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NEET MDS Synopsis

Junctional Epithelium
Periodontology

Junctional Epithelium
The junctional epithelium (JE) is a critical component of the periodontal
tissue, playing a vital role in the attachment of the gingiva to the tooth
surface. Understanding its structure, function, and development is essential for
comprehending periodontal health and disease.

Structure of the Junctional Epithelium


Composition:

The junctional epithelium consists of a collar-like band of stratified
squamous non-keratinized epithelium.
This type of epithelium is designed to provide a barrier while
allowing for some flexibility and permeability.



Layer Thickness:

In early life, the junctional epithelium is approximately 3-4
layers thick.
As a person ages, the number of epithelial layers can increase
significantly, reaching 10 to 20 layers in older
individuals.
This increase in thickness may be a response to various factors,
including mechanical stress and inflammation.



Length:

The length of the junctional epithelium typically ranges from 0.25
mm to 1.35 mm.
This length can vary based on individual anatomy and periodontal
health.




Development of the Junctional Epithelium

The junctional epithelium is formed by the confluence of the
oral epithelium and the reduced enamel epithelium during the
process of tooth eruption.
This fusion is crucial for establishing the attachment of the gingiva to
the tooth surface, creating a seal that helps protect the underlying
periodontal tissues from microbial invasion.


Function of the Junctional Epithelium

Barrier Function: The junctional epithelium serves as a
barrier between the oral cavity and the underlying periodontal tissues,
helping to prevent the entry of pathogens.
Attachment: It provides a strong attachment to the
tooth surface, which is essential for maintaining periodontal health.
Regenerative Capacity: The junctional epithelium has a
high turnover rate, allowing it to regenerate quickly in response to injury
or inflammation.


Clinical Relevance

Periodontal Disease: Changes in the structure and
function of the junctional epithelium can be indicative of periodontal
disease. For example, inflammation can lead to increased permeability and
loss of attachment.
Healing and Repair: Understanding the properties of the
junctional epithelium is important for developing effective treatments for
periodontal disease and for managing healing after periodontal surgery.

Chronic Osteomyelitis
Oral Pathology

Chronic Osteomyelitis


As soon as pus drains intra or extraorally, condition ceases to spread and chronic phase commences.
Infection is localized but persistent as bacteria are able to grow in dead bone inaccessible to body’s defenses.


Clinical features


Primary – insidious in onset , slight pain , gradual increase in jaw size.
Secondary - Pain is deep pain and intermittent, temperature fluctuations , pyrexia , cellulitis eventually leading to abscess
New bone formation leads to thickening causing facial asymmetry.
Thickened or “wooden” character of bone in cr sec osteomyelitis.
Eventually cures itself as the last sequestra is discharged.


Radiographic Features


Trabeculae in the involved area become thin or appear fuzzy & then lose their continuity.
After some time “moth eaten” appearance is seen
Sequestra appear denser on radiographs.
Where the subperiosteal new bone formation , the new bone is superimposed upon that of jaw, “fingerprint” or “orange peel” appearance is seen
Cloacae seen as dark shadows passing through opacity.


Histologic features


Areas of acute and subacute inflammation in the cancellous spaces of the necrotic bone.
Foci of acute inflammation
Active osteoclastic resorption of bone noted in peripheral portions


Chronic Subperiosteal Osteomyelitis


Cortical plate deprived of its blood supply undergoes necrosis, underlying medullary bone  is slightly affected.
Multiple small sequestra form, eventually discharged through sinuses with pus.
Following extrusion of sequestra, healing occurs.
Spontaneous drainage poor in submassetric area.
Much of  body of mandible is lost due to poor central blood supply of the region.


D/D


Paget’s disease – particularly wen periosteal bone is involved
Fibrous dysplasia
Osteosarcoma


Chronic sclerosing osteomyelitis

– focal

- diffuse

Focal Sclerosing Osteomyelitis

Clinical features


Most commonly in children and young adults, rarely in older individuals.
Tooth most commonly involved is the mandibular third molar presenting with a large carious lesion.
No signs or symptoms other than mild pain associated with infected pulp.


Radiographic features


Entire root outline always visible with intact lamina dura.
Periodontal ligament space widened.
Border smooth & distinct appearing to blend into surrounding bone


D/D for focal sclerosing osteomyelitis


Local bone sclerosis
Sclerosing cementoma
Gigantiform cementoma


Treatment & prognosis


Affected tooth may be treated endodontically or extracted.
Sclerotic bone  not attached to tooth and remains behind after tooth is removed.
This dense area may not get remodeled.
Recognizable on bone years later and is referred as bone scar.


Diffuse Sclerosing Osteomyelitis


May occur at any age, most common in older persons, esp in edentulous mandibles
vague pain, unpleasant taste.
Many times spontaneous formation of fistula seen opening onto mucosal surface to establish drainage
Slowly progressive, not particularly dangerous since it is non destructive & seldom produces complications


Radiographic features


Diffuse patchy, sclerosis of bone – “cotton wool” appearance
Radiopacity may be extensive and bilateral.
Due to diffuse nature, border between sclerosis & normal bone is often indistinct


D/D for DIFFUSE sclerosing osteomyelitis

FLORID OSSEOUS DYSPLASIA

SCLEROTIC CEMENTAL MASSES

TRUE CHR DIFFUSE SCLEROSING OSTEOMYELITIS

FIBROUS DYSPLASIA

Treatment & Prognosis


Resolution of adjacent foci of chronic infection often leads to improvement.
Usually too extensive to be removed surgically,
Acute episodes treated with antibiotics.

Nerve Supply of the Muscles of the Orbit
Anatomy

Nerve Supply of the Muscles of the Orbit (pp. 715-6)


Three cranial nerves supply the muscles of the eyeball; the oculomotor (CN III), trochlear (CN IV) and abducent (CN IV) nerves.
All three enter the orbit via the superior orbital fissure.



The trochlear nerve supplies the superior oblique muscle.
The abducent nerve supplies the lateral rectus muscle.
The oculomotor nerve supplies everything else.



A mnemonic that is used is this formula for this strange sulfate: SO4(LR6)3


Diagnostic Methods for Early Caries Detection
Conservative Dentistry

Diagnostic Methods for Early Caries Detection
Early detection of caries is essential for effective management and
treatment. Various diagnostic methods can be employed to identify caries
activity at early stages:
1. Identification of Subsurface Demineralization

Inspection: Visual examination of the tooth surface for
signs of demineralization, such as white spots or discoloration.
Radiographic Methods: X-rays can reveal subsurface
carious lesions that are not visible to the naked eye, allowing for early
intervention.
Dye Uptake Methods: Application of specific dyes that
can penetrate demineralized areas, highlighting the extent of carious
lesions.

2. Bacterial Testing

Microbial Analysis: Testing for the presence of
specific cariogenic bacteria (e.g., Streptococcus mutans) can provide
insight into the caries risk and activity level.
Salivary Testing: Salivary samples can be analyzed for
bacterial counts, which can help assess the risk of caries development.

3. Assessment of Environmental Conditions

pH Measurement: Monitoring the pH of saliva can
indicate the potential for demineralization. A lower pH (acidic environment)
is conducive to caries development.
Salivary Flow: Evaluating salivary flow rates can help
determine the protective capacity of saliva against caries. Reduced salivary
flow can increase caries risk.
Salivary Buffering Capacity: The ability of saliva to
neutralize acids is crucial for maintaining oral health. Assessing this
capacity can provide valuable information about caries risk.

GENETIC VARIATION
General Microbiology

GENETIC VARIATION

Two methods are known for genetic variation in bacteria: mutation and gene transfer.

Mutation : Any change in the sequence of bases of DNA, irrespective of detectable changes in the cell phenotype. Mutations may be spontaneous or induced by various agents which are known as mutagens. 

Spontaneous Mutations: Arise from enzymatic imperfections during DNA replications or with transient insertions of transposable elements.

Induced Mutations: Mutation by physical and chemical mutagens.

Physical mutagens  ultraviolet rays and high-energy ionizing radiations. The primary effect of UV rays on DNA is the production of pyrmidine dimers whereas ionizing radiations cause single_stranded breaks the DNA molecules.

Chemical mutagens :Affecting nucleotide sequence

(i) Agents which cause error in base pairing (e.g. nitrous acid and alkylating agents).
(ii) Agents which cause errors in DNA replication (e.g. acridine dyes such as acridine orange and profiavine).
(iii) Base analogs which are incorporated into DNA and cause replication errors (e.g. 5-bromouracil)

Gene Transfer

Transformation: Uptake of naked DNA

Transduction    : Infection by a nonlethal bacteriophage

Conjugation    : Mating between cells in contact

Protoplast fusion

Transformation: Gene transfer by soluble DNA is called as transformation. it requires that DNA be absorbed by the cell, gain entrance to the cytoplasm and undergo recombination with the host genome. 

Artificial Transformation(transfection) :Some of the bacteria (such as Escherichia coli) resist transformation until they are subjected to some special treatment such as CaCl2 to make the bacterium more permeable to DNA. Such modified cells can also take up intact double stranded DNA extracted from viruses or in the shape of plasmids. Though the process is same as transformation, it is 9 as transfection because it results in infection by an abnormal route

Transduction :The type of gene transfer in which the DNA of one bacterial cell is introduced into another bacterial cell by viral infection is known as transduction. This introduces only a small fragment of DNA. Because the DNA is protected from damage by the surrounding phage coat, transduction is an easier to perform and more reproducible process than transduction. ,

Two types of transduction are known.

- Generalized transduction When a bacteriophage picks up fragments of host DNA at random and can transfer any genes

-  Specialised transduction: phage DNA that has been integrated into the host chromosome is excised along with a few adjacent genes, which the phage can then transfer.

After entry into the host cell, the phage DNA gets incorporated into the host chromosome in such a way that the two genomes are linearly contiguous (lysogeny). The phage genome in this stage is known as prophage, The host cell acquires a significant new property as a consequence of lysogeny because it becomes immune to infection by homologous phage. This is hence called as lysogenic conversion and endow toxigenicity to Corynebacterium diphtheriae

Abortive Transduction :phage DNA fails to integrated into the host chromosome, the process is called as abortive transduction The phage DNA does not replicate and along with binary fission Of the host it goes into one of the daughter cells.

Conjugation :This is defined as the transfer of DNA directly from on bacterial. .cell to another by a mechanism that requires cell-to-cell contact. 

The capacity to donate DNA depends upon the possession of the fertility (F) factor. The F pili  also retard male-male union. Concomitant with effective male-female pair formation, the circular DNA bearing the F factor is converted to a linear form that is transferred to the female cell in a sequential manner. DNA replication occurs in the male cell and the newly synthesized, semiconserved DNA molecule remains in the male. This ensures postmating characters of the male.

Conjugation in Different Bacteria: Unusual form of plasmid transfer, called phase mediated conjugation has  been reported to occur with some strains of Staphylococcus aureus.

Protoplast Fusion: Also called as genetic transfusion. Under osmotically buffered Conditions protoplast fusion takes place by joining of cell membrane and generation of cytoplasmic bridges through which genetic material can be exchanged.

Transposons: Transposons  Tn  are  DNA sequences which are incapable of autonomous existence and which transpose blocks of genetic material back and forth between cell Chromosome and smaller replicons such as plasmids. insertion sequences (IS ) are another similar group of nucleotides which can move from one chromosome to another

Genetic material. IS and  Tn are collectively also known as transposable elements or Jumping genes. These are now recognised to play an important role in bringing about vanous types of mutations.


 

COMPONENTS OF THE CELLULAR ENVIRONMENT
Physiology

Water: comprises 60 - 90% of most living organisms (and cells) important because it serves as an excellent solvent & enters into many metabolic reactions


Intracellular (inside cells) = ~ 34 liters
Interstitial (outside cells) = ~ 13 liters
Blood plasma = ~3 liters


40% of blood is red blood cells (RBCs)

plasma is similar to interstitial fluid, but contains plasma proteins

serum = plasma with clotting proteins removed

intracellular fluid is very different from interstitial fluid (high K concentration instead of high Na concentration, for example)


Capillary walls (1 cell thick) separate blood from interstitial fluid
Cell membranes separate intracellular and interstitial fluids



Loss of about 30% of body water is fatal


 

Ions = atoms or molecules with unequal numbers of electrons and protons:


found in both intra- & extracellular fluid
examples of important ions include sodium, potassium, calcium, and chloride


Ions (Charged Atoms or Molecules) Can Conduct Electricity


Giving up electron leaves a + charge (cation)
Taking on electron produces a - charge (anion)
Ions conduct electricity
Without ions there can be no nerves or excitability

Na+ and K+ cations  
Ca2+ and Mg2+ cations  control metabolism and trigger muscle contraction and secretion of hormones and transmitters




Na+ & K+ are the Major Cations in Biological Fluids


High K+ in cells, high Na+ outside
Ion gradients maintained by Na pump (1/3 of basal metabolism)
Think of Na+ gradient as a Na+ battery- stored electrical energy
K+ gradient forms a K+ battery
Energy stored in Na+ and K+ batteries can be tapped when ions flow



Na+ and K+ produce action potential of excitable cells

Pulp
Dental Anatomy

Pulp

1. Four zones—listed from dentin inward

a. Odontoblastic layer

(1) Contains the cell bodies of odontoblasts.

 

Note: their processes remain in dentinal tubules.

 

(2) Capillaries, nerve fibers, and dendritic cells may also be present.

 

b. Cell-free or cell-poor zone (zone of Weil)

(1) Contains capillaries and unmyelinated nerve fibers.

 

c. Cell-rich zone

(1) Consists mainly of fibroblasts. Macrophages, lymphocytes, and dendritic cells may also be present.


d. The pulp (pulp proper, central zone)

(1) The central mass of the pulp.

(2) Consists of loose connective tissue, larger vessels, and nerves. Also contains fibroblasts and pulpal cells.


2. Pulpal innervation

a. When pulpal nerves are stimulated, they can only transmit one signal pain.

b. There are no proprioceptors in the pulp.

 

c. Types of nerves:

(1) A-delta fibers

(a) Myelinated sensory nerve fibers.

(b) Stimulation results in the sensation of fast, sharp pain.

(c) Found in the coronal (odontoblastic) area of the pulp.


(2) C-fibers

(a) Unmyelinated sensory nerve fibers.

(b) Transmits information of noxious stimuli centrally.

(c) Stimulation results in pain that is slower, duller, and more diffuse in nature.

(d) Found in the central region of the pulp.


(3) Sympathetic fibers

(a) Found deeper within the pulp.

(b) Sympathetic stimulation results in vasoconstriction of vessels.

? Muscles Moving the Auditory Ossicles
Anatomy

Muscles Moving the Auditory Ossicles

The Tensor Tympani Muscle


This muscle is about 2 cm long.



Origin: superior surface of the cartilaginous part of the auditory tube, the greater wing of the sphenoid bone, and the petrous part of the temporal bone.
Insertion: handle of the malleus.
Innervation: mandibular nerve (CN V3) through the nerve to medial pterygoid.



The tensor tympani muscle pulls the handle of the malleus medially, tensing the tympanic membrane, and reducing the amplitude of its oscillations.
This tends to prevent damage to the internal ear when one is exposed to load sounds.


 

The Stapedius Muscle


This tiny muscle is in the pyramidal eminence or the pyramid.



Origin: pyramidal eminence on the posterior wall of the tympanic cavity. Its tendon enters the tympanic cavity by traversing a pinpoint foramen in the apex of the pyramid.
Insertion: neck of the stapes.
Innervation: nerve to the stapedius muscle, which arises from the facial nerve (CN VII).



The stapedius muscle pulls the stapes posteriorly and tilts its base in the fenestra vestibuli or oval window, thereby tightening the anular ligament and reducing the oscillatory range.
It also prevents excessive movement of the stapes.




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