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.
Warfarin
Pharmacology
Warfarin (Coumadin):
The most common oral anticoagulant.
It is only active in vivo.
Warfarin is almost completely bound to plasma proteins. -96% to 98% bound.
Warfarin is metabolized by the liver and excreted in the urine.
Coumarin anticoagulants pass the placental barrier and are secreted into the maternal milk.
Newborn infants are more sensitive to oral anticoagulants than are adults because of lower vitamin K levels and lower rates of metabolism.
Bleeding is the most common side effect and occurs most often from the mucous membranes of the gastrointestinal tract and the genitourinary tract.
Oral anticoagulants are contraindicated in:
• Conditions where active bleeding must be avoided, Vitamin K deficiency and severe
hepatic or renal disease, and where intensive salicylate therapy is required.
Riboflavin: Vitamin B2
Biochemistry
Riboflavin: Vitamin B2
Riboflavin, or vitamin B2, helps to release energy from foods, promotes good vision, and healthy skin. It also helps to convert the amino acid tryptophan (which makes up protein) into niacin.
RDA Males: 1.3 mg/day; Females: 1.1 mg/day
Deficiency : Symptoms of deficiency include cracks at the corners of the mouth, dermatitis on nose and lips, light sensitivity, cataracts, and a sore, red tongue.
Greenstick Fractures of the Mandible
Oral and Maxillofacial SurgeryManagement of Greenstick/Crack Fractures of the Mandible
Greenstick fractures (or crack fractures) are incomplete
fractures that typically occur in children due to the flexibility of their
bones. Fracture in mandible, can often be managed
conservatively, especially when there is no malocclusion (misalignment of the
teeth).
Conservative Management
No Fixation Required:
For greenstick fractures without malocclusion, surgical fixation is
generally not necessary.
Closed Reduction: The fracture can be managed
through closed reduction, which involves realigning the fractured bone
without surgical exposure.
Dietary Recommendations:
Patients are advised to consume soft foods and
maintain adequate hydration with lots of fluids to
facilitate healing and minimize discomfort during eating.
Surgical Management Options
In cases where surgical intervention is required, or for more complex
fractures, the following methods can be employed:
Kirschner Wire (K-wire) Fixation:
Indications: K-wires can be used for both dentulous
(having teeth) and edentulous (without teeth) mandibles.
Technique: K-wires are inserted through the bone
fragments to stabilize the fracture. This method provides internal
fixation and helps maintain alignment during the healing process.
Circumferential Wiring:
Indications: This technique is also applicable for
both dentulous and edentulous mandibles.
Technique: Circumferential wiring involves wrapping
wire around the mandible to stabilize the fracture. This method can
provide additional support and is often used in conjunction with other
fixation techniques.
External Pin Fixation:
Indications: Primarily used for edentulous
mandibles.
Technique: External pin fixation involves placing
pins into the bone that are connected to an external frame. This method
allows for stabilization of the mandible while avoiding intraoral
fixation, which can be beneficial in certain clinical scenarios.
Endodontic Microbiology
EndodonticsBacterial portals to pulp: caries (most common source), exposed dentinal tubules (tubule permeability ↓ by dentinal fluid, live odontoblastic processes, tertiary and peritubular dentin)
1. Vital pulp is very resistant to microbial invasion but necrotic pulps are rapidly colonized
2. Rarely does periodontal disease → pulp necrosis
3. Anachoresis: microbes carried in blood to area of inflammation where they establish infection
Caries → pulp disease: infecting bacteria are immobile, carried to pulp by binary fission, dentinal fluid movement
1. Smooth surface and pit and fissure caries: S. mutans (important in early caries) and S. sobrinus
2. Root caries: Actinomyces spp.
3. Mostly anaerobes in deep caries.
4. Once pulp exposed by caries, many opportunists enter (e.g., yeast, viruses) → polymicrobial infection
Pulp reaction to bacteria: non-specific inflammation and specific immunologic reactions
1. Initially inflammation is a chronic cellular response (lymphocytes, plasma cells, macrophages) → formation of peritubular dentin (↓ permeability of tubules) and often tertiary dentin (irregular, less tubular, barrier)
2. Carious pulp exposure → acute inflammation (PMN infiltration → abscess formation). Pulp may remain inflamed for a long time or become necrotic (depends on virulence, host response, circulation, drainage, etc.)
Endodontic infections: most commonly Prevotella nigrescens; also many Prevotella & Porphyromonas sp.
1. Actinomyces and Propionibacterium species can persist in periradicular tissues in presence of chronic inflammation; they respond to RCT but need surgery or abx to resolve infection
2. Streptococcus faecalis is commonly found in root canals requiring retreatment due to persistent inflammation
Root canal ecosystem: lack of circulation in pulp → compromised host defense
1. Favors growth of anaerobes that metabolize peptides and amino acids rather than carbohydrates
2. Bacteriocins: antibiotic-like proteins made by one species of bacteria that inhibit growth of another species
Virulence factors: fimbriae, capsules, enzymes (neutralize Ig and complement), polyamines (↑ # in infected canals)
1. LPS: G(-), → periradicular pathosis; when released from cell wall = endotoxin (can diffuse across dentin)
2. Extracellular vesicles: may → hemagglutination, hemolysis, bacterial adhesion, proteolysis
3. Short-chain fatty acids: affect PMN chemotaxis, degranulation, etc.; butyric acid → IL-1 production (→ bone resorption and periradicular pathosis)
Pathosis and treatment:
1. Acute apical periodontitis (AAP): pulpal inflammation extends to periradicular tissues; initial response
2. Chronic apical periodontitis (CAP): can be asymptomatic (controversial whether bacteria can colonize)
3. Acute apical abscess (AAA), phoenix abscesses (acute exacerbation of CAP), and suppurative apical periodontitis: all characterized by many PMNs, necrotic tissue, and bacteria
Treatment of endodontic infections: must remove reservoir of infection by thorough debridement
1. Debridement: removal of substrates that support microorganisms; use sodium hypochlorite (NaOCl) to irrigate canals (dissolves some organic debris in areas that can’t be reached by instruments); creates smear layer
2. Intracanal medication: recommend calcium hydroxide (greatest antimicrobial effect between appointments) inserted into pulp chamber then driven into canals (lentulo spiral, plugger, or counterclockwise rotation of files) and covered with sterile cotton pellet and temporary restoration (at least 3mm thick)
3. Drainage: for severe infections to ↓ pressure (improve circulation), release bacteria and products; consider abx
4. Culturing: rarely needed but if so, sterilize tissue with chlorhexidine and obtain submucosal sample via aspiration with a 16- to 20-gauge needle
The Hard Palate
AnatomyThe Hard Palate
The anterior bony part of the palate is formed by the palatine process of the maxillae and the horizontal plates of the palatine bones.
Anteriorly and laterally, the hard palate is bounded by the alveolar processes and the gingivae.
Posteriorly, the hard palate is continuous with the soft palate.
The incisive foramen is the mouth of the incisive canal.
This foramen is located posterior to the maxillary central incisor teeth.
This foramen is the common opening for the right and left incisive canals.
The incisive canal and foramen transmit the nasopalatine nerve and the terminal branches of the sphenopalatine artery.
Medial to the third molar tooth, the greater palatine foramen pierces the lateral border of the bony palate.
The greater palatine vessels and nerve emerge from this foramen and run anteriorly into two grooves on the palate.
The lesser palatine foramen transmits the lesser palatine nerve and vessels.
This runs to the soft palate and adjacent structures.
Osteoradionecrosis
Oral Pathology
Osteoradionecrosis
Clinical features
A reduction in vascularity, secondary to endarteritis obliterans, and damage to osteocytes as a consequence of ionising
Radiotherapy can result in radiation-associated osteomyelitis or Osteoradionecrosis. The mandible is much more commonly affected than the maxilla, because it is less vascular. Pain may be severe and there may be pyrexia. The overlying oral mucosa often appears pale because of radiation damage. Osteoradionecrosis in the jaws arises most often following radiotherapy for squamous cell carcinoma.
Scar tissue will also be present at the tumour site, often in close relation to the necrotic bone.
Radiology
Osteoradionecrosis appears as rarefying osteitis within which islands of opacity (sequestra) are seen. Pathological
fracture may be visible in the mandible.
Pathology
The affected bone shows features similar to those of chronic osteomyelitis. Grossly, the bone may be cavitated
And discoloured, with formation of sequestra.
Acute inflammatory infiltrate may be present on a background of chronic inflammation, characterized by formation
Of granulation tissue around the non-vital trabeculae.
Blood vessels show areas of endothelial denudation and obliteration of their lumina by fibrosis.
Small telangiectatic vessels lacking precapillary sphincters may be present.
Fibroblasts in the irradiated tissues lose the capacity to divide and often become binucleated and enlarged.
Management
Prevention of Osteoradionecrosis is vital. Patients who require radiotherapy for the management of head and
neck malignancy should ideally have teeth of doubtful prognosis extracted at least 6 weeks prior to treatment.
The dose of radiation,
The area of the mandible irradiated and
the surgical trauma involved in the dental extractions.
Surgical management of Osteoradionecrosis is similar to osteomyelitis.
LIPOPROTIENS
Biochemistry
LIPOPROTIENS
Lipoproteins Consist of a Nonpolar Core & a Single Surface Layer of Amphipathic Lipids
The nonpolar lipid core consists of mainly triacylglycerol and cholesteryl ester and is surrounded by a single surface layer of amphipathic phospholipid and cholesterol molecules .These are oriented so that their polar groups face outward to the aqueous medium. The protein moiety of a lipoprotein is known as an apolipoprotein or apoprotein,constituting nearly 70% of some HDL and as little as 1% of Chylomicons. Some apolipoproteins are integral and cannot be removed, whereas others can be freely transferred to other lipoproteins.
There re five types of lipoproteins, namely chylomicrons, very low density lipoproteins(VLDL) low density lipoproteins (LDL), high density Lipoproteins (HDL) and free fatty acid-albumin complexes.