This document discusses space infections that can arise from dental infections. It defines fascial spaces and outlines the pathways of odontogenic (dental) infections. It describes different classifications of infections including by location (e.g. maxillary vs mandibular spaces), etiology, and causative organisms. Specific spaces that can become infected are discussed such as the canine, buccal, and infratemporal fossa. Clinical features, treatment including incision and drainage, and potential spread are covered for each space.
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.
CLINICOPATHOLOGICAL FEATURES OF PERIPHERAL OSSIFYING FIBROMA IN A SERIES OF 4...ishita1994
Peripheral ossifying fibromas are benign mesenchymal lesions that usually arise in the anterior maxilla of young female patients. Histologically they consist of spindle cell proliferation with focal mineralization. We reviewed 48 specimens from 41 patients and recorded the clinical data, sex, and age of the patients, site, and size of the lesions, treatment, and postoperative outcome. Histologically the presence of mature, woven bone, cementum, and calcifications was evaluated and evaluated immunohistochemically. Lesions were more frequent in female patients in the third and fourth decade and were usually in the lower maxilla and smaller than 2 cm. All lesions were conservatively excised, and they relapsed in eight patients. Histopathologically, the lesions were poorly circumscribed, with moderately cellular proliferation, and with no discernible architectural pattern. All tumors showed some degree of mineralization, the presence of immature bone being the most common. Immunohistochemical examination showed staining of tumoral cells for smooth muscle actin and CD68. Lesions tended to occur more commonly in female patients, but one decade later than usually reported. We found a higher recurrence rate in lesions that contained cementum-like material but without bone formation, suggesting a lack of maturation in this group. Immunohistochemical results were consistent with myofibroblastic differentiation but they added no information about the behavior of the lesions.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
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.
CLINICOPATHOLOGICAL FEATURES OF PERIPHERAL OSSIFYING FIBROMA IN A SERIES OF 4...ishita1994
Peripheral ossifying fibromas are benign mesenchymal lesions that usually arise in the anterior maxilla of young female patients. Histologically they consist of spindle cell proliferation with focal mineralization. We reviewed 48 specimens from 41 patients and recorded the clinical data, sex, and age of the patients, site, and size of the lesions, treatment, and postoperative outcome. Histologically the presence of mature, woven bone, cementum, and calcifications was evaluated and evaluated immunohistochemically. Lesions were more frequent in female patients in the third and fourth decade and were usually in the lower maxilla and smaller than 2 cm. All lesions were conservatively excised, and they relapsed in eight patients. Histopathologically, the lesions were poorly circumscribed, with moderately cellular proliferation, and with no discernible architectural pattern. All tumors showed some degree of mineralization, the presence of immature bone being the most common. Immunohistochemical examination showed staining of tumoral cells for smooth muscle actin and CD68. Lesions tended to occur more commonly in female patients, but one decade later than usually reported. We found a higher recurrence rate in lesions that contained cementum-like material but without bone formation, suggesting a lack of maturation in this group. Immunohistochemical results were consistent with myofibroblastic differentiation but they added no information about the behavior of the lesions.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
One of the most painful but easy-to-treat dental emergencies is a dry socket.
• Dry socket symptoms are experienced after a tooth extraction.
• This condition requires follow-up care by the doctor who performed the surgery, an oral surgeon or a dentist who is familiar with how to treat it.
For more information, contact :-
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
#drysocket #management #thirdmolarextraction #extractioncomplications
Brief notes on the inflammation of Alveolar bone that surrounds a tooth that has recently been extracted. It occurs as a complication of tooth extraction.
Complication of Tooth extraction and managementNusrat Fahmida
This is a brief presentation on the complications during and after tooth extraction that we face in Exodontia , prepared for a semiinar project. The contents were collected from reference books and ofcourse, internet.
One of the most painful but easy-to-treat dental emergencies is a dry socket.
• Dry socket symptoms are experienced after a tooth extraction.
• This condition requires follow-up care by the doctor who performed the surgery, an oral surgeon or a dentist who is familiar with how to treat it.
For more information, contact :-
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
#drysocket #management #thirdmolarextraction #extractioncomplications
Brief notes on the inflammation of Alveolar bone that surrounds a tooth that has recently been extracted. It occurs as a complication of tooth extraction.
Complication of Tooth extraction and managementNusrat Fahmida
This is a brief presentation on the complications during and after tooth extraction that we face in Exodontia , prepared for a semiinar project. The contents were collected from reference books and ofcourse, internet.
Everything a dentist needs to know about a periodontal abscess is here.
Along with all the relevant facts, references, definitions, classifications, and each and every statement is given with proper detail
Detailed description of diagnosis and management of maxillofacial and neck space infections. Discussion of anatomy of the spaces is also done in details. Drainage of such spaces are also discussed. Medical management is also discussed. Complications are also discussed.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
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.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
2. Content
• Introduction
• Definition
• Pathway of odontogenic infection
• Classification
• Maxillary space infection
• Mandibular space infection
• Ludwigs angina
• Cavernous sinus thrombophlebitis
3. Introduction
• Occurrence of infectious disease is determined by interaction of host ,
the microorganism and the environment
• In healthy state there is balance among these factors and when the
balance is lost disease occurs
• Most odontogenic infections arise as a sequel of pulp necrosis caused
by caries, trauma, periodontitis
4. Fascial spaces
• Definition : the fascial spaces are the potential spaces between the
various layers of fascia normally filled with loose connective tissue
and bounded by anatomical barriers , usually of bone , muscle or
fascial layers.
(Moore – 1975)
5. Pathways of odontogenic infection
• Invasion of dental pulp by bacteria after decay of a tooth
• inflammation edema and lack of blood supply
• Venous congestion ,pulpal tissue death
• Reservoir for bacterial growth
• Periodic egress of bacteria into surrounding alveolar bone
6. Odontogenic infections
• Types of infection: acute
chronic
• Acute stage
in acute stage ,infection spreading in the soft tissues can take the
following forms of in the clinical situation
Abscess
Cellulitis
Fulminating infections
7. Difference between cellulitis and abscess
cellulitis
• Acute phase
• Severe and generalized
• Large
• Diffuse borders
• Doughy to indurated
• No presence of pus
• Greater degree of seriousness
• Aerobic bacteria
abscess
• Chronic phase
• Localized
• Small in size
• Well circumscribed
• Fluctuant on palpation
• Presence of pus
• Less degree of seriousness
• Anaerobic bacteria/mixed
8. Acute infection
• The odontogenic infection present in the following forms:
1. Acute periapical abscess: abscess arises and remains in the confine
of the alveolar bone
2. Acute dentoalveolar abscess: once the infection has crossed the
confines of alveolar bone and comes to lie in the neigbouring soft
tissues and gets localized
3. Acute periodontal abscess
4. Acute pericoronal abscess
9. Differential clinical features between acute
periodontal & acute periapical abscess
Acute periapical abscess
• Pain is severe and throbbing
• Common in adults
• Pulp gets necrotic and infected
• Swelling seen over the apex
• Sinus discharge will be present
• TOP is present
• Mobility in later stages
• Arises from the pulp
Acute periodontal abscess
• Pain is severe and throbbing
• Uncommon in children
• Pulp is vital
• Swelling over the gingival third of the
alveolar process
• Sinus discharge may be present
• TOP is present
• Mobility Is seen in early stages
• Arises in relation to periodontal
pocket
11. Chronic stage
• In chronic stage the odontogenic infection present itself in the
following forms:
1. Chronic fistulous tract or sinus formation: abscess neglected for a
long period discharge intraorally or extraorally
2. Chronic osteomyelitis
3. Cervicofacial actinomycosis
12. General course of odontogenic abscess
1. Early stage: there is intrabony pus collection. The adjoining soft tissues
doesnot undergo any necrosis
2. Intermediate stage: perforation of cortex infection progresses
soft tissues becomes indurated and brawny small area of central
softening can be palpated this represents central necrosis due to
loss of blood supply
13. Microbiology
• The aerobic bacteria found in odontogenic infection are gram positive
cocci , most are viridans streptococci species , include strep.milleri
,strep.sanguis, strep.salivarius, strep.mutans.
• These oral streptococci account for more than 80% of aerobic bacteria
in odontogenic infection.
14. There are two main groups of bacteriodes
a.oropharyngeal
b. they other group found in the gut
• Oropharyngeal bacteriodes :divided into:
• Porphyromonas : includes P. assachrolyticus ,P.gingivalis,
P.endodontalis
• Prevotella:it includes p.buccal p.oralis, p.loeschii, p.denticola
prevotella intermedius , porphyromonas gingivalis ,and
porphyromonas endodontalis appears to be most pathogenic among
them
15. • Medical therapy
• Consists of supportive care –hydration soft or liquid diet rich with
protein ,analgesics and use of antiseptic mouthwashes to maintain
oral hygiene
16. Antibiotic therapy
i. In non compromised pt with well localized abscess surgical
drainage and dental therapy without antibiotic cover. In cases of
poorly localized , extensive abscess and diffuse cellulitis , antibiotic
therapy is must .
ii. In compromised pt as well as in pt with systemic signs and
symptoms like trismus, airway compromise, fever antibiotic
coverage is mandatory
17. • Penicillin is the empirical drug of choice. Later on after knowing the
lab results of culture and sensitivity testing , specific antibiotic is
instituted.
• oral clindamycin , Augmentin, 1st and 2nd generation cephalosporin
are useful in orofacial infections
• in compromised pt , clindamycin alone or in combination with
gentamicin, 1st and 2nd generation cephalosporin can be used
parenterally.
18. Surgical therapy
• Incision and drainage helps
i. To get rid of toxic purulent
ii. To decompress the edematous tissues
iii. To allow better perfusion of blood , antibiotic and defensive
elements
iv. To increase oxygenation of infected area
19. Hiltons method of incision and drainage
• The method of opening an abscess ensures that no blood vessel or nerve in the vicinity is
damaged and is called Hiltons method
• Steps
1. Topical anaesthesia
2. Stab incision: made over max fluctuation in most dependent area along the crease
3. If pus is not encountered, further deepening of surgical site is achieved with sinus
forcep
4. Closed forcep is pushed through tough deep fascia and advanced towards the pus
5. Pus flows along the sides of the beak
6. Placement of drain : a corrugated rubber drain is inserted into to the depth of the
abscess cavity and external part is secured to the wound margin with the help o suture
7. Drain left for atleast 24 hours
20.
21.
22. Purpose of keeping the drain
• Is to allow the discharge of the tissue fluids and pus from the wound
by keeping it patent .
• The drain allows for debridement of the abcess cavity by irrigation
23.
24. Spread of orofacial infection
Routes of spread
By direct continuity through the tissues
By lymphatics to the regional lymph node and eventually into the
blood stream. The spread of infection from the lymph nodes to the
tissues results in secondary area of cellulitis or tissue space abscess
By blood stream: local thrombophlebitis may propagate along the
veins entering the cranial cavity via emissary veins to produce
cavernous sinus thrombophlebitis. The microorganism or the infected
emboli may get swept away in to the blood stream leading to
bacteraemia, septicaemia or pyaemia with the development of
embolic abscess.
25. Potential routes of spread of periapical
infection
Muscles and fascial attachments determine the direction of spread.
Extensions beyond this attachments lead to deep space involvement
26. Factors influencing spread
• General factors
a) Host resistance :depends upon : humoral factor
cellular factor
i. Humoral factors involve immunoglobulins derived from B
lymphocytes or plasma cells
ii. Cellular factors include pmn leucocytes , monocytes ,lymphocytes
and tissue macrophages
27. b. Virulence of micro organisms : determined by invasiveness of the
causative micro organisms. These include production of lytic enzymes ,
potent endotoxins & exotoxins
c. Compromised host defences : uncontrolled metabolic diseases, such
as alcoholism , malnutrition , severe diabetes
2. Suppressing diseases: leukaemia , lymphoma , malignant tumours
3. Suppressing drugs: cancer chemotherapeutic drugs ,
immunosuppressive drugs
28. Local factors
• Intact anatomical barriers:
i. alveolar bone : first local limiting barrier to further spread of
periapical infection
ii. Periosteum : this structure is better developed in mandible and
hence can delay further spread leading to the development of a
sub periosteal abscess
iii. Adjacent muscles and fascia : next site for localization
29. Evaluation of patient with orofacial infection
• If the patient
i. Is toxic
ii. Exhibits CNS changes
iii. Airway compromise
• Then,
i. Immediate hospitalization
ii. Aggressive medical treatment
iii. Aggressive surgical intervention
30. History taking
• Physical examination
General examination
Regional examination
Extra oral examination
• Inspection
• Palpation
Intra oral examination
Radiological examination
33. Primary max space
• Canine
• Buccal
• infratemporal
Primary mandibular
space
• Submental
• Sublingual
• Submandibular
• buccal
Secondary fascial
spaces
• Pterygomandibular
• Superficial and deep
temporal
• Masseteric
• Pharyngeal
• Retropharyngeal
• Prevertebral
• parotid
34. Based on etiology
General classification
• Odontogenic
• Traumatic
• Implant surgery
• Reconstructive surgery
• Infection arising from contaminated needle puncture
• Others( including from factors such as infected antrum , salivary gland
afflictions)
35. On the basis of causative organism
• Bacterial infection
• Fungal
• Viral
• Odontogenic infection
• Non odontogenic infection
Tonsillar infection
Nasal infection
Furuncle overlying skin
36. Canine fossa involvement [infraorbital space]
• Odontogenic infection
• Nasal infection
• Periapical abscess of cuspids.
periapical abscess which discharges bucally from an upper
canine or first premolar may lead to accumulation of pus in
canine fossa
37. • Involvement :teeth which frequently give rise to abscess are maxillary
canine and premolars and sometimes mesiobuccal root of maxillary
first molar
• The periapical abscess discharges bucally superior to origin of
canninus muscle and pus accumulates in
canine fossa
39. Clinical features
• Swelling of the cheek and upper lip
• Obliteration of nasolabial fold
• Drooping of the angle of mouth
• Edema of the lower eye lid
• extra oral –early phase: on first or second day,inflamma-
tory enlargement of upper lip, and angle of mouth is
seen to drop.
• late phase-usually occur on the second or third day
• Marked periorbital edema forcing eyelid to close
• Redness and marked tenderness of the facial tissues
40. • When the infection progress to chronic stage, it may result in
production of chronic fistula in the cleft area between levator labii
superiors alaque nasi and zygomaticus minor muscle near the medial
canthus of eye
• intraoral: the offending teeth is mobile and is tender on percussion
41. Treatment
• Incision and drainage :
• The approach to this area is through the mucosa of buccal vestibule in
the region of lateral incisor and canine. A curved mosquito forcep is
inserted superior to the attachment of caninus muscle ,and the
infraorbital space is entered.
42. Buccal space involvement
• Buccal space is the potential space between buccinator and masseter
BOUNDARIES
• Anteromedially :buccinator
• Posteromedially:masseter overlying the anterior border
of ramus of mandible
• Laterally :platysma muscle
• Inferiorly:limited by the attachment of deep fascia to
the mandible and by depressor anguli oris
• Superiorly: the zygomaticus process of the maxilla and zygomaticus major and
minor muscle
43. • Contents :buccal pad of fat, stensons duct, facial artery
• TEETH COMMONLY INVOLVED
maxillary and mandibular molars and premolars
44. CLINICAL FEATURES
• Gum boil is seen in the vestibule
• Prominent dome shaped extraoral swelling extending from lower
border of mandible to the infraorbital margin and
from the anterior margin of masseter muscle to
the corner of the mouth.
SPREAD: continuation with the pterygomandibular
space to infratemporal space along the fascia
45. Treatment
• Incision and drainage :horizontal incision thro the oral mucosa of the cheek
in the premolar ,molar region.
• If the pus is lateral to the muscle then the muscle is penetrated with the
mosquito forcep to enter the buccal space
46.
47. Infratemporal fossa space
• Also called retrozygomatic space
as it is situated behind the zygomatic bone
• Involvement :infections arise from
infection of buccal roots of the
max 2nd and 3rd molar
• Local anaesthesia injection with
contaminated needle in the area
of tuberosity
48. BOUNDARIES
• Bounded laterally by ramus of mandible temporalis muscle and its tendon
• Medially by medial pterygoid plate ,lateral
pterygoid muscle lower part of temporal fossa
of the skull and lateral wall of pharynx
• Superiorly by infratemporal surface of greater
wing of sphenoid and by zygomatic arch
• Inferiorly by the lateral pterygoid muscle which
forms the floor of the fossa
• Anteriorly infratemporal surface of maxilla
• Posteriorly parotid gland
49. Clinical features
Extraoral:
• Trismus
• Bulging of temporalis muscle
• Marked swelling of the face on the affected side infront of the ear
• The eye is often closed
Intraoral: swelling of the tuberosity.
• Elevation of temperature up o 104 F
50. Incision and drainage
• Intraoral approach: if trismus is not marked and fluctuation is
detected early , intraoral incision is given in the buccal vestibule .
• extraoral approach: incision is made at upper and posterior end of
the temporalis muscle within the hairline .the sinus is then directed
upwards and medially and pus is evacuated.
51. Potential primary spaces related to lower jaw
SUBMENTAL SPACE
• Involvement: originating from the six anterior mandibular teeth; then
perforate the cortical plate below the origin of mentalis muscle labially and
mylohyoid lingually.
BOUNDARIES:
Lateral: lower border of the mandible and anterior
bellies of digastric muscle
Superior: mylohyoid muscle
Inferior: suprahyoid portion of the investing layer of
deep cervical fascia which is in turn covered by
platysma
52. Contents: submental lymph node and jugular veins .the lymph nodes lies
embedded in adipose tissues and hence submental abscess tend to remain
well circumscribed.
CLINICAL FEATURES:
Extraoral finding :distinct firm swelling in
the midline, beneath the chin.
Intraoral findings : ant teeth are either
non vital fractured or carious .
• The offending tooth may exhibit tenderness
to percussion and may show mobility
• Pt may experience discomfort on swallowing
53. Incision and drainage
• Performed by making transverse incision in the
skin below the symphysis of mandible.
Dissection is carried by inserting sinus forcep
through the incision, upward and backward.
• SPREAD posteriorly to involve the
submandibular space
• It may discharge on the face in the submental
region.
54. Submandibular space
• The space lies between ant and post bellies of digastric muscle. The upper part lies beneath
the inferior border of mandible and the lower part lies deep to the investing layer of deep
cervical fascia .
• Involvement: infections originating from mandibular molars.
• The pus perforates the lingual cortical plate of mandible inferior to the attachment of
mylohyoid muscle and passes directly to the submandibular space
• It is involved as an extension of infection from submental space
• Also involved by an infection originating from
post part of sublingual space
• Also involved from infection originating
from middle third of the tongue ,posterior
• part of the floor of the mouth, maxillary teeth
cheek , maxillary sinus and palate.
55.
56. BOUNDARIES
• Anteromedially ,the floor is formed by the mylohyoid muscle which is covered by
loose areolar tissue and fat
• Posteromedially ,the floor is formed by the
hyoglossus muscle
• Superolaterally,medial surface of mandible
below the mylohyoid ridge
• Anterosuperiorly,anterior belly of digastric
• Posterosupriorly, post belly of digastric stylohyoid
and stylopharyngeus muscle
• Laterally , platysma and the skin
57. Clinical features
Extraoral :firm swelling in submandibular region ,below the inferior
border of the mandible
• Some degree of tenderness
• Redness of the overlying skin
Intraoral: teeth are sensitive to percussion
• Teeth are mobile
• Dysphagia
• Moderate trismus
58. Incision and drainage
• Incision of about 1.5 to2cm length is made 2 cm below the lower
mandible in the skin creases .
• Skin and subcutaneous tissues are incised .
• The sinus forcep is inserted thro the incision superiorly and
posteriorly on the lingual side of the mandible below the mylohyoid
to release the pus from the submandibular space
59. spread
• There are no major anatomic barrier between the two submandibular
and submental spaces
• There are no major anatomic barrier hence infection can spread easily
across the midline and involve submandibular space on the
contralateral side
• Infection can spread backwards to involve para pharyngeal space
• The submandibular space communicates with the sub lingual space
around the posterior border of mylohyoid muscle.
61. Sublingual space
• This space is v shaped trough lying lateral to the muscle of the tongue
including hyoglossus genioglosssus and geniohyoid
• Involvement : teeth involved are mandibular incisors canines premolars
• The infection perforates lingual plate below the level of the mucosa of the
floor of the mouth and passes into the sublingual space.
62. Boundaries
• Superiorly by the mucosa of the floor of the mouth
• Inferiorly :mylohyoid muscle
• Laterally: medial side of the mandible
• Medially :hyoglossus genioglossus and
geniohyoid muscles
• Posteriorly :hyoid bone
• Laterally and inferiorly by the mylohyoid muscle and the lingual side of the
mandible
63. Contents
• Includes genioglossus geniohyoid hyoglossus muscle
• It also contains
• deep part of submandibular salivary gland
• sublingual salivary gland
• Lingual nerve
• Hypoglossal nerve
64. Clinical features
• Extraoral : there is little or no swelling .the lymph node may be enlarged and
tender
• Pain and discomfort on deglutition
• Speech may be affected
• Intraoral: firm painful swelling seen in the floor of
the mouth
• The tongue may be pushed superiorly. this will
bring
about airway obstruction
• The ability to protrude the tongue beyond the
vermillion border of upper lip is affected
65. Incision and drainage
• Intraorally:incision is made close to the lingual cortical plate as the
imp structure at this site is sublingual nerve which is deeply placed
and less likely to be damaged by this approach. The sinus forcep is
inserted and opened to evacuate pus.
• Extraoral: drained via skin incision placed in the sub mental region.
66. spread
• Infection always crosses the midline, and can affect the spaces on the
opposite side
• Infection can also spread via the lymphatics to the submental or
submandibular lymph nodes.
67. Masticatory spaces
• It comprises of the following spaces
1. pterygomandibular
2. submasseteric
3. temporal –superficial temporal
4. deep temporal
68. Submassetric space
• When the pus accumulates between the ramus of the mandible and
the masseter muscle , it produces a submassetric space abscess.
• Involvement :infection originates from the lower 3rd molar resulting
from(i) pericoronitis
• (ii) periapical abscess
69. Boundaries
• Anterior : ant border of masseter muscle
and buccinators
• Posterior : parotid gland and posterior
part of masseter
• Inferior : attachment of masseter to lower
border of mandible
• Medial : lateral surface of ramus of mandible
• Lateral : medial surface of masseter
70. Contents
• masseteric nerve , superficial temporal artery , transverse facial
artery
• It contains muscle of mastication, ramus ,posterior
• part of mandible and branches of mandibular division of
• trigeminal nerve
71. Clinical features
• External facial swelling is moderate in size :swelling extending from
lower border of mandible to the zygomatic arch and anteriorly to the
ant border of masseter and posteriorly
to the post border of the mandible
• Tenderness over the angle of the
mandible
• Almost complete limitation of mouth
opening
• pyrexia
72. Incision and drainage
• Intraoral approach: incision made vertically over the lower part of
anterior border of the ramus of the mandible ,deep to the bone.
• A sinus forcep is passed along the lateral surface of the ramus
downwards and backwards.
• Extraoral approach : when the mouth cannot be opened ,an incision
is placed in the skin behind the angle of mouth to open the abscess
by Hiltons method
73. • Involvement : pericoronitis related to mandibular 3rd molar
• Infection can also be because of contaminated needle used for an
IANB
• At times can also originate from max 3rd molar following PSA injection
Pterygomandibular space infection
74. Boundaries
• Lateral: medial surface of ramus of mandible
• Medial : lateral surface of medial pterygoid muscle
• Posterior: parotid gland
• Anterior :pterygomandibular raphe
• Superior :lat pterygoid muscle forms the roof to pterygomandibular
space
• Contents: lingual nerve , mandibular nerve , inferior alveolar artery ,
mylohyoid nerve and vessel
75. Clinical features
• Even the established cases of pterygomandibular space infection
doesnot cause much swelling of face over the submandibular region .
• Severe degree of limitation of mouth opening
• Tenderness over the area of swollen tissues medial to ant border of
ramus of mandible
• Dysphagia is present
• Redness and the edema of the area around the 3rd molar
• Uvula is swollen
• Difficulty in breathing
76. Incision and drainage
• Intraoral :Vertical incision approx. 1.5 cm in length is made on
anterior and medial aspect of ramus of mandible . Sinus forcep is
inserted in the abscess cavity , opened and
closed and withdrawn . The pus is evacuated
• Extraoral :incision is taken in the skin below
the angle of the mandible. A sinus forcep is
inserted towards the medial side of the
ramus in an upward and backward direction
• . Pus is evacuated
77. Spread
• Infection may spread superiorly along the medial surface of the ramus
to involve the infratemporal fossa
• Infection may spread posteriorly to lateral pharyngeal space and then
to retropharyngeal space
• Can also spread around the front of ramus of mandible to involve the
buccal space
78. Life threatening complication of orofacial
infection
• Which may be classified as
• Those relate to lower jaw
(a)ludwigs angina
(b) descending deep cellulitis of the neck
(c) carotid sheath invasion
• Those related to upper jaw
(a)cavernous sinus thrombosis ,Dural meningitis ,osteomyelitis of
skull
(b) retro bulbar cellulitis with possibility of blindness
79. Ludwig's angina
• Definition;it is the massive firm brawny cellulitis/induration and acute
toxic stage involving simultaneously ,the submandibular, sublingual
and submental spaces bilaterally .
• the term Ludwig angina was coined by Camerer in 1837
• this condition had established its unique identity with three ” f ”s
• It was to be FEARED
• rarely becomes FLUCTUANT
• it was often FATAL
80. Etiology
1.Odontogenic :
a) Acute dentoalvelolar abscess
b) Acute periodontal abscess
c) Acute pericoronal abscess: in relation to erupting 2nd and 3rd molar
which can extend to following spaces
i. Submandibular spaces
ii. Buccal space
iii. Sublingual space
iv. Pterygomandibular space
81. 2. Iatrogenic : use of contaminated needle for giving LA
3. Traumatic injuries to orofacial region :mandibular fractures ,deep
lacerations and penetrating injuries
4. Osteomyelitis
5. Sublingual and submandibular sialadenitis
6. Cervical lymphoid tissues
82. Pathology
• The condition is a cellulitis – a diffuse inflammation of soft tissues
which is not circumscribed or confined to one area but in contrast to
the abscess ,tends to the spread thro tissues spaces and along fascial
planes.
• Involvement : mandibular 2nd and 3rd molars
83. Clinical features
• Pt looks very toxic , very ill and dehydrated
• There is pyrexia anorexia chills and malaise
• Dysphagia
• Impaired speech
• Hoarseness of voice
84. Extraoral examination
• Firm and brawny hard swelling in the bilateral submandibular and submental
regions which soon extends down to the anterior part of the neck to the clavicle.
• Swelling is non pitting minimally or non fluctuant associated with severe
tenderness
• Classically shows ill defined borders with induration.
• Severe muscle spasm may lead to trismus.
• Typically mouth may remain open due to edema of the sublingual tissues leading
to raised tongue almost touching the palatal vault
• Airway obstruction
• There may be dilatation of alae nasi , raising of thoracic inlet by the scalene and
sternocleidomastoid muscle and indrawing of the tissues above the clavicle
85. • Cyanosis may occur due to hypoxia
• Fatal death may occur in untreated cases of Ludwig's
angina within 10 to 24 hours due to asphyxia
• Intraorally: swelling develops rapidly which involves
sublingual tissues and distends or raises the floor of
the mouth, woody edema of the floor of the mouth
and the tongue
• Increased salivation , stiffness of tongue movement
and difficulty in swallowing
• Backward spread of infection leads to edema of
glottis, resulting in respiratory obstruction
• Stridor being alarming sign of this fatal extension
needing emergency intervention to keep airway
patent
86. Spread
• Due to anatomical continuity of various spaces with submandibular space infection may track to
• submasseteric
petrygomandibular space
parapharyngeal space
para tonsillar spaces
Worsening the airway
87. • Infection from the submandibular region may spread downwards
along and the deep investing layer of deep cervical fascia , towards
the clavicle and subsequently to mediastinum.
88.
89.
90. Principles of treatment
• The treatment is based on combination of following factors
• Early diagnosis
• Maintenance of patent airway
• Intense and prolonged antibiotic therapy
• Extraction of offending tooth
• Surgical drainage or decompression of fascial spaces
91. Airway maintenance
• Intubation of patient: blind intubation should be avoided .
Nasoendotacheal intubation is far more reliable.
• surgical airway: required in case of severe upper resp obstruction .
• Laryngotomy cricothyroidotomy (tracheotomy) is preferred over
tracheostomy because of :
• Identification of landmarks is difficult due to associated massive
edema and tissue distortion
• The surgery itself may lead to spread of infection to deeper tissues
due to additional incision required .
92. Surgical intervention
• It has two aims: (i) remove the cause
(ii) Surgical decompression
Removal of the cause : removing of offending tooth may facilitate the
evacuation of the pus
Surgical decompression : it reduces pressure of edematous tissues on
the airway reducing respiratory embarassement
• It allows prompt drainage
93. Antibiotic therapy
• Plays a vital role in managing Ludwig's angina.
• Penicillin are first line antibiotics in treating such infections as it
covers majority of aerobic gram +ve microbial flora .
• Administerd in the form of aqueous Pn g 2 to 4 million units IV 4 to 6
hourly or;500 mg six hourly orally .
• Ampicillin or amoxicillin ; 500mg 6 and 8 hourly IV and orally
respectively
• Cloxacillin; 500mg orally 8 hourly
• In case of allergic to Pn; erythromycin 600mg 6 to 8 hourly
94. • Gentamicin 80mg IM B.D
• Clindamycin IV 300 to 600 mg 8 hourly
• Metronidazole 400mg 8 hourly
95. Hydration
• Pt should be encouraged to have liquids and if required iv ,fluids can
maintain hydration and calories.
96. A simple prototype protocol
A. Preoperative
1.Airway assessment
2.Etiological findings :further radiographs OPG, and other radiograph
3.Risk factor consideration: diabetes immunodeficiency status
4.Hydration :pulse and urine output
5.Chest radiograph to rule out pneumonia
6.Evaluate lab data: blood counts
97. B.Perioperative
i. Intubation
ii. Removal of cause
iii. Antibiotics
C .postoperative
i. Extubate after confirming adequate airway
ii. Irrigations of drains periodically
iii. Culture reports to adjust antibiotics accordingly
iv. Regular follow up
98.
99. Cavernous sinus thrombophlebitis
• Occur as a result of superior spread of odontogenic infection via
haematogenous route
• Formation of thrombus in cavernous sinus / communicating branches
• Unusual occurrence ,rarely result of infected tooth
• Serious, life threatening infection
102. Microbiology
streptococci and staphylococci and gram –
ve bacteria
Clinical features
• Swelling of the face and eye
• Pain in the eye
• Edema of conjunctiva
• Pulsating exopthalmus
104. Conclusion
we being dental surgeons must understand
anatomy of fascial spaces ,spread of infection and
proper management for the prevention of further
complications and betterment of health of the
patient.