term discarded by medical pathologists)
16. Synonyms – Periostitis ossificans, Chronic non suppurative
osteomyelitis of Garre, Garre’s proliferative periostitis,
Chronic sclerosing inflammation of the jaws, Chronic
osteomyelitis with proliferative periostitis and many more
Carl Garre in 1893 – in his historical article,
Described special forms & complications of – acute infective
osteomyelitis.
Did not describe new type of osteomyelitis.
Enjoyed great acceptance in medical & dental literature till
recently (1994)
17. Alveolar osteitis or Dry socket
Localized form
3 types – alveolitis simplex, alveolitis granulomatosa,
alveolitis sicca
In alveolar osteomyelitis – absence of invasion in to bone
& hence not considered as form of osteomyelitis
Due to breakdown of clot by fibrinolysins released by
bacteria or trauma
Bacteria remain on the surface of exposed bone & do not
invade
18. Osteoradionecrosis & Radioosteomyelitis
Still an observed condition, (in spite of advances)
Initiated by bacteria - hence the term – ‘radiation induced
osteomyelitis or radioosteomyelitis’
Marx in 1983 – as radiation induced avascular necrosis of
bone due to 3- H - Hypoxic, Hypocellular and Hypovascular
tissue -------- chronic non healing wound ----super
infection ---------- osteomyelits
19. Osteochemonecrosis
Caused by drugs (anti cancer, corticosteroids & others)
chemicals (phossy jaw or phosphorous necrosis due to
white P in matchbox industry)
Recent years – “Bisphosphonate induced osteo-
chemo necrosis of jaws” – Due to Bisphosphonates
drugs, used for osteoporosis, Paget’s disease, bone
cancer metastasis, multiple myeloma etc.
20. “Juvenile chronic osteomyelitis” – Resembles Garre’s
, peaks in puberty, with voluminous expansion of
bone, periosteal apposition, & mixed sceroticolytic
appearance
21. classification
Waldvogel is credited with the first classification
system for osteomyelitis.This system categorizes based
upon pathogenesis. He describes three categories of
osteomyelitis:
1) hematogenous osteomyelitis
2) osteomyelitis secondary to a contiguous focus of
infection and
3) osteomyelitis associated with peripheral vascular
disease.
22. From:- topazian 4° edition chapter 10
Suppurative Osteomyelitis
Acute suppurative osteomyelitis
Chronic suppurative osteomyelitis
Primary – no acute phase
preceding
Secondary – Follows acute
phase
Infantile osteomyelitis
Non suppurative osteomyelitis
Diffuse sclerosing osteomyelitis
Focal sclerosing osteomyelitis
Proliferative periostitis
Osteoradionecrosis
Classification of Osteomyelitis of the jaws
23. I. Acute forms of
osteomyelitis (suppurative
or nonsuppurative)
A. Contagious focus
1. Trauma
2. Surgery
3. Odontogenic Infection
B. Progressive
1. Burns
2. Sinusitis
3. Vascular insu!ciency
C. Hematogenous(metastatic)
1. Developing skeleton
(children)
II. Chronic forms of osteomyelitis
A. Recurrent multifocal
1. Developing skeleton (children)
2. Escalated osteogenic (activity< age 25 years)
B. Garrè's
1. Unique proliferative
subperiosteal reaction
2. Developing skeleton (children
and young adults)
C. Suppurative or nonsuppurative
1. Inadequately treated forms
2. Systemically compromised
forms
3. Refractory forms (chronic recur-
rent multifocal osteomyelitis
CROM)
D. Diffuse sclerosing
1. Fastidious microorganisms
2. Compromised host/pathogen
interface
Classification based on clinical picture and radiology
24. Classification based on clinical picture,
radiology, pathology, and etiology
I. Acute suppurative
osteomyelitis (rarefactional
osteomyelitis)
II. Chronic suppurative
osteomyelitis
(sclerosing osteomyelitis)
III. Chronic focal sclerosing
osteomyelitis
(pseudo-paget, condensing
osteomyelitis)
IV. Chronic diffuse
sclerosing osteomyelitis
V. Chronic osteomyelitis
with proliferative periostitis
(Garre's chronic nonsuppurative
sclerosing osteitis,ossifying
periostitis)
VI. Specific osteomyelitis
1. Tuberculous osteomyelitis
2. Syphilitic osteomyelitis
3. Actinomycotic osteomyelitis
25. CLASSIFICATION BASED ON PATHOGENESIS
I. Hematogenous osteomyelitis
II. Osteomyelitis secondary to a contigu-
ous focus of infection
III. Osteomyelitis associated with or with-
out peripheral vascular disease
26. Dual classification based on pathological
anatomy and pathophysiology
I. Anatomic Types
Stage I: medullar osteomyelitis –
involved medullar bone without
cortical involvement; usually
hematogenous
Stage II: super$cial osteomyelitis –
• less than 2 cm bony defect without
cancellous bone
Stage III: localized osteomyelitis –
o less than 2 cm bony defect on
radiograph, defect does not appear
to involve both cortices
Stage IV: diffuse osteomyelitis –
o defect greater than 2 cm. Pathologic
fracture, infection, nonunion
II. Physiological class
A host: normal host
B host: systemic compromised host,
local compromised host
C host: treatment worse than disease
27.
28. MICROBIOLOGY
Staphylococcus aureus account for 80% of the cases of osteomyelitis
of the jaws.
Others include
Streptococcus epidermis
Staphylococcus albus and Salmonella.
In addition Mycobacterium tuberculosis, Treponema palladium and
Actinomyces israelli produce certain specific forms of osteomyelitis.
30. pATHOGENESIS
It is usually initiated from a contiguous focus of infection or by
hematogenous spread.
This is primarily caused by odontogenic infection originating
from the pulpal or periodontal tissues. It is polymicrobial in nature
as compared with that of long bone osteomyelitis, in which
classically Staphylococcus aureus is the infecting organism.
Trauma, especially compound fractures is the second leading
cause.
31. 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
⇃
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)
32. CLINICAL PRESENTATION
• Pain
• Swelling and erythema of overlying tissues
• Adenopathy
• Fever
• Paresthesia of the inferior alveolar nerve
• Trismus
• Malaise
33. Acute suppurative osteomyelitis
It may have appearance of typical odontogenic infection.
It can be localised or widespread
Aetiology :
Odontogenic infections
Compond fractures of jaws
Local traumatic injuries
Peritonsillar abscess
34. Clinical Features
Generalised constitutional symptoms
Deep seated boring, continuous and intense pain
Facial cellulitis
Trismus
Established cases may present with
Fetid odour
Purulent discharge with sinuses
Dehydration, acidosis and toxemia
Regional lymphadenopathy is usually present
35. Chronic focal sclerosing osteomyelitis
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.
This form of osteomyelitis arises
most commonly in young persons
below 20yrs.
The tooth most commonly involved is
first molar, which presents as a large
carious lesion.
There may be no signs or symptoms of
the disease other than mild pain
associated with an infected pulp.
36. Periapical radiograph show
Well-circumscribed radio-opaque mass of
sclerotic bone surrounding and extending
below the apex of involved tooth.
The border of this lesion, abutting the
normal bone, may be smooth and distinct
or appear to blend into the surrounding
bone.
Treatment consists of endodontic therapy
or extraction of involved tooth following
which the bony lesion may remodel or
remain distinct.
37. Chronic diffuse sclerosing osteomyelitis
Chronic diffuse sclerosing
osteomyelitis also represents a
proliferative reaction of bone to low
grade infection.
Here the portal of entry of
infection is mainly through the
periodontium.
This might occur at any age, but
most commonly in older persons,
especially in edentulous mandibular
jaws. It is more common in females.
38. Radiographically there is diffuse sclerosis of bone. Radio-opaque
lesions may be extensive. Border between normal bone and sclerotic bone is
indistinct.
Treatment of chronic diffuse sclerosing osteomyelitis is mainly
conservative. It consists of removal of source of infection and antibiotic
administration.
39. Garre’s osteomyelitis
This was 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
This is seen primarily in
children and young adults.
Clinically it is characterised by
a localized, hard, non-tender
swelling over the mandible.
40. Intra-oral periapical radiograph will often
reveal a carious tooth opposite the hard bony
mass.
Occlusal view will show a focal overgrowth of
bone on the outer surface of the cortex, which
may be described as a duplication of the
cortical layer of bone. This mass of bone is
smooth and rather well calcified.
Treatment is by removal of the involved
tooth along with biopsy of the lesion to confirm
the diagnosis. Remodeling of the bone occurs
gradually following removal of the offending
tooth.
41. INFANTILE OSTEOMYELITIS
Osteomyelitis of the jaws in infants is not a common disease.
It is seen a few weeks after birth and usually involves maxilla.
It is thought to 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 or artificial
nipples have also been implicated as sources of infant infection.
42. Intra-orally
The maxilla on the affected side is swollen both bucally and
palatally
Fluctuance is often present and
Fistulas may exist in the alveolar mucosa.
During the early acute phase, little radiographic changes are noted and
leucocytosis is generally present.
Clinically the patient presents with a Facial
cellulitis centered about the orbit.
Irritability and malaise precede frank cellulitis, which
are followed by hyperpyrexia, anorexia and dehydration.
Convulsions and vomiting may occur.
43. ACTINOMYCOTIC OSTEOMYELITIS
Actinomycosis 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.
Actinomycotic osteomyelitis of jaws are rare but may present as
A periostitis as a result of the involvement of the adjacent soft
tissues.
An Actinomycotic osteomyelitis in which the mandible is
thickened and honeycombed by narrow tracts in which the micro-
organisms is embedded in granulation tissue. Eventually sequestration of
the bone occurs.
A chronic infection of a fracture of the jaw bone and produce a
chronic facial sinus.
44. Diagnosis is by microscopic examination of the pus. Sulphur granules are
rarely present when the patient has already received antibiotic therapy.
Treatment entails prolonged antibiotic therapy with penicillin 500mg 6th
hourly or amoxycillin 500mg 8th hourly orally for 6-8 weeks Surgical
intervention will be required to remove any sequestra, which have formed.
45. TUBERCULOUS OSTEOMYELITIS
This condition of the jaws is rare. Infection of bone
by Mycobacterium tuberculosis is usually brought
about by hematogenous spread and is almost always
secondary to a primary focus in respiratory or
alimentary tract.
Localised osteomyelitis may follow tooth extraction
performed on tuberculous patient. Active
tuberculosis infection of the tooth socket is seen
both in patients with pulmonary TB with a positive
sputum and in patients with active infection in
cervical lymphnodes.
Primary tuberculous osteomyelitis of the mandible: a case report
Dentomaxillofacial Radiology (2008) 37, 415–420
46. The diagnosis is confirmed on biopsy.
If the infection of mandible is left
untreated it may spread into soft tissues
and form an indolent, chronic facial
sinus.
Treatment consists of local
surgery and anti-tuberculous therapy
(a) Part of an enhanced panoramic
radiograph of the left side of the
mandible showing healing of the bony
lesion 6 months after the initiation of
antituberculous chemotherapy (arrows).
(b) Occlusal view of the left side of the
mandible showing healing of the bone
6 months after the initiation of
antituberculous chemotherapy
47. Syphilitic osteomyelitis
Infection by Treponema palladium may affect the bones in
syphilis in both the secondary and tertiary stages and also in
cases of congenital syphilis
At the site of the lesion there is a chronic, inflammatory
granulomatous and necrotising periarterial infiltrate
accompanied by partial destruction of bone. As the disease
progress the vascularity of the area become diminished and the
bone tends to become sclerosed. Osteosclerosis with new bone
formation is more common than osteoporosis and rarefaction
48. In neonatal syphilis the involvement of the skeleton takes place
approximately at the end of the fifth month of intrauterine life
and the characteristic bone changes are seen at birth.
Gummatous destruction of the nasal septum and hard palate are
common. This result in saddle shaped nose due to subsidence
of the bridge of the nose and perforations of the palate.
Radiologically, the cranium has a worm-eaten appearance due
to subperiosteal gummas. In the absence of treatment,
separation of the circular sequestra from the base of ulcerating
gummatous lesions may lead to complete perforation of the
bone
49. In acquired syphilis bony changes are seldom seen before
tertiary stage. The palate, nose, skull and tibia are the bone
most commonly affected. The changes seen are in the form of
periosteal or central gumma. Bone is resorbed at the site of the
gumma producing radiolucency with a poorly defined margin
Syphilitic osteomyelitis of the jaws cannot be distinguished
from pyogenic osteomyelitis on clinical and radiologic
examination. Diagnosis may be missed, unless a gumma is
seen or evidence of tertiary syphilis is found elsewhere in the
body or a serological test to show presence of syphilis. The
condition rapidly improves with use of penicillin or
erythromycin.
50. DIAGNOSTIC IMAGING
The increasing availability of 3-dimensional imaging, magnetic
resonance imaging (MRI), scintigraphy, and, now, PET/CT imaging has
made it much easier to precisely delineate the extent of the disease process
in a timely manner.
The newest imaging modalities, such as scintigraphy and PET scan,
are able to highlight biological as well as anatomic activity
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
51. Conventional Radiography
Although the standard for many
decades, the role of this modality is limited
in detection of and therapy for
osteomyelitis because it only shows
changes after extensive bone abnormality
has been present for prolonged periods.
However, it is readily available and
exposes patients to minimal radiation.
Panoramic projection is most useful in
most maxillofacial cases
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
52. Once osteomyelitis has become well established,
radiographic changes usually demonstrate one of
the following sets of characteristics (Worth 1969)
Scattered areas of bone destruction - a moth-
eaten appearance
Bone destruction of varied extent in which there are
islands that is sequestra. A sheath of new bone
(involucrum) is often found separated from
sequestra by a zone of radiolucency.
Stippled or granular densification of bone
caused by subperiosteal deposition of new bone.
53. COMPUTED TOMOGRAPHY
The addition of cone beam
computerized tomography,
which is highly useful for
imaging hard tissues of the
head and neck in multiplanar
slices, is ideal for visualizing
decortications and periosteal
changes. Soft tissue changes can
also be visualized in medical-
grade CT scans by adding
contrast medium .
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
54. mri Use of gadolinium as a contrast agent can show early osteomyelitis
changes in tissue by highlighting nonspecific disturbances in tissue-blood
interfaces, which are common in infection, inflammation, trauma, or
tumors. The changes are most often noted in the soft tissues and can also
be noticed in the medullary portion of the affected bone
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
55. scintigraphy The radioactive substances used to
identify altered bone physiology are
technetium 99m— labeled methylene
diphosphonate, gallium 67, and
indium 111.
The most common scintigraphic agent
is technetium 99m , which is used to
delineate increased bone turnover,
and it is often coupled with the
gallium 67 to distinguish the
osteomyelitis lesions from tumor and
trauma because gallium is sensitive to
inflammatory changes
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
56. Recent advances
Pet/ct
The application of PET scan using fludeoxyglucose F 18 has shown
promise in the identification of osteo myelitis in the jaws especially when
applied with traditional CT. The 2 scanning modalities fuse together
anatomic findings and a metabolic state finding in a real-time frame.
Alveolar Osteitis and Osteomyelitis of the jaws
Oral and Maxillofacial Surg Clin N Am 23 2011 401-413
57. Treatment principle
1.Early Diagnosis
2. Elimination of the source of infection
3.Establishment of surgical drainage
4. Bacteriologic identification and antibiotic sensitivity testing
5. Appropriate antibiotic coverage
6. Surgical debridement
7. Supportive care
8. Reconstruction.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
58. Antibiotics
Aqueous Peicillin-2 million units every 4 hourly or
Oxacillin 1g IV every 4 hourly
When patient has been asymptomatic for 48-72 hours then
switch to Dicloxacillin 250mg 4 hourly orally for 4 to 6
weeks.
If patient is allergic to penicillin
2nd choice – Clindamycin 600mg 6 hourly
3rd Choice- Cephalosporins
4th Choice – Erythromycin 500 mg every 6 hourly
59.
60. Hyperbaric O2 in treatment of OML
Hyperbaric oxygen therapy consists of breathing 100% oxygen through a face
mask or hood in a monoplace or a large chamber at 2.4 absolute
atmospheres pressure for 90 min session or dives for as many as 5 days a
week totaling 30 or more sessions often followed by another 10 or more
sessions
Action of HBO therapy:
1.Enhancement of lysosomal degradation potential of polymorphonuclear
leukocytes and O2 radicals.Formation of these enzymes is decreased in
hypoxic environment as in OML.
2. Free radicals of O2 are toxic to many anaerobes(bactericidal).
61. 2)Exotoxin liberated by microorganisms are rendered inert by
exposure to elevated partial pressure of O2
3)Tissue hypoxia is reversed by HBO
4)Postive enhancement of neoangiogenesis
Clinical effects
It aids in healing of draining sinus
Improves osteogenesis in lytic areas
Reduces destruction of bone and soft tissues
Sequestra undergo rapid dissolution without suppuration &
healing eliminates the need for surgical intervention.
62. Marx protocol
Stage – 1
Response
Stage-2
Response
Stage-3
•30 (100% O2 for 90 min at 2.4ATA)
•Examine the exposed bone
•Surgery
•10(100% 02 for 90min at 2.4 ATA)
•Excision of nonviable bone
•Fixation of mandibular segment
•10(100%02 for 90 min at 2.4 ATA)
•Reconstruction after 3 months
•No further HBO required
•10(100% 02 for 90 min at 2.4
ATA) (stage 1 responder)
Healing without exposed
bone (stage 2 responder)
64. Surgical debridement of the osteomyelitic jaw may encompass a series of
procedures. The removal of infected and devitalized teeth and associated
soft tissue is a preliminary treatment of osteomyelitis.
The removal of necrotic and chronically infected bone is essential to
the successful management of the infection. Multiple procedures over a
period of days or weeks may be required to eradicate the infection from the
affected jaw. The procedures include Sequestrectomy, Saucerization,
Decortication, Resection, and Reconstruction.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
66. Sequestrectomy
Sequestrectomy is the removal of
infected devitalized bony fragments in the
infected area of the jaw. The sequestrum
is often surrounded by a sheath or
membrane of new bone, termed an
involucrum. The removal of sequestra is
important because it enables the
penetration of high concentrations of
antibiotics into an area of previously poor
vascularity
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
67.
68. SAUCERIZATION
Saucerization is frequently performed in conjunction with
sequestrectomy. This procedure removes the margins of necrotic bone to expose
the medullary spaces for further exploration and removal of necrotic tissue.
The procedure is usually performed intraorally, giving direct
access to the infected bone. After the procedure the wound may be packed open
to allow irrigation and examination during the early healing of the defect. Once
a bed of healthy granulation tissue is formed, the packing may be removed.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
69.
70. decortication
Decortication is the removal of lateral and inferior cortical plates of bone to
gain access to the infected medullary cavity. Avascular bone is removed
until a 1- to 2-cm margin of vital bone is achieved.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
71. resection
Long-term osteomyelitic infections
may lead to pathologic fractures,
continuing infection after decortication, . In
such cases, resection and eventual
reconstruction may be indicated to
eradicate the disease.
The resection margins should be in a
viable bone 1 to 2 cm from the site of
infection.
How can we diagnose and treat osteomyelitis of the jaws as early as possible?
Oral and Maxillofac Surg Clin N Am (23) 2011 557-567
73. Long term antibiotics and calcitonin in the treatment
of chronic osteomyelitis of the mandible: Case report
British Journal of Oral and Maxillofacial Surgery 46 (2008) 400–402
Recent advances
Calcitonin and parathyroid hormone regulate
bone turnover, and therefore maintain calcium
balance and homeostasis.
It is used for relief of bone pain in Paget’s
disease, neoplastic bone disease and post-
menopausal osteoporosis.
Its analgesic properties result from inhibition of
prostaglandins and stimulation of production of
endorphins.
Radiographs have shown good healing, but
further clinical studies are required to asses the
true effect of calcitonin and its use as an
adjunct to antimicrobial and surgical treatment
74. references
Topazian 4° edition
Osteomyeltis of jaw mark baltensperger
Radiographic imaging in osteomyelitis: the role of plain radiography,
computed tomography, ultrasonography, magnetic resonance imaging, and
scintigraphy
Osteomyelitis: a review of current literature and concepts nicholas h.
MAST, MD and DANIEL HORWITZ, MD
Diagnosis and classification of mandibular osteomyelitis. Yoshikazu suei,
DDS, phd,a akira taguchi, DDS, phd,a and keiji tanimoto, DDS, phd,
hiroshima, japan. OOO Vol. 100 no. 2 august 2005
Editor's Notes
Classification based on clinical picture and radiology.
The two major groups (acute and chronic osteomyelitis) are differentiated by the clinical course of the disease after onset, relative to surgical and antimicrobial therapy. The arbitrary time limit of 1 month is used to differentiate acute from chronic
osteomyelitis (Marx 1991; Mercuri1991;Koorbusch1992).
In most incidences periapical and periodontal infections are localized by a protective pyogenic membrane or so. tissue abscess wall which serves as a certain barrier (Schroeder 1991). As mentioned above, this condition represents a carefully balanced equilibrium between microorganisms and host resistance preventing further spreading of the infection. If the causative bacteria are sufficient in number and virulence, this barrier can be destroyed. Furthermore, permanent or temporary reduction of host resistance factors for various reasons mentioned previously facilitate deep bone invasion of the microorganisms. this invasion induces a cascade of inflammatory host responses causing hyperemia, increased capillary permeability, and local inflammation of granulocytes. Proteolytic enzymes are released during this immunological reaction creating tissue necrosis, which further progresses as destruction of bacte ria and vascular thrombosis ensue. Accumulation of pus inside the medullary cavity, consisting of necrotic tissue and dead bacteria within white blood cells, increases in tramedullary pressure. €is leads to vascular collapse, venous stasis, thrombosis, and hence local ischemia. Pus travels through the haversian and nutrient canals and accumulates bneath the periosteum, elevating it from the cortical bone and thereby further reducing the vascular supply
In mandibular osteomyelitis, the increased intramedullary pressure also leads to direct compression of the neurovascular bundle, accelerating thrombosis and ischemia resulting in dysfunction of the inferior alveolar nerve, known as Vincent’s symptom.