Download 1. Concrete aims

MINISTRY of PUBLIC HEALTH of UKRAINE
VINNITSYA NATIONAL PIROGOV MEMORIAL
MEDICAL UNIVERSITY
It is "confirmed"
on a methodical meeting of
department of pediatric dentistry
head-chair
doc.Filimonov Yu.V._____
"____ " ___________ in20
Methodical recommendation for 4d year students
of dental faculty
Educational discipline
Module ¹
Rich in content module ¹
Topic
Course
Faculty
Autor
Pediatric surgery
1
1
Odontogenic
acute
osteomyelitis.
pathogenesis, manadement
4
Dental
Isakova N.M.
Vinnitsya 2012
Etiology,
Actuality of theme:
1. Concrete aims:
Osteomyelitis of jaws is an infectiously-allergic festering-necrotizing process
which develops in a bone under the action of both external (physical, chemical,
biological) and internal factors on a background previous sensitization of
organism.This definition is confirmed by the results of morphologic
investigations of foci purulent infiltration of the bone marrow , thrombosis and
purulent infiltration of the bone.
3.Educator aims:
To develop sense of professional responsibility for the timeliness of
diagnostics of osteomyelitis jaws in children and rightness of determination of
medical tactics of doctor-stomatology.
3 Base knowledges, abilities, habits which are necessary for study the topic.
Names of previous disciplines
Skills are got
1. General anatomy
The structure of the maxillofacial region, the
blood and nerve supply
2. Gistology
Histological structure of the oral mucous
cavity. The mechanism of development and
phase of inflammation
3. Therapy, pediatrics
Know the features of a child's body. Know
the basic diseases of importance in
conducting the diagnosis of major dental
diseases
4. Task for independent work during preparation to employment.
4.1. List of basic terms, parameters, descriptions which a student must
master at preparation to employment :
Term
Determination
1. Preventive means
Sanation of the oral cavity, radical treatment of all forms
of chronic periodontitis with toothextraction
2. Chronic periostitis
Excessive formation of periosteal stack layering, which
are to be removed surgically due to indications
3. Granulomatous
periodontitis
Formed on the area of the root apex granulomais
detected only radiographically.
4.2. Theoretical questions to employment:
1. Able to diagnose sharp serous and purulent osteomyelitis of
children and define medical tactics them.
2. Able to conduct differential diagnostics of sharp osteomyelitis
children with tumours and inflammatory diseases of jaws on the
intensifying.
3. Able to conduct differential diagnostics of chronic osteomyelitis
children with tumours and inflammatory diseases of jaws.
jaws for
jaws for
stage of
jaws for
4.3 Practical works (tasks)
To conduct the different types of the local anaesthetizing on phantoms.
5. A plan and organizational structure of lesson in discipline.
№
Stages of
Distribution Types of control
employment
of time
1.
practical tasks,
Preparatory stage 15 min
situatioonal tasks,
1.11.1OThe
organizational
verbal crossquestions.
1.2 Forming
of
examination at
motivation.
standart list of
1.3 Control of
questions.
initial
level
of
preparation.
2.
55 min
Basic
stage.
3.
3.1.
3.2.
3.3
20 min
Final stage
Control of eventual
level of preparation.
General estimation
of studing activity of
student.
Informing
of
students about the
theme
of
next
employment.
test tasks
Maintenance of theme
Facilities of
studies
Text-books,
methodical
recommendations.
The words, ossews in Latin means bony, andosteon in Greek means bone, and
myelos means marrow; and in Greek means inflammation.
By meaning OML is an inflammation of medullary portion of bone or bone
marrow or cancellous bone. However, the process is rarely confined to medulla. It
involves cortical bone and periosteum as well. Therefore, OML may be defined as
an inflammatory condition of bone, that begins as an infection of medullary cavity
and haversian systems of the cortex and extends to involve the periosteum of the
affected area.
The inflammation may be acute, subacute or chronic. It may be localized; or
may involve a larger portion of bone. It may besuppurative or nonsuppurative.
OML of the jaws was once a common and dreaded disease; because of its
prolonged therapy and the resultant disfigurement and dysfunction, due to loss of
major portion of the jaw bone.
In the contemporary world, the incidence of OML of the jaws has become less,
because of the worldwide avail-ability of newer antimicrobials, better awareness,
and better dental health care. However, we do come across a few cases of OML;
the causes can be attributed to the following: (i) development of certain strains of
organisms, which are resistant to certain antibiotics, and (ii) presence of more
cases of medically handicapped individuals in the present population. It is an
opportunistic disease, as presented by the host to the pathogenic microbe.
Predisposing Factors
The factors that predispose to OML are as follows:
(i) conditions affecting host resistance or defences,
(ii)
compromised vascular integrity and perfusion in the host bone, at the local,
regional or systemic level, and
(iii)
virulence of microorganisms. These factors play an important role in the
onset and severity of OML.
1. Conditions that alter host defences would include chronic debilitating systemic
diseases: such as diabetes mellitus, agranulocytosis, leukaemia, severe anaemia,
malnutrition, drug abuse, chronic alcoholism, sickle cell disease, and febrile
illnesses such as typhoid.
2.Conditions that alter vascularity of bone include therapeutic irradiation,
osteoporosis, Paget's disease, fibrous dysplasia, bone malignancy, metallic bone
necrosis (caused by mercury, bismuth, and arsenic). An intrinsic and extrinsic
vascular component has a more profound influence, both in onset of occurrence
as well as in resolution outcome.
3. Virulence of organisms certain organisms precipitate thrombi formation by
virtue of their destructive lysosomal enzymes (Hudson 1993) (Table 1).
Lysosomal and enzymatic degradation of host tissue, along with microvascular
thrombosis brought about by pathogen borne bioactive peptides and chemo
attracted leukocytic purulence, forms a protective barrier for the infectious foci,
allowing organisms to proliferate in anenriched host medium while protected
from the host immunity.
Brodie's abscess of long bone osteomyelitis is the classic example of this
isolational phenomenon, which can also occur in osteomyelitis of tooth bearing
bone, but to a lesser extent.
1. Non-compliant patients refractory to health care delivery,
2. Systemic, metabolically compromised individuals who can befurther
categorized into the following subsets; (a) age of patients,(b) malnutrition, (c)
immunosuppression, (d) congenital oracquired pathophysiology disrupting
microvascular perfusion of the calcified tissue structure and investing soft tissue
envelope.
3. Inaccessibilty to health care delivery
The process of OML is initiated by invasion of bacteria into the cancellous bone,
followed by acute inflammation:hyperaemia, increased capillary permeability; and
infiltration of granulocytes. The failure of microcirculation in the cancellous bone
is a critical factor in the establishment of the osteomyelitis. The infection spreads
along the path of least resistance. Since the involved area becomes ischaemic and
bone becomes necrotic, bacteria can then proliferate, because normal blood-borne
defences do not reach the tissue and osteomyelitis spreads, until it is stopped by
medical and surgical therapy.
Etiology
Osteomyelitis of the jaws is caused by the following:
1. Odontogenic infections Primarily odontogenic infections originating from pulpal
or periodontal tissues, pericoronitis, infected socket, infected cyst, tumour, etc.
2.Trauma It is the second leading cause: (a) especially, compound fracture, and (b)
surgery-iatrogenic
3. Infections of orofacial regions—derived from (a) periostitis following gingival
ulceration, (b) lymph nodes infected from furuncles, and (c) lacerations (d)
peritonsillar abscess.
4. Infections derived by hematogenous route Furuncle on face, wound on the skin,
upper respiratory tract infection, middle ear infection, mastoiditis, systemic
tuberculosis.
The infections from the last two groups account for a small percentage of cases.
Pathogenesis
Osteomyelitis is initiated from a contiguous focus of infection or by hematogenous
spread. 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.
The important factor in establishment of OML is the compromise in the blood
supply. It is worth considering the blood supply and venous drainage of mandible.
1. Blood supply (a) Primary supply: The mandible is supplied by inferior alveolar
artery, except coronoid process, which is supplied by temporalis muscle vessels,
(b) Secondary Supply: It is the 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.
2. Venous drainage of mandible There are two routes: (i) Via inferior alveolar vein;
it runs upwards, and joins pharyngeal plexus, and (ii) It runs downwards, and
joins external jugular veins.
Waldron (1943) gave an exhaustive morphologic description of vascular
morphology of mandible and associated structures 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 occurrence 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:
i. These tend 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.
ii. When afferent vessels anastomose with medullary channels, there is a
possibility of a decrease in venous flow with associated areas of greater
turbulence.
iii. There may be a reduction in host immune defense mechanism associated with
these vascular channels in calcified tissue.
A true osteomyelitic infectious process does not occur in the maxilla despite the
presence of tooth follicle or anatomic respiratory sinus cavities, including the nose.
Osteomyelitis in Maxilla
Osteomyelitis in maxilla is rare; due to: (i) extensive blood supply and significant
collateral blood flow in midface, (ii) porous nature of membranous bone, (iii) thin
cortical plates, and (iv) abundant medullary spaces. These preclude confinement of
infections within bone; and permit dissipation of edema and pus into soft tissues
and paranasal air sinuses.
The mechanism of formation and accumulation of pus is worth understanding.
The process leading to osteomyelitis is initiated by acute inflammation,
hyperaemia, increased capillary permeability and infiltration of granulocytes.
Tissue necrosis occurs as proteolytic enzymes are liberated and as destruction of
bacteria and vascular thombosis continues, there is a pus formation. The pus is a
combination of necrotic tissue and dead bacteria and WBC accumulate. When pus
accumulates, the intramedullary pressure increases resulting in vascular collapse,
venous stasis, and ischaemia. Subsequently, pus travels through haversia 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, ischaemia, and infarction, later
resulting in paraesthesia and sequestrum formation.
Extensive periosteal elevation is seen more frequently in children, since
periosteum is presumed to be less firmly bound to bone. If pus continues to
accumulate, the periosteum is penetrated; mucosal and cutaneous abscesses and
fistulae develop. As natural host defences and therapy begin to be effective, the
process may become chronic, inflammation regresses, granulation tissue is formed;
new blood vessels cause lysis of bone, thus separating fragments of necrotic bone
(sequestrum) from viable bone.
Small sections of bone may be completely lysed, whereas larger ones may be
isolated by a bed of granulation tissue encased in a sheath of new bone
(Involucrum). Sequestra, may be revascularized, remain quiescent, or continue to
be chronically infected and require surgical removal. Occasionally, involucrum
gets penetrated by channels, known as "cloacae", through which pus escapes from
sequestrum to an epithelial surface.
Radiographically, the bone surrounding sequestrum appears less densely
mineralized than sequestrum itself, since vascularity of vital bone creates relative
demineralization. Ischaemia causes increase in C02 level, which attracts Calcium
due to change in pH. The calcium deposition leads to increase in mineralization of
the sequestrum.
Microbiology
In the past, the etiology of OML was associated with skin surface bacteria, S
aureus; and to a lesser extents epidermidis, or hemolytic streptococci. However,
the picture of S.aureus as primary offending pathogen does not hold true with
regard to OML of toothbearing bone. Sinus tractculture results, especially in the
jaws, are often misleading, as they are usually contaminated with Staphylococcus
organisms.
Most of the cases are caused by aerobic streptococci (a hemolytic streptococci,
Strep
viridans),
anaerobic streptococci;
and
other anaerobes, such
as
peptostreptococci, fusobacteria, and Bacteroides (Peterson 1999). Sometimes,
anaerobic or microaerophilic cocci, Gram-negativeorganisms such as Klebsiella,
Pseudomonas and Proteus are also found. 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, as well as
other opportunistic bacteria. Marx et al (1992) identified Actinomycoses, Eikenella
and Arachnia as pathogens in some of the more refractory forms of OML of jaws.
Other unusual organisms such as Coccidioides, tuberculous bacilli, Treponema
and Klebsiella have also been implicated as causative agents. The change in
bacterial pattern is not because of ecology. It is attributable to the employment of
more sophisticated culture methods.
Classification and Staging
Due to the long-standing existence of OML as a clinical entity, a variety of
classifications of this disease process have evolved. A variety of classifications of
various forms of the disease are given, which are as follows:
1. Historically accepted classification It is based on clinical course: (a) acute, and
(b) chronic. The arbitrary time limit,to identify acute from chronic forms, is of one
month
Hudson's classification of OML of the jaws
Acute forms of OML (Suppurative or non-suppurative) include:
a. Contiguous focus: (i) Trauma, (ii) Surgery, and (iii) Odontogenic infections.
b. Progressive: (i) Burns, (ii) Sinusitis, and (iii) Vascular insufficiency.
c. Hematogenous (Metastatic): Developing skeleton (children) Chronic forms of
OML
a. Recurrent multifocal: (i) Developing skeleton (children), (ii) Escalated
osteogenic activity ( age < 25 years)
b. Garre's: (i) Unique proliferative subperiosteal reactior (ii) Developing
skeleton (children to young adults)
c. Suppurative or non-suppurative: (i) Inadequately treated forms, (ii)
Systemically compromised forms, and (iii) Refractory forms (CROM:
Chronic refractory OML).
d. Diffuse sclerosing: (i) Fastidious organisms, and (ii) Compromised
host/pathogen interface
2. Classification based on pathogenesis of altered vascular perfusion as a major
contributing factor to the presence and persistence of OML as a clinical disease.
(Vibhagool et al 1993): There are three types:
• Hematogenous OML
• OML secondary to a contiguous focus of infection
• OML associated with or without peripheral vascular disease
3. Classification based on presence or absence of suppuration
4.
Cierny
et
classification
location
status
al
and
of
of
the
(1985)
staging
and
Vibhagool
(1993)
system;
based
infectious
process,
and
host
systemic
(iii)
or
on
(i)
(ii)
local
developed
a
anatomic
physiological
factors
affecting
immune system, metabolism, and local vascularity.
Acute Pyogenic OML (Acute suppurative OML)
Acute pyogenic OML may have the appearance of a typical odontogenic infection.
It can be localised and It involved medullary bone without cortical involvement;
usually hematogenous Less than 2 cm of bony defect without cancellous bone.
Less than 2 cm bony defect seen on radiograph, defect does not appear to involve
both cortices. The defect is less than 2 cm, pathological fracture, infection, and
nonunion
II. Physiological types
A host: Normal host
В
host:
Systemic
compromise
(Bs);
local
compromise
(Bl)
C host: Treatment is worse than the disease.
HI. Systemic or local factors that affect immune surveillance, metabolism, and
local vascularity
(i) Malnutrition, (ii) Renal or hepatic failure, (iii) Diabetes mellitus, (iv) Chronic
hypoxia, (v) Immune deficiency or suppression, (vi) Malignancy, (vii) Extremes of
age, (viii) Autoimmune disease, and (ix) Tobacco and alcohol abuse: (i) Chronic
lymphedema, (ii) Venous stasis, (iii) Major vessel disease,(iv) Arteritis, (v)
Extensive scarring, (vi) Radiation fibrosis, (vii) Small vessel disease, and (viii)
Loss of local sensation
widespread, with extensive sequestration and possible pathological fracture.
Microbiology It is caused by pyogenic organisms. OML in the toothbearing area is
polymicrobial in nature. The most commonly found organisms found in
odontogenic OML is Staph aureus; and also Strep pyogenes. Vincent's
Spirochaetes may also be present. Gram-negative bacilli may also be present (E.
coli)
Etiology
1. Odontogenic infections These are the common local causes of OML. These
infections may result from (i) periapical disease secondary to pulp pathosis, (ii)
periodontal disease, (iii) pericoronitis of long duration, (iv) infected odontogenic
cyst, and (v) infection of an extraction wound or fracture site.
2. Local traumatic injuries (a) Injuries of gingiva, are usually insignificant;
however, may become serious in patients with low resistance (Ivy and Cook
1942), and (b) Instruments used for extraction of teeth.
3. Peritonsillar abscess It has been reported as a cause of OML of ascending
ramus.
4. Furunculosis ofskinlt is a rare cause of OML. Hoenigef al (1931) have reported
such a case.
5. Hematogenous infection It may cause multiple sites of OML. The organisms
enter the blood stream through a minor wound in the skin, or infection of upper
respiratory tract, or infection of middle ear. The predisposing factors include: (i)
undernourished children, (ii)lowered general resistance of body, (iii) generalised
body diseases: such as; diabetes, leukaemia, and agranulocytosis, and (iv) acute
illnesses, such as influenza, measles, scarlet fever, pertussis and pneumonia,
etc.Blair et al (1931) reported one case following tonsillitis, one following
measles, and one following diphtheria. Galli (1926) reported a case of OML of
maxilla associated with renal complication. Recently, with the use of newer
antibiotics and early institution of antibiotics hematogenous spread is not
commonly seen.
6. Infected compounded odontome(Romer 1955).
7. Compound fractures of jaws are complicated by OML.
Clinical features Occurrence 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).
A. Early cases are characterised by:
1. Generalised constitutional symptoms: High inter mittent fever, malaise,
nausea, vomiting, anorexia.
2. Deep seated boring, continuous intense pain in the affected area.
3. Intermittent paraesthesia or anaesthesia of the lower lip, which helps the
clinician to differentiate this condition from alveolar abscess.
4. Facial cellulitis, or indurated swelling of moderate size, which is more
confined to the periosteal envelop and its contents: (i) thrombosis of inferior
alveolar vasa nervorum, (ii) rise in pressure from edemain inferior alveolar
canal, (iii) teeth are tender to percussion and loose
5. Trismus: In children: (i) fulminating, (ii) severe and serious, (iii) involvement
of maxilla or mandible, (iv) complicated by the presence of unerupted
developing teeth buds, which become necrotic and act as foreign bodies and
prolong the disease process. Long-term involvement of TMJ can cause
ankylosis of TMJ and subsequently affect the growth and development of
facial structures.
Laboratory Studies: show mild leucocytosis (PMNL) and albuminuria.
B. Established cases are characterized by:
1. Deep pain, malaise, fever, dehydration, anorexia.
2. Teeth in involved area begin to loosen and become sensitive to percussion.
3. Purulent discharge through sinuses: (a) intra-orally; (i) around gingival sulcus:
or (ii) through buccal vestibule, and (b) extra-orally on the face, through
cutaneous fistulae.
4. Foetid odour is often present.
5. Trismus may be present.
6. Dehydration, acidosis and toxaemia.
7. Regional lymphadenopathy is usually pesent.
Laboratory studies show (i) moderate leucocytosis
(PMNL), and (ii) slightly elevated ESR, (iii) anaemia, and (iv) albuminuria.
Blood cultures, wound culture and sensitivity, and complete blood count along
with peaks and troughs on any antimicrobial prescribed should be assessed on a
regular basis. Radiological changes are absent initially.
Literature.
Basic:
1.Lectures which are read on the department of pediatric dentistry.
2. Pinkham J.R. Pediatric dentistry. – 2nded.- W.B. Sounders Company. – 1994.647 p.
3. Pediatric dentistry /Ed. R.R.Welbury.- Oxford, 1997 – 584p.
Additional:
1. Хирургическая стоматология.: Учебник /Т.Г.Робустовой. - М.: Medicine,
1990, 327.
2. Стоматология детского возраста: Учебник / А.А.Колесова. - М.: Medicine,
1991.
3. Танфильев Д.Е. Удаление зубов. - Л.: Medicine. 1976. - 160 с.
4. Соловьев М. М., Игнатов Ю.Д., Конобевцев О. Ф. Обезболивание at
лечении зубов in детей. - М.: Medicine, 1985. - 184 с.
5. Рузин Г.П., Бурых М. М. Основы технологии операций в хирургической
стоматологии и челюстно-лицевой хирургии. - Харьков, 2000. - 291 с.