NEET MDS Synopsis
Window of Infectivity
Conservative DentistryWindow of Infectivity
The concept of the "window of infectivity" was introduced by Caufield in 1993
to describe critical periods in early childhood when the oral cavity is
particularly susceptible to colonization by Streptococcus mutans, a key
bacterium associated with dental caries. Understanding these windows is
essential for implementing preventive measures against caries in children.
Window of Infectivity: This term refers to specific
time periods during which the acquisition of Streptococcus mutans occurs,
leading to an increased risk of dental caries. These windows are
characterized by the eruption of teeth, which creates opportunities for
bacterial colonization.
First Window of Infectivity
A. Timing
Age Range: The first window of infectivity is observed
between 19 to 23 months of age, coinciding with the
eruption of primary teeth.
B. Mechanism
Eruption of Primary Teeth: As primary teeth erupt, they
provide a "virgin habitat" for S. mutans to colonize the oral
cavity. This is significant because:
Reduced Competition: The newly erupted teeth have
not yet been colonized by other indigenous bacteria, allowing S.
mutans to establish itself without competition.
Increased Risk of Caries: The presence of S.
mutans in the oral cavity during this period can lead to an
increased risk of developing dental caries, especially if dietary habits
include frequent sugar consumption.
Second Window of Infectivity
A. Timing
Age Range: The second window of infectivity occurs
between 6 to 12 years of age, coinciding with the eruption
of permanent teeth.
B. Mechanism
Eruption of Permanent Dentition: As permanent teeth
emerge, they again provide opportunities for S. mutans to colonize
the oral cavity. This window is characterized by:
Increased Susceptibility: The transition from
primary to permanent dentition can lead to changes in oral flora and an
increased risk of caries if preventive measures are not taken.
Behavioral Factors: During this age range, children
may have increased exposure to sugary foods and beverages, further
enhancing the risk of S. mutans colonization and subsequent
caries development.
4. Clinical Implications
A. Preventive Strategies
Oral Hygiene Education: Parents and caregivers should
be educated about the importance of maintaining good oral hygiene practices
from an early age, especially during the windows of infectivity.
Dietary Counseling: Limiting sugary snacks and
beverages during these critical periods can help reduce the risk of S.
mutans colonization and caries development.
Regular Dental Visits: Early and regular dental
check-ups can help monitor the oral health of children and provide timely
interventions if necessary.
B. Targeted Interventions
Fluoride Treatments: Application of fluoride varnishes
or gels during these windows can help strengthen enamel and reduce the risk
of caries.
Sealants: Dental sealants can be applied to newly
erupted permanent molars to provide a protective barrier against caries.
Space Maintainers
PedodonticsSpace Maintainers: A fixed or removable appliance designed
to maintain the space left by a prematurely lost tooth, ensuring proper
alignment and positioning of the permanent dentition.
Importance of Primary Teeth
Primary teeth serve as the best space maintainers for the permanent
dentition. Their presence is crucial for guiding the eruption of permanent
teeth and maintaining arch integrity.
Consequences of Space Loss
When a tooth is lost prematurely, the space can change significantly within a
six-month period, leading to several complications:
Loss of Arch Length: This can result in crowding of the
permanent dentition.
Impaction of Permanent Teeth: Teeth may become impacted
if there is insufficient space for their eruption.
Esthetic Problems: Loss of space can lead to visible
gaps or misalignment, affecting a child's smile.
Malocclusion: Improper alignment of teeth can lead to
functional issues and bite problems.
Indications for Space Maintainers
Space maintainers are indicated in the following situations:
If the space shows signs of closing.
If using a space maintainer will simplify future orthodontic treatment.
If treatment for malocclusion is not indicated at a later date.
When the space needs to be maintained for two years or more.
To prevent supra-eruption of opposing teeth.
To improve the masticatory system and restore dental health.
Contraindications for Space Maintainers
Space maintainers should not be used in the following situations:
If radiographs show that the succedaneous tooth will erupt soon.
If one-third of the root of the succedaneous tooth is already calcified.
When the space left is greater than what is needed for the permanent
tooth, as indicated radiographically.
If the space shows no signs of closing.
When the succedaneous tooth is absent.
Classification of Space Maintainers
Space maintainers can be classified into two main categories:
1. Fixed Space Maintainers
These are permanently attached to the teeth and cannot be removed
by the patient. Examples include band and loop space maintainers.
Common types include:
Band and Loop Space Maintainer:
A metal band is placed around an adjacent tooth, and a wire loop
extends into the space of the missing tooth. This is commonly used
for maintaining space after the loss of a primary molar.
Crown and Loop Space Maintainer:
Similar to the band and loop, but a crown is placed on the
adjacent tooth instead of a band. This is used when the adjacent
tooth requires a crown.
Distal Shoe Space Maintainer:
This is used when a primary second molar is lost before the
eruption of the permanent first molar. It consists of a metal band
on the first molar with a metal extension (shoe) that guides the
eruption of the permanent molar.
Transpalatal Arch:
A fixed appliance that connects the maxillary molars across the
palate. It is used to maintain space and prevent molar movement.
Nance Appliance:
Similar to the transpalatal arch, but it has a small acrylic
button that rests against the anterior palate. It is used to
maintain space in the upper arch.
2. Removable Space Maintainers
These can be taken out by the patient and are typically used when more
than one tooth is lost. They can also serve to replace occlusal function and
improve esthetics.
Common types include:
Removable Partial Denture:
A prosthetic device that replaces one or more missing teeth and
can be removed by the patient. It can help maintain space and
restore function and esthetics.
Acrylic Space Maintainer:
A simple acrylic appliance that can be used to maintain space.
It is often used in cases where esthetics are a concern.
Functional Space Maintainers:
These are designed to provide occlusal function while
maintaining space. They may include components that allow for
chewing and speaking.
Types of Removable Space Maintainers
Non-functional: Typically used when more than one tooth
is lost.
Functional: Designed to provide occlusal function.
Advantages of Removable Space Maintainers
Easy to clean and maintain proper oral hygiene.
Maintains vertical dimension.
Can be worn part-time, allowing circulation of blood to soft tissues.
Creates room for permanent teeth.
Helps prevent the development of tongue thrust habits into the
extraction space.
Disadvantages of Removable Space Maintainers
May be lost or broken by the patient.
Uncooperative patients may not wear the appliance.
Lateral jaw growth may be restricted if clasps are incorporated.
May cause irritation of the underlying soft tissues.
Post viral cirrhosis
General Pathology
Post viral (post hepatitic) cirrhosis (15-20%)
Cause:- Viral hepatitis (mostly HBV or HCV)
Acute hepatitis → chronic hepatitis → cirrhosis.
Pathology
Liver is shrunken. Fatty change is absent (except with HCV). Cirrhosis is mixed.
M/E :-
Hepatocytes-show degeneration, necrosis as other types of cirrhosis.
Fibrous septa -They are thick and immature (more cellular and vascular).
- Irregular margins (piece meal necrosis).
- Heavy lymphocytic infiltrate.
Prognosis:- - More rapid course than alcoholic cirrhosis.Hepatocellular carcinoma is more liable to occur
FORMATION OF THE PERMANENT DENTITION
Dental Anatomy
FORMATION OF THE PERMANENT DENTITION
Twenty deciduous tooth buds are formed initially.
Proliferative activity of the dental lamina during the bell stage that leads to formation of permanent tooth buds (cap stage) lingual of each deciduous tooth germ.
Molars have no predecessors; they are formed by posterior proliferation of the dental lamina.
HARD TISSUE FORMATION
Hard tissue formation starts at the late stages of the bell stage.
Differentiatioin of cells into odontoblasts and ameloblasts.
The cells of the inner dental epithelium will become ameloblasts.
The cells of the dental papilla opposite to the inner dental epithelium will become odontoblasts.
Dentin is formed before enamel.
Dentin initiates the formation of enamel.
ROOT FORMATION
The root of the tooth is composed by dentin and cementum.
Dentinogenesis is initiated by the odontoblasts.
Odontoblasts are formed as epithelial cells continue to proliferate from the cervical loop as a double layer of cells known as Hertwig's root sheath.
TOOTH SHAPE
The shape of the crowns results from the interaction of inner dental epithelium and the dental papilla.
The cells of the inner dental epithelium have a programmed proliferation.
This internal program determines the tooth form.
The fate of the dental lamina
Rests of Serres
The rest of Serres are rests of the dental lamina identified in the gingival soft tissues.
They are round to ovoid aggregates of epithelial cells that have clear cytoplasm (glucogen rich).
They result from early breakup of the dental lamina during bell stage.
Rests of Malassez
The rests of Malassez result from breakup of the Hertwig's root sheath during root formation.
They can be identified in the periodontal ligament and are responsible for the development of radicular cysts.
Huntington’s disease
General Pathology
Huntington’s disease
a. Causes dementia.
b. Genetic transmission: autosomal dominant.
c. Characterized by the degeneration of striatal neurons, affecting cortical and basal ganglia function.
d. Clinically, the disease affects both movement and cognition and is ultimately fatal.
Mixed Narcotic Agonists-Antagonists
Pharmacology
Mixed Narcotic Agonists/Antagonists
These drugs all produce analgesia, but have a lower potential for abuse and do not produce as much respiratory depression.
A. Pentazocine
Has a combination of opiate analgesic and antagonist activity.
Orally, it has about the same analgesic potency as codeine.
In contrast to morphine, cardiac workload tends to increase due to an increase in pulmonary arterial and cerebrovascular pressure. Blood pressure and heart rate both also tend to increase.
Adverse reactions to Pentazocine
• Nausea, vomiting, dizziness.
• Psychotomimetic effects, such as dysphoria, nightmares and visual hallucinations.
• Constipation is less marked than with morphine.
B. Nalbuphine
Has both analgesic and antagonist properties.
Resembles pentazocine pharmacologically.
Analgesic potency approximately the same as morphine.
Appears to be less hypotensive than morphine.
Respiratory depression similar to morphine, but appears to peak-out at higher doses and to reach a ceiling.
Like morphine, nalbuphine reduces myocardial oxygen demand. May be of value following acute myocardial infarction due to both its analgesic properties and reduced myocardial oxygen demand.
Most frequent side effect is sedation.
C. Butorphanol
Has both opiate agonist and antagonist properties.Resembles pentazocine , pharmacologically., 3.5 to 7 times more potent than morphine., Produces respiratory depression, but this effect peaks out with higher doses. The respiratory depression that does occur lasts longer than that seen following morphine administration.
Butorphanol, like pentazocine, increases pulmonary arterial pressure and possibly the workload on the heart.
Adverse reactions include sedation, nausea and sweating.
D. Buprenorphine
A derivative of eto`rphine. Has both agonist and antagonist activity. 20 to 30 times more potent than morphine.Duration of action only slightly longer than morphine, but respiratory depression and miosis persist well after analgesia has disappeared.
Respiratory depression reaches a ceiling at relatively low doses.
Approximately 96% of the circulating drug is bound to plasma proteins.
Side effects are similar to other opiates:
sedation, nausea, vomiting,
dizziness, sweating and headache.
Immunoglobulins.
General Pathology
Immunoglobulins. (Ig)
These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)
Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).
Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.
Characteristics of Immunoglobulin subclasses
I. Ig G:
(i) Predominant portion (80%) of Ig.
(ii) Molecular weight 150, 000
(iii) Sedimentation coefficient of 7S.
(iv) Crosses placental barrier and to extra cellular fluid.
(v) Mostly neutralising effect. May be complement fixing.
(vi) Half life of 23 days.
2.IgM :
(i) Pentamer of Ig.
(ii) Molecular weight 900, 000
(iii) 19S.
(iv) More effective complement fixation and cells lysis
(v) Earliest to be produced in infections.
(vi) Does not cross placental barrier.
(vii) Halflife of 5 days.
3. Ig A :
Secretory antibody. Found in intestinal, respiratory secretions tears, saliva and urine also.
Secreted usually as a dinner with secretory piece.
Mol. weight variable (160,000+)
7 S to 14 S.
Half life of 6 days.
4.Ig D :
Found in traces.
7 S.
Does not cross placenta.
5. Ig E
Normally not traceable
7-8 S (MoL weight 200,000)
Cytophilic antibody, responsible for some hypersensitivity states,
Osteomyelitis
Oral Pathology
Osteomyelitis
Osteomyelitis is an extensive inflammation of a bone. It involves the cancellous portion, bone marrow, cortex, and periosteum
Conditions that alter HOST IMMUNITY
Leukemia, Severe anemia, Malnutrition, AIDS, IV- drug abuse, Chronic alcoholism, Febrile illnesses, Malignancy, Autoimmune disease, Diabetes mellitus, Arthritis, Agranulocytosis
Conditions that alter vascularity of bone
Osteoporosis, Paget’s disease, Fibrous dysplasia, Bone malignancy, Radiation, Virulence of the organisms
Certain organisms precipitate thrombi formation by virtue of their destructive lysosomal enzymes.
Organisms proliferate in enriched host medium while protected from host immunity.
Etiology
- Odontogenic infections
- Trauma
- Infections of oro facial region
- Infections derived from hematogenous route
- Compound fractures of the jaws.
PATHOGENESIS
DEV . OF INFECTION --> BACTERIAL INVASION --> PUS FORMATION --> SPREAD OF INFECTION --> INCREASED INTRAMEDULLARY PRESSURE , BLOOD FLOW , OSTEOCLASTIC ACTIVITY --> INFLAMMATORY RESPONSES --> INCREASED PERIOSTEAL PRESSURE --> PROCESS BECOMES CHRONIC GRANULATION TISSUE FORMATION --> LYSIS OF BONE --> SEQUESTRUM FORMATION
Classification
Classification based on clinical picture, radiology, and etiology
Suppurative osteomyelitis
I. Acute suppurative osteomyelitis
II. Chronic suppurative osteomyelitis
– Primary chronic suppurative osteomyelitis
– Secondary chronic suppurative osteomyelitis
III. Infantile osteomyelitis
Nonsuppurative osteomyelitis
I. Chronic sclerosing osteomyelitis
– Focal sclerosing osteomyelitis
– Diffuse sclerosing osteomyelitis
II. Garre's sclerosing osteomyelitis
III. Actinomycotic osteomyelitis
IV. Radiation osteomyelitis and necrosis