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Muscles of the Soft Palate
Anatomy

Muscles of the Soft Palate

The Levator Veli Palatini (Levator Palati)


Superior attachment: cartilage of the auditory tube and petrous part of temporal bone.
Inferior attachment: palatine aponeurosis.
Innervation: pharyngeal branch of vagus via pharyngeal plexus.
This cylindrical muscle runs inferoanteriorly, spreading out in the soft palate, where it attaches to the superior surface of the palatine aponeurosis.
It elevates the soft palate, drawing it superiorly and posteriorly.
It also opens the auditory tube to equalise air pressure in the middle ear and pharynx.


 

The Tensor Veli Palatini (Tensor Palati)


Superior attachment: scaphoid fossa of medial pterygoid plate, spine of sphenoid bone, and cartilage of auditory tube.
Inferior attachment: palatine aponeurosis.
Innervation: medial pterygoid nerve (a branch of the mandibular nerve).
This thin, triangular muscle passes inferiorly, and hooks around the hamulus of the medial pterygoid plate.
It then inserts into the palatine aponeurosis.
This muscle tenses the soft palate by using the hamulus as a pulley.
It also pulls the membranous portion of the auditory tube open to equalise air pressure of the middle ear and pharynx.


 

The Palatoglossus Muscle


Superior attachment: palatine aponeurosis.
Inferior attachment: side of tongue.
Innervation: cranial part of accessory nerve (CN XI) through the pharyngeal branch of vagus (CN X) via the pharyngeal plexus.
This muscle, covered by mucous membrane, forms the palatoglossal arch.
The palatoglossus elevates the posterior part of the tongue and draws the soft palate inferiorly onto the tongue.


 

The Palatopharyngeus Muscle


Superior attachment: hard palate and palatine aponeurosis.
Inferior attachment: lateral wall of pharynx.
Innervation: cranial part of accessory nerve (CN XI) through the pharyngeal branch of vagus (CN X) via the pharyngeal plexus.
This thin, flat muscle is covered with mucous membrane to form the palatopharyngeal arch.
It passes posteroinferiorly in this arch.
This muscle tenses the soft palate and pulls the walls of the pharynx superiorly, anteriorly and medially during swallowing.


 

The Musculus Uvulae


Superior attachment: posterior nasal spine and palatine aponeurosis.
Inferior attachment: mucosa of uvula.
Innervation: cranial part of accessory through the pharyngeal branch of vagus, via the pharyngeal plexus.
It passes posteriorly on each side of the median plane and inserts into the mucosa of the uvula.
When the muscle contracts, it shortens the uvula and pulls it superiorly.

Piroxicam
Pharmacology

Piroxicam:

Half‐life of 45 hrs. Once‐daily dosing. Delay onset of  action.

High doses inhibits PMN migration, decrease oxygen  radical production, inhibits lymphocyte function. 

used to relieve the symptoms of  arthritis, primary dysmenorrhoea, pyrexia; and as an analgesic,non-selective  cyclooxygenase (COX) inhibitor

The risk of adverse side efects is nearly ten times higher than with other NSAIDs. Peptic ulcer (9.5 higher)

Sterilization
Conservative Dentistry

Sterilization in Dental Practice
Sterilization is a critical process in dental practice, ensuring that all
forms of life, including the most resistant bacterial spores, are eliminated
from instruments that come into contact with mucosa or penetrate oral tissues.
This guide outlines the accepted methods of sterilization, their requirements,
and the importance of biological monitoring to ensure effectiveness.

Sterilization: The process of killing all forms of
life, including bacterial spores, to ensure that instruments are free from
any viable microorganisms. This is essential for preventing infections and
maintaining patient safety.

Accepted Methods of Sterilization
There are four primary methods of sterilization commonly used in dental
practices:
A. Steam Pressure Sterilization (Autoclave)

Description: Utilizes steam under pressure to achieve
high temperatures that kill microorganisms.
Requirements:
Temperature: Typically operates at 121-134°C
(250-273°F).
Time: Sterilization cycles usually last from 15 to
30 minutes, depending on the load.
Packaging: Instruments must be properly packaged to
allow steam penetration.



B. Chemical Vapor Pressure Sterilization (Chemiclave)

Description: Involves the use of chemical vapors (such
as formaldehyde) under pressure to sterilize instruments.
Requirements:
Temperature: Operates at approximately 132°C
(270°F).
Time: Sterilization cycles typically last about 20
minutes.
Packaging: Instruments should be packaged to allow
vapor penetration.



C. Dry Heat Sterilization (Dryclave)

Description: Uses hot air to sterilize instruments,
effectively killing microorganisms through prolonged exposure to high
temperatures.
Requirements:
Temperature: Commonly operates at 160-180°C
(320-356°F).
Time: Sterilization cycles can last from 1 to 2
hours, depending on the temperature.
Packaging: Instruments must be packaged to prevent
contamination after sterilization.



D. Ethylene Oxide (EtO) Sterilization

Description: Utilizes ethylene oxide gas to sterilize
heat-sensitive instruments and materials.
Requirements:
Temperature: Typically operates at low temperatures
(around 37-63°C or 98.6-145°F).
Time: Sterilization cycles can take several hours,
including aeration time.
Packaging: Instruments must be packaged in
materials that allow gas penetration.




Considerations for Choosing Sterilization Equipment
When selecting sterilization equipment, dental practices must consider
several factors:

Patient Load: The number of patients treated daily will
influence the size and capacity of the sterilizer.
Turnaround Time: The time required for instrument reuse
should align with the sterilization cycle time.
Instrument Inventory: The variety and quantity of
instruments will determine the type and size of sterilizer needed.
Instrument Quality: The materials and construction of
instruments may affect their compatibility with certain sterilization
methods.


Biological Monitoring
A. Importance of Biological Monitoring

Biological Monitoring Strips: These strips contain
spores calibrated to be killed when sterilization conditions are met. They
serve as a reliable weekly monitor of sterilization effectiveness.

B. Process

Testing: After sterilization, the strips are sent to a
licensed reference laboratory for testing.
Documentation: Dentists receive independent
documentation of monitoring frequency and sterilization effectiveness.
Failure Response: In the event of a sterilization
failure, laboratory personnel provide immediate expert consultation to help
resolve the issue.


Pit and Fissure Sealants
Pedodontics

Pit and Fissure Sealants
Pit and fissure sealants are preventive dental materials used to protect
occlusal surfaces of teeth from caries by sealing the grooves and pits that are
difficult to clean. According to Mitchell and Gordon (1990), sealants can be
classified based on several criteria, including polymerization methods, resin
systems, filler content, and color.

Classification of Pit and Fissure Sealants
1. Polymerization Methods
Sealants can be differentiated based on how they harden or polymerize:


a) Self-Activation (Mixing Two Components)

These sealants harden through a chemical reaction that occurs when
two components are mixed together. This method does not require any
external light source.



b) Light Activation

Sealants that require a light source to initiate the polymerization
process can be further categorized into generations:
First Generation: Ultraviolet Light
Utilizes UV light for curing, which can be less common due
to safety concerns.


Second Generation: Self-Cure
These sealants harden through a chemical reaction without
the need for light, similar to self-activating sealants.


Third Generation: Visible Light
Cured using visible light, which is more user-friendly and
safer than UV light.


Fourth Generation: Fluoride-Releasing
These sealants not only provide a physical barrier but also
release fluoride, which can help in remineralizing enamel and
providing additional protection against caries.







2. Resin System
The type of resin used in sealants can also classify them:

BIS-GMA (Bisphenol A Glycidyl Methacrylate)
A commonly used resin that provides good mechanical properties and
adhesion.


Urethane Acrylate
Offers enhanced flexibility and durability, making it suitable for
areas subject to stress.



3. Filled and Unfilled
Sealants can be categorized based on the presence of fillers:


Filled Sealants

Contain added particles that enhance strength and wear resistance.
They may provide better wear characteristics but can be more viscous and
difficult to apply.



Unfilled Sealants

Typically have a smoother flow and are easier to apply, but may not
be as durable as filled sealants.



4. Clear or Tinted
The color of the sealant can also influence its application:


Clear Sealants

Have better flow characteristics, allowing for easier penetration
into pits and fissures. They are less visible, which can be a
disadvantage in monitoring during follow-up visits.



Tinted Sealants

Easier for both patients and dentists to see, facilitating
monitoring and assessment during recalls. However, they may have
slightly different flow characteristics compared to clear sealants.



Application Process

Sealants are applied in a viscous liquid state that enters the
micropores of the tooth surface, which have been enlarged through acid
conditioning.
Once applied, the resin hardens due to either a self-hardening catalyst
or the application of a light source.
The extensions of the hardened resin that penetrate and fill the
micropores are referred to as "tags," which help in retaining the sealant on
the tooth surface.

Hormones of the Hypothalamus
Physiology

Gonadotropin-releasing hormone (GnRH)

GnRH is a peptide of 10 amino acids. Its secretion at the onset of puberty triggers sexual development.

 

Primary Effects

FSH and LH Relaese

 

Secondary Effects

 

Increases estrogen and progesterone (in females)

testosterone Relaese (in males)

Growth hormone-releasing hormone (GHRH)

GHRH is a mixture of two peptides, one containing 40 amino acids, the other 44.  GHRH stimulates cells in the anterior lobe of the pituitary to secrete growth hormone (GH).

Corticotropin-releasing hormone (CRH)

CRH is a peptide of 41 amino acids. Its acts on cells in the anterior lobe of the pituitary to release adrenocorticotropic hormone (ACTH) CRH is also synthesized by the placenta and seems to determine the duration of pregnancy.  It may also play a role in keeping the T cells of the mother from mounting an immune attack against the fetus

Somatostatin

Somatostatin is a mixture of two peptides, one of 14 amino acids, the other of 28. Somatostatin acts on the anterior lobe of the pituitary to


inhibit the release of growth hormone (GH)
inhibit the release of thyroid-stimulating hormone (TSH)


Somatostatin is also secreted by cells in the pancreas and in the intestine where it inhibits the secretion of a variety of other hormones.

Antidiuretic hormone (ADH) and Oxytocin

These peptides are released from the posterior lobe of the pituitary

Classification for antiasthmatic drugs.
Pharmacology

SYMPATHOMIMETICS 

β2 -agonists are invariably used in the symptomatic treatment of asthma. 

Epinephrine and ephedrine are structurally related to the catecholamine norepinephrine, a neurotransmitter of the adrenergic nervous system 

Some of the important β 2 agonists like salmeterol, terbutaline and salbutamol are invariably used as bronchodilators both oral as well as
aerosol inhalants 

SALBUTAMOL
It is highly selective β2 -adrenergic stimulant h-aving a prominent bronchodilator action.
It has poor cardiac action compared to isoprenaline.


TERBUTALINE
It is highly selective β2  agonist similar to salbutamol, useful by oral as well as inhalational route.


SALMETEROL

Salmeterol is long-acting analogue of salbutamol 

BAMBUTEROL

It is a latest selective adrenergic β2 agonist with long plasma half life and given once daily in a dose of 10-20 mg orally.


METHYLXANTHINES (THEOPHYLLINE AND ITS DERIVATIVES)


THEOPHYLLINE
Theophylline has two distinct action:
smooth muscle relaxation (i.e. bronchodilatation) and suppression of the response of the airways to stimuli (i.e. non-bronchodilator prophylactic effects). 

ANTICHOLINERGICS

Anticholinergics, like atropine and its derivative ipratropium bromide block cholinergic pathways that cause airway constriction.

MAST CELL STABILIZERS

SODIUM CROMOGLYCATE

It inhibits degranulation of mast cells by trigger stimuli. 
It also inhibits the release of various asthma provoking mediators e.g. histamine, leukotrienes, platelet activating factor (PAF) and interleukins (IL’s) from mast cell 

KETOTIFEN
It is a cromolyn analogue. It is an antihistaminic (H1  antagonist) and probably inhibits airway inflammation induced by platelet activating factor (PAF) in primate. 
It is not a bronchodilator. It is used in asthma and symptomatic relief in atopic dermatitis, rhinitis, conjunctivitis and urticaria.

LEUKOTRIENE PATHWAY INHIBITORS

MONTELUKAST

It is a cysteinyl leukotriene receptor antagonist indicated for the management of persistent asthma. 

Growth and spread of tumours
General Pathology

Growth and spread of tumours

Growth in excess of normal is a feature of all tumours but extension to tissue away from the site of origin is a feature of malignant tumours.

Modes of spread of malignant tumours

- local, invasion. This is a feature of all malignant tumors and  takes place along tissue spaces and facial planes
    o    Lymphatic spread. Most often seen in carcinomas. This can be in the form of 
    o    Lymphatic permeation:  Where the cells extend along the lymphatics as a  solid core 
    o    Lymphatic embolisation: Where a group of tumour cells break off and get carried to the draining mode

-Vascular spread :  This is a common and early mode of spread for sarcomas but certain carcinomas like renal cell carcinoma and chorio carcinoma have a predilection to early vascular spread.

Vascular spread is most often due .to invasion of venous channels and can be by permeation or embolisation.

Lungs, liver, bones and brain are the common sites for vascular metastasis but
different tumours have different organ preference for metastasis, e.g. : Bronchogenic carcinoma often spreads to liver and adrenals.

-Body cavities and natural passages
    o    Gastrointestinal carcinomas spread to ovaries (Krukenberg’s tomour)
 

Adrenocortical Hyperfunction
General Pathology

Adrenocortical Hyperfunction (Hyperadrenalism)

Hypercortisolism (Cushing Syndrome) is caused by any condition that produces an elevation in glucocorticoid levels. The causes of this syndrome are 
A. Exogenous through administration of exogenous glucocorticoids; the most common causeB. Endogenous 
1. Hypothalamic-pituitary diseases causing hypersecretion of ACTH (Cushing disease)
2. Adrenocortical hyperplasia or neoplasia 
3. Ectopic ACTH secretion by nonendocrine neoplasms (paraneoplastic)


Pathological features 

- The main lesions of Cushing syndrome are found in the pituitary and adrenal glands. 
- The most common change in the pituitary, results from high levels of endogenous or exogenous  glucocorticoids, is termed Crooke hyaline change. In this condition, the normal granular, basophilic cytoplasm of the ACTH-producing cells in the anterior pituitary is replaced by homogeneous, lightly basophilic material. This is due to accumulation of intermediate keratin filaments in the cytoplasm. 
- There is one of four changes in the adrenal glands, which depends on the cause.
1. Cortical atrophy 
2. Diffuse hyperplasia
3. Nodular hyperplasia 
4. Adenoma, rarely a carcinoma 

1. In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the cortex by ACTH. In cases of endogenous hypercortisolism, in contrast, the adrenals either are hyperplastic or contain a cortical neoplasm. 
2. In Diffuse hyperplasia the adrenal cortex is diffusely thickened and yellow, as a result of an increase in the size and number of lipid-rich cells in the zonae fasciculata and reticularis. 
3. Nodular hyperplasia, which takes the form of bilateral, up to 2.0-cm, yellow nodules scattered throughout the cortex. 

4. Primary adrenocortical neoplasms causing Cushing syndrome may be benign or malignant. The  adrenocortical adenomas are yellow tumors surrounded by capsules, and most weigh < 30 gm .

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