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.
This document provides information on osteomyelitis of the jaw, including its classification, etiology, pathogenesis, microbiology, clinical findings, imaging, and treatment. It discusses the different types of osteomyelitis (acute suppurative, secondary chronic, primary chronic, non-suppurative). It also covers osteoradionecrosis of the jaw, its definition, clinical findings, radiological features, treatment with hyperbaric oxygen therapy, and prevention. Microorganisms commonly involved include viridans streptococci and anaerobes such as Peptostreptococcus and Fusobacterium. Imaging tools like radiography, CT, MRI, and radionuclide bone scanning can aid in diagnosis
The document discusses chronic osteomyelitis, defining it as a severe, persistent bone infection lasting over 1 month with dead bone present. It covers the pathogenesis, classification, clinical features, and Cierny-Mader staging system for chronic osteomyelitis, which considers anatomical factors like location of infection and physiological factors like immune status to determine treatment approach. Chronic osteomyelitis is challenging to treat due to biofilm formation, poor vascularity of infected bone, and host immune compromise in many cases.
The document discusses chronic osteomyelitis, defining it as a severe, persistent bone infection lasting over 1 month with dead bone present. It covers the pathogenesis, classification, clinical features, and Cierny-Mader staging system for chronic osteomyelitis, which considers anatomical factors like location of infection and physiological factors like immune status to determine treatment approach. Chronic osteomyelitis is challenging to treat due to biofilm formation, poor vascularity of infected bone, and host immune compromise in many cases.
This document discusses osteomyelitis and septic arthritis. It defines osteomyelitis as inflammation of the bone and marrow usually due to infection. Common causative organisms include bacteria such as Staphylococcus aureus and mycobacteria. Pyogenic osteomyelitis is described along with its clinical features, diagnosis, and treatment. Tuberculous osteomyelitis and its features are also outlined. Infectious arthritis is discussed, noting the bacteria commonly involved and characteristics of joint fluid. Risk factors, clinical features, and complications are summarized for both conditions.
Osteomyelitis is an inflammation of bone caused by bacterial infection. It can be acute (<2 weeks), subacute (2-6 weeks), or chronic (>6 weeks) depending on duration and symptoms. Common causative organisms are Staphylococcus aureus and other staph species. In children, S. aureus and group B streptococcus are frequent causes. Chronic osteomyelitis is characterized by necrotic bone (sequestrum) surrounded by inflammatory tissue (involucrum). Symptoms include pain, swelling, and draining sinuses. The metaphysis of long bones is a common site due to its vascular anatomy.
The document discusses osteomyelitis, which is an inflammatory condition of bone that begins as an infection of the medullary cavity and spreads to involve the periosteum. It can be acute or chronic, and is caused by bacteria or fungi entering via trauma or a blood-borne route. Symptoms include pain, swelling, and pus drainage. Diagnosis involves medical imaging and biopsy. Treatment involves antibiotics, drainage of pus, debridement of infected tissue, and sometimes surgery. Chronic osteomyelitis can be difficult to treat and may require repeated surgeries. Risk factors include reduced blood supply to bone from conditions like diabetes.
This document discusses osteomyelitis, an infection of bone. It describes the classification systems of Waldvogel and Cierny-Mader, which categorize osteomyelitis based on duration, pathogenesis, anatomical involvement, and host physiology. Common types include hematogenous osteomyelitis from bacteremia and contiguous osteomyelitis from a nearby soft tissue infection. Diagnosis involves imaging, labs, and bone biopsy for culture and pathology. Staphylococcus aureus is a frequent pathogen.
This document provides information on osteomyelitis of the jaw, including its classification, etiology, pathogenesis, microbiology, clinical findings, imaging, and treatment. It discusses the different types of osteomyelitis (acute suppurative, secondary chronic, primary chronic, non-suppurative). It also covers osteoradionecrosis of the jaw, its definition, clinical findings, radiological features, treatment with hyperbaric oxygen therapy, and prevention. Microorganisms commonly involved include viridans streptococci and anaerobes such as Peptostreptococcus and Fusobacterium. Imaging tools like radiography, CT, MRI, and radionuclide bone scanning can aid in diagnosis
The document discusses chronic osteomyelitis, defining it as a severe, persistent bone infection lasting over 1 month with dead bone present. It covers the pathogenesis, classification, clinical features, and Cierny-Mader staging system for chronic osteomyelitis, which considers anatomical factors like location of infection and physiological factors like immune status to determine treatment approach. Chronic osteomyelitis is challenging to treat due to biofilm formation, poor vascularity of infected bone, and host immune compromise in many cases.
The document discusses chronic osteomyelitis, defining it as a severe, persistent bone infection lasting over 1 month with dead bone present. It covers the pathogenesis, classification, clinical features, and Cierny-Mader staging system for chronic osteomyelitis, which considers anatomical factors like location of infection and physiological factors like immune status to determine treatment approach. Chronic osteomyelitis is challenging to treat due to biofilm formation, poor vascularity of infected bone, and host immune compromise in many cases.
This document discusses osteomyelitis and septic arthritis. It defines osteomyelitis as inflammation of the bone and marrow usually due to infection. Common causative organisms include bacteria such as Staphylococcus aureus and mycobacteria. Pyogenic osteomyelitis is described along with its clinical features, diagnosis, and treatment. Tuberculous osteomyelitis and its features are also outlined. Infectious arthritis is discussed, noting the bacteria commonly involved and characteristics of joint fluid. Risk factors, clinical features, and complications are summarized for both conditions.
Osteomyelitis is an inflammation of bone caused by bacterial infection. It can be acute (<2 weeks), subacute (2-6 weeks), or chronic (>6 weeks) depending on duration and symptoms. Common causative organisms are Staphylococcus aureus and other staph species. In children, S. aureus and group B streptococcus are frequent causes. Chronic osteomyelitis is characterized by necrotic bone (sequestrum) surrounded by inflammatory tissue (involucrum). Symptoms include pain, swelling, and draining sinuses. The metaphysis of long bones is a common site due to its vascular anatomy.
The document discusses osteomyelitis, which is an inflammatory condition of bone that begins as an infection of the medullary cavity and spreads to involve the periosteum. It can be acute or chronic, and is caused by bacteria or fungi entering via trauma or a blood-borne route. Symptoms include pain, swelling, and pus drainage. Diagnosis involves medical imaging and biopsy. Treatment involves antibiotics, drainage of pus, debridement of infected tissue, and sometimes surgery. Chronic osteomyelitis can be difficult to treat and may require repeated surgeries. Risk factors include reduced blood supply to bone from conditions like diabetes.
This document discusses osteomyelitis, an infection of bone. It describes the classification systems of Waldvogel and Cierny-Mader, which categorize osteomyelitis based on duration, pathogenesis, anatomical involvement, and host physiology. Common types include hematogenous osteomyelitis from bacteremia and contiguous osteomyelitis from a nearby soft tissue infection. Diagnosis involves imaging, labs, and bone biopsy for culture and pathology. Staphylococcus aureus is a frequent pathogen.
This document discusses various inflammatory diseases of bone, focusing on osteomyelitis. It defines osteomyelitis as an infection and inflammation of bone and bone marrow. The document categorizes osteomyelitis as either acute or chronic, describes their signs and symptoms, causes, and treatments. It also discusses other conditions involving bone inflammation including osteitis, periostitis, sclerosing osteomyelitis, osteoradionecrosis, and alveolar osteitis.
osteomyelitis of jaw bones / dental implant courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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1. Osteomyelitis is an infection of bone that can be caused by various systemic infectious diseases spreading to the bone or directly through injuries or surgery.
2. Pyogenic osteomyelitis is usually caused by bacterial infection, most commonly Staphylococcus aureus, and presents differently in developing versus developed countries.
3. Tuberculous osteomyelitis is caused by Mycobacterium tuberculosis spreading hematogenously from sites like the lungs and can lead to caseous necrosis and bone destruction if left untreated.
Osteomyelitis is an infection of the bone that can be acute or chronic. It is most commonly caused by Staphylococcus aureus bacteria entering through the bloodstream (hematogenous spread), through a penetrating injury or surgery (contiguous spread), or spreading from a skin infection in patients with vascular disease. It typically presents with bone pain, swelling, and fever. Treatment involves antibiotics, sometimes for prolonged periods, and potentially surgical drainage if an abscess forms. Chronic osteomyelitis is difficult to treat and characterized by long-term infection that results in the formation of dead bone (sequestrum).
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.
This document discusses inflammatory diseases of the bones and joints, focusing on osteomyelitis. It defines osteomyelitis as inflammation of all bone anatomical structures that is typically caused by common bacteria like Staphylococcus aureus. It describes the pathogenesis of hematogenous osteomyelitis, how it spreads through the bones, and can lead to complications like sepsis and fractures. Diagnosis involves x-rays and CT scans to identify features like periosteal reaction and bone destruction. Treatment involves antibiotics, surgery to debride infected areas, and managing complications.
This document discusses chronic infections of the jaws, including:
- Types of infections like periostitis, osteitis, and osteomyelitis and their characteristics.
- Causative factors like bacteria, trauma, and dental infections.
- Classification systems based on features like pathogenesis, clinical presentation, and anatomy.
- Presentation and management of specific types like acute suppurative osteomyelitis, chronic sclerosing osteomyelitis, and Garre's osteomyelitis.
- Role of predisposing conditions like diabetes and factors like poor vascularity that increase risk.
1) Acute osteomyelitis is a bacterial infection of bone that typically affects children under 5 years old. It spreads hematogenously from sites like skin infections.
2) Symptoms include fever, bone pain, and refusal to use the affected limb. Diagnosis involves blood tests, imaging like x-rays and MRIs, and aspirating fluid from bone or abscesses.
3) Treatment consists of antibiotics, drainage of abscesses, and sometimes drilling into bone to relieve pressure. Complications include spread to joints, bones, or internally. Without proper treatment, it can become chronic osteomyelitis.
This document discusses osteomyelitis, an infection of the bone marrow. It begins by defining osteomyelitis and discussing its etiology, or causes. Common causes include dental infections, trauma, and hematogenous spread. The pathogenesis, or mechanism by which it develops, is then explained. Bacterial infection leads to inflammation, tissue necrosis, and vascular damage within the bone. Over time, this can progress to form sequestra - dead bone fragments. Symptoms vary depending on whether the infection is acute or chronic, but may include pain, swelling, fever, and bone destruction visible on x-rays. The document continues with further sections on classification, diagnosis, and treatment of osteomyelitis.
This document provides an overview of chronic osteomyelitis. It begins with definitions and describes the pathogenesis as bacteria reaching the metaphysis, causing inflammation and tissue necrosis. Imaging can detect bone changes like lytic lesions. Diagnosis involves biopsy for culture and histology. Chronic osteomyelitis is characterized by infected dead bone (sequestrum) surrounded by sclerotic bone (involucrum) that forms draining sinus tracts. Multiple organisms are often present and biofilm formation complicates treatment. Differential diagnosis includes tuberculosis, soft tissue infection, and tumors.
This document discusses osteomyelitis and bone infections. It covers the definition of osteomyelitis as a bone infection, modes of spread including direct introduction through the skin or bloodstream, and general aspects such as inflammation and bone necrosis. It also describes acute pyogenic infection, acute hematogenous osteomyelitis in children and adults, clinical features, diagnostic imaging including X-rays, and treatment involving identifying the organism, drainage, debridement and antibiotics.
Osteomyelitis is an inflammation of bone caused by an infecting organism. Staphylococcus aureus is the most common cause. Acute hematogenous osteomyelitis usually involves the metaphysis of long bones in children. Diagnosis is based on clinical features like localized tenderness and lab tests showing elevated inflammatory markers. Plain X-rays may initially only show soft tissue swelling and osteopenia before lytic bone changes appear in subacute or chronic cases.
Osteomyelitis is a progressive bone or bone marrow infection, usually caused by bacteria such as Staphylococcus aureus. It can affect any bone and is more common in long bones and vertebrae. Symptoms include bone pain, swelling, and limited movement. Diagnosis involves medical history, physical exam, blood tests, imaging like MRI, bone scan, or CT, and bone biopsy. Treatment consists of prolonged antibiotic therapy and sometimes surgery to remove infected bone and tissue. Complications include bone abscesses, fractures, and chronic osteomyelitis.
Osteomyelitis is defined as bone inflammation caused by a circulating infection. It is characterized by progressive bone destruction. Common symptoms include severe pain, fever, and unwillingness to use the affected limb. Investigation may include blood tests, bone biopsy for culture and sensitivity, and imaging like x-rays, MRI, or bone scan. Treatment depends on factors like patient health, injury severity, and location; and may involve antibiotics, surgery, or both to clear the infection. Complications can include persistent or spreading infection, amputation, sepsis, or malignant transformation of chronic draining sinuses.
This document discusses acute osteomyelitis, beginning with a definition and classification. It describes how the infection can spread from the initial site in bone to surrounding tissues. Common causative organisms are discussed for both children and adults. Clinical features vary depending on the patient's age but may include pain, fever, and localized swelling. Diagnostic imaging tools like x-ray, MRI, and bone scans are described. Treatment involves aspirating pus for culture and treating with antibiotics.
The document discusses bone infection or osteomyelitis, including causes such as bacterial infection spreading through the bloodstream or nearby tissue, symptoms like fever and bone pain, diagnosis through tests like blood work, x-rays and biopsies, and treatment involving long-term antibiotic therapy and sometimes surgery to drain infections and remove damaged tissue. Osteomyelitis can affect people of all ages but is more common in infants, children, and older adults.
This document discusses osteomyelitis, an inflammation of bone and bone marrow that can result from odontogenic infection. It describes the different types of osteomyelitis including acute suppurative, chronic suppurative, chronic focal sclerosing (condensing osteitis), and chronic diffuse sclerosing osteomyelitis. Specific details are provided on the clinical, radiographic, and histopathologic features of acute suppurative osteomyelitis as well as chronic osteomyelitis with proliferative periostitis (Garre's osteomyelitis). The pathogenesis and potential complications of acute suppurative osteomyelitis are also summarized.
Osteomyelitis is an inflammation of bone and bone marrow caused by an infecting organism. It can be classified based on duration, mechanism of infection, anatomical involvement, and host factors. Acute hematogenous osteomyelitis most commonly affects the metaphysis of long bones in children under 2 years old. It is caused by hematogenous spread from another infection and presents with fever, pain, and swelling as the infection destroys bone and spreads. Proper classification and treatment is important to prevent complications like bone deformity, joint involvement, and chronic infection.
The document discusses osteomyelitis, including its pathophysiology, risk factors, presentation, diagnosis, and treatment. Osteomyelitis is a bone infection that can occur due to hematogenous spread, direct inoculation from trauma/surgery, or contiguous spread from nearby infected structures. Diagnosis involves blood tests, imaging like x-rays and MRI, and bone biopsy. Treatment requires a multidisciplinary approach including surgical debridement combined with long-term IV and oral antibiotics based on isolated pathogens.
This document discusses various inflammatory diseases of bone, focusing on osteomyelitis. It defines osteomyelitis as an infection and inflammation of bone and bone marrow. The document categorizes osteomyelitis as either acute or chronic, describes their signs and symptoms, causes, and treatments. It also discusses other conditions involving bone inflammation including osteitis, periostitis, sclerosing osteomyelitis, osteoradionecrosis, and alveolar osteitis.
osteomyelitis of jaw bones / dental implant courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
1. Osteomyelitis is an infection of bone that can be caused by various systemic infectious diseases spreading to the bone or directly through injuries or surgery.
2. Pyogenic osteomyelitis is usually caused by bacterial infection, most commonly Staphylococcus aureus, and presents differently in developing versus developed countries.
3. Tuberculous osteomyelitis is caused by Mycobacterium tuberculosis spreading hematogenously from sites like the lungs and can lead to caseous necrosis and bone destruction if left untreated.
Osteomyelitis is an infection of the bone that can be acute or chronic. It is most commonly caused by Staphylococcus aureus bacteria entering through the bloodstream (hematogenous spread), through a penetrating injury or surgery (contiguous spread), or spreading from a skin infection in patients with vascular disease. It typically presents with bone pain, swelling, and fever. Treatment involves antibiotics, sometimes for prolonged periods, and potentially surgical drainage if an abscess forms. Chronic osteomyelitis is difficult to treat and characterized by long-term infection that results in the formation of dead bone (sequestrum).
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.
This document discusses inflammatory diseases of the bones and joints, focusing on osteomyelitis. It defines osteomyelitis as inflammation of all bone anatomical structures that is typically caused by common bacteria like Staphylococcus aureus. It describes the pathogenesis of hematogenous osteomyelitis, how it spreads through the bones, and can lead to complications like sepsis and fractures. Diagnosis involves x-rays and CT scans to identify features like periosteal reaction and bone destruction. Treatment involves antibiotics, surgery to debride infected areas, and managing complications.
This document discusses chronic infections of the jaws, including:
- Types of infections like periostitis, osteitis, and osteomyelitis and their characteristics.
- Causative factors like bacteria, trauma, and dental infections.
- Classification systems based on features like pathogenesis, clinical presentation, and anatomy.
- Presentation and management of specific types like acute suppurative osteomyelitis, chronic sclerosing osteomyelitis, and Garre's osteomyelitis.
- Role of predisposing conditions like diabetes and factors like poor vascularity that increase risk.
1) Acute osteomyelitis is a bacterial infection of bone that typically affects children under 5 years old. It spreads hematogenously from sites like skin infections.
2) Symptoms include fever, bone pain, and refusal to use the affected limb. Diagnosis involves blood tests, imaging like x-rays and MRIs, and aspirating fluid from bone or abscesses.
3) Treatment consists of antibiotics, drainage of abscesses, and sometimes drilling into bone to relieve pressure. Complications include spread to joints, bones, or internally. Without proper treatment, it can become chronic osteomyelitis.
This document discusses osteomyelitis, an infection of the bone marrow. It begins by defining osteomyelitis and discussing its etiology, or causes. Common causes include dental infections, trauma, and hematogenous spread. The pathogenesis, or mechanism by which it develops, is then explained. Bacterial infection leads to inflammation, tissue necrosis, and vascular damage within the bone. Over time, this can progress to form sequestra - dead bone fragments. Symptoms vary depending on whether the infection is acute or chronic, but may include pain, swelling, fever, and bone destruction visible on x-rays. The document continues with further sections on classification, diagnosis, and treatment of osteomyelitis.
This document provides an overview of chronic osteomyelitis. It begins with definitions and describes the pathogenesis as bacteria reaching the metaphysis, causing inflammation and tissue necrosis. Imaging can detect bone changes like lytic lesions. Diagnosis involves biopsy for culture and histology. Chronic osteomyelitis is characterized by infected dead bone (sequestrum) surrounded by sclerotic bone (involucrum) that forms draining sinus tracts. Multiple organisms are often present and biofilm formation complicates treatment. Differential diagnosis includes tuberculosis, soft tissue infection, and tumors.
This document discusses osteomyelitis and bone infections. It covers the definition of osteomyelitis as a bone infection, modes of spread including direct introduction through the skin or bloodstream, and general aspects such as inflammation and bone necrosis. It also describes acute pyogenic infection, acute hematogenous osteomyelitis in children and adults, clinical features, diagnostic imaging including X-rays, and treatment involving identifying the organism, drainage, debridement and antibiotics.
Osteomyelitis is an inflammation of bone caused by an infecting organism. Staphylococcus aureus is the most common cause. Acute hematogenous osteomyelitis usually involves the metaphysis of long bones in children. Diagnosis is based on clinical features like localized tenderness and lab tests showing elevated inflammatory markers. Plain X-rays may initially only show soft tissue swelling and osteopenia before lytic bone changes appear in subacute or chronic cases.
Osteomyelitis is a progressive bone or bone marrow infection, usually caused by bacteria such as Staphylococcus aureus. It can affect any bone and is more common in long bones and vertebrae. Symptoms include bone pain, swelling, and limited movement. Diagnosis involves medical history, physical exam, blood tests, imaging like MRI, bone scan, or CT, and bone biopsy. Treatment consists of prolonged antibiotic therapy and sometimes surgery to remove infected bone and tissue. Complications include bone abscesses, fractures, and chronic osteomyelitis.
Osteomyelitis is defined as bone inflammation caused by a circulating infection. It is characterized by progressive bone destruction. Common symptoms include severe pain, fever, and unwillingness to use the affected limb. Investigation may include blood tests, bone biopsy for culture and sensitivity, and imaging like x-rays, MRI, or bone scan. Treatment depends on factors like patient health, injury severity, and location; and may involve antibiotics, surgery, or both to clear the infection. Complications can include persistent or spreading infection, amputation, sepsis, or malignant transformation of chronic draining sinuses.
This document discusses acute osteomyelitis, beginning with a definition and classification. It describes how the infection can spread from the initial site in bone to surrounding tissues. Common causative organisms are discussed for both children and adults. Clinical features vary depending on the patient's age but may include pain, fever, and localized swelling. Diagnostic imaging tools like x-ray, MRI, and bone scans are described. Treatment involves aspirating pus for culture and treating with antibiotics.
The document discusses bone infection or osteomyelitis, including causes such as bacterial infection spreading through the bloodstream or nearby tissue, symptoms like fever and bone pain, diagnosis through tests like blood work, x-rays and biopsies, and treatment involving long-term antibiotic therapy and sometimes surgery to drain infections and remove damaged tissue. Osteomyelitis can affect people of all ages but is more common in infants, children, and older adults.
This document discusses osteomyelitis, an inflammation of bone and bone marrow that can result from odontogenic infection. It describes the different types of osteomyelitis including acute suppurative, chronic suppurative, chronic focal sclerosing (condensing osteitis), and chronic diffuse sclerosing osteomyelitis. Specific details are provided on the clinical, radiographic, and histopathologic features of acute suppurative osteomyelitis as well as chronic osteomyelitis with proliferative periostitis (Garre's osteomyelitis). The pathogenesis and potential complications of acute suppurative osteomyelitis are also summarized.
Osteomyelitis is an inflammation of bone and bone marrow caused by an infecting organism. It can be classified based on duration, mechanism of infection, anatomical involvement, and host factors. Acute hematogenous osteomyelitis most commonly affects the metaphysis of long bones in children under 2 years old. It is caused by hematogenous spread from another infection and presents with fever, pain, and swelling as the infection destroys bone and spreads. Proper classification and treatment is important to prevent complications like bone deformity, joint involvement, and chronic infection.
The document discusses osteomyelitis, including its pathophysiology, risk factors, presentation, diagnosis, and treatment. Osteomyelitis is a bone infection that can occur due to hematogenous spread, direct inoculation from trauma/surgery, or contiguous spread from nearby infected structures. Diagnosis involves blood tests, imaging like x-rays and MRI, and bone biopsy. Treatment requires a multidisciplinary approach including surgical debridement combined with long-term IV and oral antibiotics based on isolated pathogens.
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
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2. The words, “osseous” in latin means bony, and
“osteon” in Greek means “bone”, and ‘‘myleos’’
means marrow; and “itis” in Greek means
inflammation.
In 1834, Nelaton first coined the word
“Osteomyelitis”.
By definition osteomyelitis (OML) is an
inflammation of medullary portion of bone or bone
marrow or cancellous bone.
3. Osteomyelitis is an extensive inflammation of a
bone. It involves the cancellous portion, bone
marrow ,cortex and periosteum. ( Laskin1989)
4. The inflammation may be acute, subacute or
chronic.
It may be localized ; or may involve a larger portion
of bone.
It may be suppurative or nonsuppurative.
5. The factors that predispose to osteomyelitis are:
1. Conditions affecting host resistance or defenses
2. Compromised vascular integrity and perfusion in
the host bone, at the local, regional or systemic level
3. Virulence of microorganisms
6. 1. Conditions that alter host defenses would
include chronic debilitating diseases, such as
diabetes mellitus, agranulocytosis, leukemia ,
severe anemia, malnutrition, drug abuse, chronic
alcoholism, sickle cell disease, and febrile
illnesses such as typhoid, tuberculosis.
2. Conditions that alter vascularity of bone include
therapeutic irradiation, osteoporosis, Paget’s
disease, fibrous dysplasia, peripheral vascular
disease, bone malignancy, metallic bone necrosis
(caused by mercury, bismuth, and arsenic).
7. 3. Virulence of organisms: Certain organisms precipitate
thrombi formation by virtue of their destructive
lysosomal enzymes (Hudson 1993). Lysosomal and
enzymatic degradation of host tissue, along with
microvascular thrombosis brought about by pathogen
borne bioactive peptides and chemoattracted leukocytic
purulence, forms a protective barrier for the infectious
foci, allowing organisms to proliferate in an enriched
host medium, while protected from the host immunity.
8. Osteomyelitis of the jaws is caused by:
Odontogenic infections: Primarily odontogenic infections
originating from pulpal or periodontal tissues,
pericoronitis, infected socket, infected cyst, tumor, etc.
Trauma: Is the second leading cause : (a) Especially,
compound fracture and (b) Surgery – iatrogenic cause.
Infections of orofacial regions derived from : Periostitis
following gingival ulceration, lymph nodes infected from
furuncles, lacerations, peritonsillar abscess.
9. Infections derived by hematogenous route: Furuncle on
face, wound on the skin, upper respiratory tract infection,
middle ear infection, mastoiditis, systemic tuberculosis.
The medications linked to osteomyelitis are steroids,
chemotherapeutic agents and bisphosphonates. Local
conditions that adversely affect the blood supply can also
predispose the host to a bony infection.
10. Osteomyelitis is initiated from a contiguous focus of
infection or by hematogenous spread
Primary hematogenous osteomyelitis is rare in the
maxillofacial region , generally occurring in the very young
patients
The adult process is initiated by an inoculation of bacteria
into the jaw bones
11. The initial causative insult results in a bacteria induced
inflammation or cascade
In normal healthy patient, this process will be self-limiting
Osteomyelitis is an infectious process of the medullary
myeloid cavity of bone
In the craniofacial skeleton , only the mandible and the
calvarium have myeloid compartments
12. The important factor in the establishment of osteomyelitis
is the compromise in the blood supply .
13.
14.
15. Primary supply: The mandible is supplied by inferior alveolar
artery, except coronoid process, which is supplied by
temporalis muscle vessels.
Secondary supply: It is periosteal supply, which generally
runs parallel to cortical surface of bone, giving off nutrient
vessels, those penetrate cortical bone and anastomose with
the branches of inferior alveolar artery.
Venous drainage of mandible: There are two routes: (1) Via
inferior alveolar vein ; it runs upwards, and joins pharyngeal
plexus, and (2) It runs downwards, and joins external jugular
veins.
Waldron(1943) , gave an exhaustive morphologic description
of vascular morphology of mandible and associated structures
16. to account for spread of OML. He described mandibular
vascular support as being provided through multiple
arterial loops from a single major vessel, which renders
large portion of bone susceptible to necrosis with the
occurence of major vessel infectious thrombosis.
Waldervogel (1970): described its relationship to vascular
support of long bones of developing and adult human
skeleton . He made several conclusions :
There tends to be segregation of vascular channels, which
act like “end organs”, due to lack of terminal collateral
anastomosis, ultimately, leading to vascular plugging by
bacteria, microthrombi or both.
When afferent vessels anastomose with medullary
channels
17. , there is a possibility of a decrease in venous flow with
associated areas of greater turbulence.
There may be a reduction in host immune defense
mechanism associated with these vascular channels in
calcified tissue.
18. A true osteomyelitis infectious process does not occur in
the maxilla despite the presence of tooth follicle or
anatomic respiratory sinus cavities, including the nose.
It is rare , due to: (1) Extensive blood supply and
significant collateral blood flow in midface,
(2) Porous nature of membranous bone,
(3) Thin cortical plates, and
(4) Abundant medullary spaces. These preclude
confinement of infections within bone ; and permit
dissipation of edema and pus into soft tissues and
paranasal air sinuses.
19.
20. The process of leading to OML is initiated by acute
inflammation, hyperemia, increased capillary permeability
and infiltration of granulocytes. Tissue necrosis occurs, as
proteolytic enzymes are liberated and as destruction of
bacteria and vascular thrombosis continues, there is a pus
formation.
The pus is a combination of necrotic tissue and dead
bacteria and white blood cells accumulate. When pus
accumulates, the intermedullary pressure increases
resulting in vascular collapse, venous stasis, and ischemia.
21. Subsequently, pus travels through Haversian and
nutrient canals and accumulates beneath the periosteum,
elevating it from the cortex ; and thereby further
reducing vascular supply. Compression of neurovascular
bundle accelerates thrombosis, ischemia, and infarction,
later resulting in paresthesia and sequestrum formation.
A sequestrum is defined as a portion of bone that
becomes separated from sound bone during the process of
necrosis.
Radiographically, the bone surrounding sequestrum
appears less densely mineralized than sequestrum itself,
since vascularity of vital bone creates relative
demineralization.
22. In the past, etiology of OML was associated with skin
surface bacteria, Staphylococcus aureus, and to a lesser
extent Staphylococcus epidermidis, or hemolytic
streptococci. However, the picture of S.aureus as primary
offending pathogen does not hold true with regard to OML
of tooth bearing bone.
Most of the cases are caused by aerobic Streptococci (alpha
hemolytic streptococci, Streptococcus viridans), anaerobic
streptococci; and other anaerobes, such as
Peptostreptococci, fusobacteria, and Bacteroides.
23. Other organisms, such as M. tuberculosis , T. Pallidum,
and Actinomyces species produce their respective specific
forms of OML.
Hence, established acute OML is usually a polymicrobial
disease and includes : Streptococci, Bacteroides,
Peptostreptococci and Fusobacteria.
24. A variety of classifications of various forms of the disease
are:
Historically accepted classification : It is based on clinical
course. (A) Acute, (B) Chronic. The arbitrary time limit, to
identify acute from chronic form is of 1 month (Koorbusch
et al. 1992, Marx; 1992, and Mercuri ; 1992) .
27. Cierny et al. (1985) and Vibhagool (1993) developed a
classification and staging system; based on:
1. Anatomic location of infectious process,
2. Physiological status of the host,
3. Systemic or local factors affecting immune system,
metabolism, and local vascularity.
28.
29. It may have the appearance of a typical
odontogenic infection. It can be localized and
widespread, with extensive sequestration and
possible pathological fracture.
30. It is caused by pyogenic organisms. OML in the tooth
bearing area, is polymicrobial in nature. The most
commonly found organisms in odontogenic OML is
Staphylococcus aureus, and Streptococcus pyogenes.
31. 1. Odontogenic infections
2. Local traumatic injuries
3. Peritonsillar abscess
4. Furunculosis
5. Hematogenous infections
6. Infected compounded odontoma
7. Compound fractures of jaws are complicated by OML.
32. These are the common local cause of OML. These
infections may result from: periapical disease secondary to
pulp pathology, periodontal disease, pericoronitis of long
duration, infected odontogenic cyst, and infection of an
extraction wound or fracture site.
33.
34. Injuries of gingiva are usually insignificant;
however may become serious in patients with low
resistance (Ivy and Cook, 1942).
Instruments used for extraction of teeth.
35. PERITONSILLAR ABSCESS: It has been
recorded as a cause of OML of ascending ramus.
FURUNCULOSIS: Of skin is a rare cause of
OML.
HEMATOGENOUS INFECTION : It may
cause multiple sites of OML. The organisms enter
the bloodstream through a minor wound in the
skin, or infection of upper respiratory tract, or
infection of middle ear.
36. 1. Undernourished children
2. Lowered general resistance of body
3. Generalized body diseases, such as : diabetes,
leukemia and agranulocytosis
4. Acute illnesses such as influenza, measles,
scarlet fever, pertussis and pneumonia, etc.
37. OCCURENCE: In adults, it is more common in
mandible and involves alveolar process, angle of
mandible, posterior part of ramus and coronoid process.
OML of condyle is reportedly rare (Linsey, 1953).
Early cases are characterized by :
Generalized constitutional symptoms: high
intermittent fever, malaise, nausea, vomiting,
anorexia.
Continuous intense pain in the affected area.
38. Intermittent paresthesia or anesthesia of the lower lip,
which helps the clinician to differentiate this condition
from alveolar abscess.
Facial cellulitis, or indurated swelling of moderate size,
which is more confined to the periosteal envelope and its
contents (I) Thrombosis of inferior alveolar vasa
nervorum, (II) Rise in pressure from edema in inferior
alveolar canal (III) Teeth are tender to percussion and
loose, and presence of trismus.
In children : fluminating, severe and serious, involvement
of maxilla or mandible, complicated by the presence of
unerupted developing teeth buds, which become necrotic
39. and act as foreign bodies and prolong the disease
process.
Long- term involvement of temporomandibular joint
(TMJ) can cause ankylosis of TMJ and subsequently
affect the growth and development of facial
structures.
Laboratory studies : Show mild leukocytosis [poly-
morphonuclear leukocytes (PMNL)] and
albuminuria.
40. Established cases are characterized by :
Deep pain, malaise, fever, dehydration, anorexia
Teeth in involved area begin to loosen and become
sensitive to percussion.
Purulent discharge through sinuses :
(a) Intraorally, around gingival sulcus or through buccal
vestibule, and
(b) Extraorally on the face, through cutaneous fistulae
Fetid odor is often present .
Dehydration, acidosis and toxemia.
Regional lymphadenopathy is usually present.
41. Laboratory studies show: moderate leukocytosis, slightly
elevated erythrocyte sedimentation rate (ESR) and C
reactive protien, anemia and albuminuria.
MANAGEMENT –
Removal of the cause and debridement with antibiotic
cover.
42. It can be primary: resulting from organisms which are less
virulent, and secondary occuring after acute OML, when
the treatment did not succeed in eliminating the infection
43. The clinical features are usually limited to :
Pain and tenderness : the pain is minimal
Nonhealing bony and overlying soft tissue wounds with
induration of soft tissues,
Intraoral or extraoral draining fistulae.
Thickened or “wooden” character of bone.
Enlargement of mandible because of deposition of
subperiosteal new bone .
Sterile abscess (Brodie’s abscess) , common to long bones
is rare in jaws.
Teeth in the area tend to become loose and sensitive to
palpation and percussion.
44. It is made on basis of : history, clinical examination and
radiological findings — 1) Presence of sequestra, (2)
Areas of suppuration involving the tooth –bearing area of
jaw bone, not responding to debridement and
conservative therapy, (3) Regional or systemic
compromise of immune response, microvascular
decompensation or both.
45. Several sequalae/complications can occur as a result of
OML of jaws.
Neoplastic transformation: With chronic OML,
neoplastic conversion of inflammatory metaplasia to
squamous cell carcinoma is noted. The incidence
reported is 0.2-1.5%.
Discontinuity defects: The defects can be (a)
spontaneous (b) surgically induced, necessitating jaw
reconstruction ; once infection is resolved.
46.
47. Progressive diffuse sclerosis : It involves the medullary
and cortical portions of maxillofacial skeleton, especially
mandible, over a period of time.
48. The overall treatment modalities include:
1. Conservative treatment
2. Surgical treatment
The goal of the treatment is to:
1. Attentuate and eradicate proliferating pathological
organisms
2. Promote healing
3. Re-establish vascular permeability.
49. Successful treatment is based on the following
fundamental principles :
1. Early diagnosis with radiographic evaluation and tissue
histopathology diagnosis
2. Bacterial culture and sensitivity testing
3. Adequate, appropriate and prompt antibiotic therapy
4. Adequate pain control
5. Proper surgical intervention
6. Reconstruction, where indicated.
50. Complete bed rest
Supportive therapy: It includes – nutritional support, in
the form of high protein and high caloric diet, and
adequate multivitamins
Dehydration: Hydration orally or through
administration of IV fluids
Blood transfusion : In case, RBCs and hemoglobin is
low
Control of pain: It is controlled with analgesics.
Sedation may be employed for keeping patient
comfortable and allow to sleep.
51. Antimicrobial agents : Begin with empiric dual drug
therapy— Penicillin and metronidazole or single drug
Clindamycin. Definitive antimicrobial therapy can be
started after final culture and sensitivity test results are
obtained.
Antibiotics of value in treatment of OML include:
penicillins, penicillinase-resistant penicillins, clindamycin,
cephalosporins and erythromycins. Some of the newer
antibiotics which provide effective coverage include:
metronidazole, clindamycin, ticarcillin, clavulanic acid,
cephalosporins, vancomycin in combination with other
antibiotics, and fluoroquinolones.
52. Recommended antibiotic regimens for OML of jaws are as
follows:
Regimen I (1st choice) : As empirical therapy, penicillin
(penicillin V) is given.
Aqueous penicillin: 2 million units IV every 4 hourly.
Oxacillin: 1g IV every 4 hourly.
When the patient has been asymptomatic for 48-72 hours,
then switch to—penicillin V orally 500mg every 4 hourly,
with dicloxacillin 250 mg orally every 4 hourly for 2-4 weeks.
Regimen II: It is based on culture and sensitivity results.
Penicillinase penicillinase-resistant penicillins, such as
oxacillin, cloxacillin, dicloxacillin, or flucloxacillin may be
given.
53. In case of allergy to penicillin, the following antibiotics are
prescribed, in order of preference: (i) Clindamycin 300-600
mg orally 6 hourly, (ii) Cephalosporin 250-500mg orally
every 6 hourly: (a) Cefazolin 500 mg 8 hourly, or (b)
Cephalexin 500 mg 6 hourly, (iii) Erythromycin 2g every 6
hourly IV, then 500 mg every 6 hourly orally.
Second choice: Clindamycin: It is effective against
penicillinase producing staphylococci, streptococci and
anaerobic bacteria including Bacteroides. It is used because
of its ability to diffuse widely in bone. It is nkt
recommended as first choice; as it is bacteriostatic, and
causes diarrhea due to pseudomembranous colitis.
54. Third choice : Cefazolin or Cephalexin : It is effective
against most cocci including penicillinase –producing
staphylococci, Gram-negative aerobic bacilli viz. E. coli ,
Klebsiella, and Proteus.
Cephalosporins are not recommended as first choice
because these are moderately effective against anaerobes
and because of broad spectrum coverage, which increases
antibiotic complications.
Fourth choice: Erythromycin : These drugs cannot be used
as first choice, as these are : (i) Bacteriostatic, and (ii)
rapidly develop resistant strains.
55. Over the last several decades, HBO therapy has
emerged as :
(i) a potent alternative to surgical reperfusion, and
(ii) as an adjunctive enhancement to host –immune
response.
Its use has increased in the treatment of refractory OML
and osteoradionecrosis (ORN) .
The hyperbaric oxygen therapy is indicated in cases of
osteomyelitis , which do not respond to routine
treatment due to presence of certain associated
conditions like irradiated jaw , osteosclerosis ,
osteoporosis , and geriatric patients.
56. It facilitates the healing of the bone and also helps in
combating the infection .
The HBO therapy involves the intermittent ,twice daily,
inhalation of 100% humidified oxygen under 2 atmospheric
pressure for 90 minutes .
HBO reduces the hypoxia within the affected tissues and
stimulates angiogenesis in the hypovascular tissues.
It enhances phagocytic activity of leukocytes to stimulate
fibroblast growth , increase in collagen formation and
promote growth of new capillaries.
57. Hyperbaric oxygen chamber : The patient is placed in a
chamber. Oxygen is given by mask or by hood .It is given for
5 days per week for 30, 60, or more dives at 2.4 ATA for 90
minutes , while breathing 100% oxygen twice daily.
Marx protocol (1983 ):
• 30 initial dives, if improved then 60 dives completed
• Otherwise , sequestrectomy +30 dives
• If wound dehiscence , resection + 60 dives and 20 dives after
10 weeks
• Patient with pathological fracture , orocutaneous fistula are
given 30 dives more prior going to resection.
58.
59. The surgical treatment modalities include:
1. Incision and drainage
2. Extraction of loose or offending teeth
3. Debridement
4. Decortication
5. Continuous or intermittent indwelling close catheter
irrigation
60. 6. Sequestrectomy
7. Saucerization
8. Resection of jaw
9. Trephination
10. Immediate or delayed reconstruction with bone
graft.
Surgical intervention is done under antibiotic cover,
started atleast, 1-2 days prior to the procedure.
61. It should be done as soon as possible. It relieves the
pressure and pain caused by the accumulation of pus.
Incision of abscesses should be carried out intraorally or
extraorally depending upon the location. Evacuation of
pus by drainage, lessens absorption of toxic products and
prevents further spread of infection in the bone, thus,
helping in its localization. The consistency, color and odor
of the pus may provide important clues to the diagnosis
and initial treatment. Patients with compromised
systemic conditions or toxemia, surgical interference may
be postponed for 2-3 days.
62. The various methods employed for causing drainage from
the bone include: (i) Opening up the pulp chamber, (ii) By
making fenestration through cortical plate over the apical
area with a drill, (iii) In an edentulous area, especially,
posterior maxilla or maxillary tuberosity region, by making
an incision over the alveolar crest, and by making a
window, pus is evacuated and (iv) OML at the angle of
mandible or ascending ramus, drainage can be achieved by
a small incision made over the point of the greatest
tenderness, or just below the mandible.
Extraction of loose or offending teeth: Sometimes,
drainage is achieved by extraction of offending teeth.
63. Debridement : followed by incision and drainage, thorough
debridement of affected area should be carried out. The area
may be irrigated with hydrogen peroxide and saline. Any
foreign body, necrotic tissue or small sequestrum should be
removed.
Decortication: Removal of dense chronically infected and
poorly vascularized, lateral and inferior cortical plates of
bone 1-2 cm beyond the area of involvement. Thus, an access
is provided to medullary cavity. Obwegeser (1960) advocated
this procedure, as it shortens healing time.
Decortication and mobilization of muscle flaps to achieve or
improve regional and systemic vascular supply to the involved
area have been used to bring the overlying vascular soft
tissue envelope to a closer proximity to infected spongiosa.
64. This will increase the blood supply and healing of the affected
area.
The steps in decortication are:
Creation of buccal flap by crestal incision extending along the
necks of the teeth.
Reflection of mucoperiosteal flap to the inferior border.
Removal of teeth in the involved area.
Removal of cortical plates —lateral and inferior border, with
chisel in one piece. Bone must be cut back to uninvolved
areas.
Bony bed should be thoroughly debrided and flaps should be
closed primarily and dead space is eliminated by applying
pressure bandage placed to keep vascularized soft tissue in
contact with bony bed.
65. Irrigation tubes should be placed through separate stab
incision and closed suction should be employed.
66. Continuous or intermittent indwelling closed catheter
irrigation : After intraoral sequestrectomy and
saucerization or decortication, two small pediatric
nasogastric feeding tubes, catheters or polyethylene drain
tubes, 3-4 mm in diameter and 6-10 inches long in length,
are placed against the bony bed through separate skin
incisions at some distance and secured with sutures. One
tube is connected to the low – pressure suction to allow
drainage of pus and serum and another is kept patent to
provide a route through which locally antibiotics may be
instilled in very high concentrations. Daily, first saline
irrigation followed by antibiotic instillation should be
repeated, until negative cultures are obtained. Systemic
antibiotics are also continued for atleast 2-3 months
following cessation of clinical evidence of disease.
67. Sequestrectomy: An integral part of definitive therapy. It helps
in establishment of local microvascular proliferation. It should
be undertaken through an intraoral incision; or extraoral (
submandibular) approach, depending upon the site of
sequestrum.
Saucerization: Excision of margins of necrotic bone overlying a
focus of OML. It is useful in chronic form, since it permits
removal of formed and forming sequestra with better
visualization. It is performed when removal of sequestrum
leaves a large cavity, and to eliminate the dead space to avoid
reinfection of extensive clot. It is performed with a large round
bur, so that when wound is closed, the soft tissues eliminate a
dead space. The buccal cortex is reduced to the level of
unattached mucosa, producing a saucer like defect.
68.
69.
70. Sequestrectomy and saucerization are to be carried out after
the acute phase has subsided; and the defense mechanism of
host and antimicrobial therapy have overcome the virulence
of organisms. In certain circumstances, after performing the
necessary surgical procedures, where the soft tissues cannot
be closed without leaving dead space, or because of rigid
fibrosis ; the wound may be packed with 2” ribbon gauze
soaked with Whitehead varnish.
Trephination Or fenestration is the creation of bony holes or
windows in the overlying cortical bone adjacent to the
infectious process for tissue ammoniation and
decompression of the medullary compartment. Drilling of
holes into the cortex and reaching medulla provides multiple
71.
72. surgical transcortical ports, that allow vascular
communication between the periosteum and the medullary
cavity.
Resection : It is rarely required. When full thickness of
segment of jaw is involved and a conservative approach
has failed to cure, resection of the part should be
considered. However, while exposing the affected area, the
only soft tissue related to the necrotic bone should be
elevated, to avoid devitalization of the adjoining cortex.
73.
74. Immediate and/or delayed reconstruction : It has been
used successfully in cases of: (i) pathological fracture, (ii)
persistence of infection after decortication, and (iii) when
both cortical plates are markedly diseased . Iliac crest is
a desirable graft. A block of corticocancellous iliac crest
can be used or cancellous marrow is used. Stabilization
may be achieved with vitallium or titanium mesh that
also serves as a tray to contain the graft. Immediate
reconstruction offers the obvious advantage of shortening
the period of illness and speeding recovery and
rehabilitation. In cases, where immediate bone grafting
is contraindicated, a reconstruction plate is fixed as a
spacer.
75. Secondary bone grafting: This should be considered when
the wound has healed completely and is free of infection.
Postoperative care: It includes the following :(i) Continued
use of antibiotics, analgesics, and hot saline mouth rinses,
(ii) Adequate hydration, complete rest, removal of
sequestra, in case they are in the alveolar part of bone. The
wound is closed preferably primarily, with a drain.
Prognosis : If proper aggressive and comprehensive
therapy is instituted on time, then, the recovery of acute
and chronic OML is always good. But, in cases of chronic
refractory or diffuse sclerosing OML, associated with
regional or systemic disease, such as microvascular or
immunosuppressive disorders, the treatment may be worse
than the disease itself.
76. In these cases, attempt should be done to provide long – term
conservative therapy than major surgical debridement. Long
term use of salicylates, nonsteroidals or steroids with
laboratory monitoring is advised in some of these cases.
The treatment regimen will have to be modified depending
on the status of general health of the patient.
77.
78. Infantile OML( OML Maxillaries Neonatorum,
Maxillitis of infancy) :It is a rare type of OML seen in
infants involving maxilla. Wilensky (1932) described
OML in infants in a comprehensive manner.
ETIOLOGY: (1)Trauma: The access may be through a
break in the mucosa. Perinatal trauma caused to oral
mucosa during delivery. (2) Infection of maxillary sinus
(3) Paunz (1926) and Ramon et al. (1977) believe that
the disease is caused by infections from the nose. (4)
Hematogenous invasion by streptococci and
pneumococci
79. Clinical features-
Almost seen a few weeks after birth. There is sudden
onset and acute course. The disease may also have slow
onset and a chronic course. In acute stage , severe pain
and high fever ; and with chronic course there is moderate
pain and slight fever.
General constitutinal manifestations : Pyrexia, anorexia,
dehydration, convulsions, or vomitting may occur.
Treatment-
The treatment should be prompt and aggressive.
Antibiotics preferably be given by IV route. Penicillins or
80. penicillinase – resistant penicillins like flucloxacillin, or
broad – spectrum antibiotics may be given for 2-4 weeks.
Incision and drainage of fluctuant areas : It is indicated
in the presence of of periosteal or palatal abscesses.
Irrigations: In case of sinus tracts, irrigations are done
frequently.
Supportive therapy: (i) Analgesics and antipyretics, (ii)
fluids (iii) Proper diet.
Sequestrectomy or removal of necrotic tooth germs:
Removal of sequestra is undertaken when they are
completely separated, and on the basis of clinical and
radiological findings. Surgical interference should be
conservative; as loss of bone and teeth leads to severe
deformities later in life.
81. Children who have undergone sequestrectomies, should be
followed up by an orthodontist to aid in the development of
the arch and maintenance of occlusion.
Garre’s Sclerosing Osteomyelitis: Also known as chronic
nonsuppurative sclerosing OML, chronic OML with
proliferative periostitis, and periostitis ossificans . It was
first described Carl Garre (1893) , as irritation induced focal
thickening of periosteum and cortical bone of tibia. It is a
nonsuppurative inflammatory process; where there is
peripheral subperiosteal bone deposition caused by mild
irritation and infection.
Pathogenesis : The etiological agents can be a carious tooth,
or the overlying soft tissue infection. The infectious process
localizes in periosteum or beneath the periosteal covering of
82. cortex and spreads slightly into the inferior of bone .
Clinical features: It is characterized by: (i) localized hard,
nontender bony swelling of lateral and inferior aspects of
mandible, (ii) lymphadenopathy, hyperpyrexia and
leukocytosis usually not found
Treatment: It is directed towards removing sources of
inflammation : (a) Removal of infected tooth and curettage
of socket, (b) Surgical recontouring : This is done to
recontour the cortical expansion of the jaw. This is
attempted only if there is obvious expansion, (c)
Endodontic therapy , (d) Antibiotics : If signs of infection
are present and (e) follow – up.
83. Chronic Sclerosing OML (focal and diffuse) :
The various other names are sclerosing osteitis, ossifying
OML, sclerosing cementoma, gigantiform cementoma,
and sclerotic cemental masses.
Focal form: (I) Below the age of twenty, (II) More common
in mandible, (III) Associated with infected pulp of lower
molars /premolars, (iv) Appears as circumscribed
radiopaque mass of sclerotic bone associated with tooth
roots, (v) Margins may be distinct or may blend into
surrounding bone.
Treatment: Endodontic therapy or Extraction.
84. Multiple form: These occur in both maxilla and mandible
(resembles chronic suppurative OML). Pain is a prominent
feature. Suppuration is usually absent.
Treatment: Debridement, antibiotic therapy, alveolectomy,
and HBO2, etc.
Actinomycotic OML of jaws : It is a chronic infection
manifesting both granulomatous and suppurative features ;
and usually involved soft tissues and occasionally bone.
Pathogenesis: Organisms gain entry into soft tissues directly
or by extension from bone through (i) Periapical, or (ii)
Periodontal lesions and (iii) Fractures, or (iv) Extraction
sites.
85. Clinical features:
Soft or firm tissue masses on the skin ; which have
purplish, dark red, oily areas with occasional small zones
of fluctuation.
Spontaneous drainage of serous fluid containing granular
material. These granules are yellowish substances called
sulfur granules , and represent colonies of bacteria.
Regional lymph nodes are occasionally enlarged.
Trismus: Not common ; unless secondary infection
Pyrexia
86. Management: In the past, many therapeutic agents and
techniques were used including: (a) Iodides (b)
Radiation (c) Incision and drainage (d) Excision of soft
tissues and bone. Currently, iodides and radiotherapy
are considered to be ineffective.
87.
88. Mucormycosis is a rare opportunistic fungal infection with
high morbidity and mortality
3rd most common Angio- invasive fungal infection (after
candidiasis and aspergillosis)
Majority of the patient has underlying risk factor
Immuno-compromised patient
Mucormycosis is caused by the fungal organisms of the
family of Mucorale (Mucor, Rhizopus and Absida).
89. Represents 8.3%-13% of all fungal infections
In developed countries, the disease remain uncommon is
mostly seen in patients with diabetes mellitus and
hematological malignancies undergoing chemotherapy.
In developing countries, especially in India,
mucormycosis cases although sporadic, occur mainly in
patients with uncontrolled diabetes or trauma.
90. Inoculation occurs when spores reach the nasal cavity
during inhalation.
Tiny spores then become airborne and land on the oral and
nasal mucosa of humans.
Angio-invasion
Vessel thrombosis
Tissue necrosis
Hematogenous spread to other organs can occur.
97. Palatal involvement is usually the result of direct
extension of disease from the maxillary sinus and in the
distribution of the nasopalatine and greater palatine
arteries.
98. Oral and skin ulcerations are present with pain and
swelling
99. Plain orbit or sinus radiography
CT
MRI
Early diagnosis: small, focal lesions can often be surgically
excised before they progress to involve critical structures.
Antifungal therapy:
Amphotericin B : Initially a test dose- 1mg in 20 ml of
5%dextrose in water is infused intravenously over 20-30
minutes
100. With careful monitoring for side effects (i.e, chills, fever, and
anaphylaxis) every 30 minutes for 2to4 hours.
If this dose is well tolerated – An initial dose of 0.1 to 0.3
mg/kg/day is then prepared as a 0.1mg /ml infusion and
delivered slowly over 6-24 hours .
Gradually increased by 5 to 10 mg per day, upto a total
dose of 0.7to1 mg /kg/day.
But a single dose should exceed 1.5 mg/kg /day ; as
overdoses can result in cardiorespiratory arrest.
Liposomal Amphotericin B:
First line recommended agent
Can be given as 5mg/kg/day to 10 mg/kg/day
101. Surgery + Liposomal Amphotericin B increases survival
rates and cure rates.
Posaconazole :
Dose : 800 mg/day divided in 4
Isavuconazole:
Available in oral and intravenous formulations.
Administered with a loading dose of 200 mg 3 times a
day for 2 days and 200 mg daily thereafter.
Fluconazole , voriconazole, and itraconazole do not have
reliable activity against mucormycosis.
102. Surgical debridement:Extensive and early surgical
debridement is necessary.
Therefore, debridement of necrotic tissues may be
important for complete eradication of mucormycosis.
Surgical management include:
Debridement of the necrotic part
Drainage of the sinuses
Total and subtotal maxillectomy
Palatectomy
Sphenoid and ethmoid sinusectomy
103. Exerts a fungistatic effect
Aids in neovascularization
Dose: exposure to 100% oxygen for 1 and ½ hours
at pressures from 2-2.5 atm with 1or 2 exposures
daily for a total of 40 treatments.
104. Mucormycosis is a fatal infection.
Early recognition will prevent further dissemination of
disease.
Medical as well as surgical management plays equal role
in its treatment.
Osteomyelitis, although uncommon, continues to be seen
and treated by dentists and oral and maxillofacial
surgeons.
Complete therapy involves both medical and surgical
approaches in an effort to achieve total care.