NEET MDS Synopsis
Dentinogenesis
Dental Anatomy
Dentinogenesis
Dentin formation, known as dentinogenesis, is the first identifiable feature in the crown stage of tooth development. The formation of dentin must always occur before the formation of enamel. The different stages of dentin formation result in different types of dentin: mantle dentin, primary dentin, secondary dentin, and tertiary dentin.
Odontoblasts, the dentin-forming cells, differentiate from cells of the dental papilla. They begin secreting an organic matrix around the area directly adjacent to the inner enamel epithelium, closest to the area of the future cusp of a tooth. The organic matrix contains collagen fibers with large diameters (0.1-0.2 μm in diameter). The odontoblasts begin to move toward the center of the tooth, forming an extension called the odontoblast process. Thus, dentin formation proceeds toward the inside of the tooth. The odontoblast process causes the secretion of hydroxyapatite crystals and mineralization of the matrix. This area of mineralization is known as mantle dentin and is a layer usually about 150 μm thick.
Whereas mantle dentin forms from the preexisting ground substance of the dental papilla, primary dentin forms through a different process. Odontoblasts increase in size, eliminating the availability of any extracellular resources to contribute to an organic matrix for mineralization. Additionally, the larger odontoblasts cause collagen to be secreted in smaller amounts, which results in more tightly arranged, heterogenous nucleation that is used for mineralization. Other materials (such as lipids, phosphoproteins, and phospholipids) are also secreted.
Secondary dentin is formed after root formation is finished and occurs at a much slower rate. It is not formed at a uniform rate along the tooth, but instead forms faster along sections closer to the crown of a tooth. This development continues throughout life and accounts for the smaller areas of pulp found in older individuals. Tertiary dentin, also known as reparative dentin, forms in reaction to stimuli, such as attrition or dental caries.
The dentin in the root of a tooth forms only after the presence of Hertwig's epithelial root sheath (HERS), near the cervical loop of the enamel organ. Root dentin is considered different than dentin found in the crown of the tooth (known as coronal dentin) because of the different orientation of collagen fibers, the decrease of phosphoryn levels, and the less amount of mineralization.
Pouring the Final Impression
Conservative DentistryPouring the Final Impression
Technique
Mixing Die Stone: A high-strength die stone is mixed
using a vacuum mechanical mixer to ensure a homogenous mixture without air
bubbles.
Pouring Process:
The die stone is poured into the impression using a vibrator and a
No. 7 spatula.
The first increments should be applied in small amounts, allowing
the material to flow into the remote corners and angles of the
preparation without trapping air.
Surface Tension-Reducing Agents: These agents can be
added to the die stone to enhance its flow properties, allowing it to
penetrate deep into the internal corners of the impression.
Final Dimensions
The impression should be filled sufficiently so that the dies will be
approximately 15 to 20 mm tall occluso-gingivally after trimming. This
height is important for the stability and accuracy of the final restoration.
Chronic hepatitis
General Pathology
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.
SPECIAL VISCERAL AFFERENT (SVA) PATHWAYS
Physiology
SPECIAL VISCERAL AFFERENT (SVA) PATHWAYS
Taste
Special visceral afferent (SVA) fibers of cranial nerves VII, IX, and X conduct signals into the solitary tract of the brainstem, ultimately terminating in the nucleus of the solitary tract on the ipsilateral side.
Second-order neurons cross over and ascend through the brainstem in the medial lemniscus to the VPM of the thalamus.
Thalamic projections to area 43 (the primary taste area) of the postcentral gyrus complete the relay.
SVA VII fibers conduct from the chemoreceptors of taste buds on the anterior twothirds of the tongue, while SVA IX fibers conduct taste information from buds on the posterior one-third of the tongue.
SVA X fibers conduct taste signals from those taste cells located throughout the fauces.
Smell
The smell-sensitive cells (olfactory cells) of the olfactory epithelium project their central processes through the cribiform plate of the ethmoid bone, where they synapse with mitral cells. The central processes of the mitral cells pass from the olfactory bulb through the olfactory tract, which divides into a medial and lateral portion The lateral olfactory tract terminates in the prepyriform cortex and parts of the amygdala of the temporal lobe.
These areas represent the primary olfactory cortex. Fibers then project from here to area 28, the secondary olfactory area, for sensory evaluation. The medial olfactory tract projects to the anterior perforated substance, the septum pellucidum, the subcallosal area, and even the contralateral olfactory tract.
Both the medial and lateral olfactory tracts contribute to the visceral reflex pathways, causing the viscerosomatic and viscerovisceral responses.
Age Groups and Radiographs
Radiology
Age Groups and Radiographs
Age 2:
Anterior IOPA's: 2
Posterior IOPA's: 4
Bitewings: 2
Total Films: 12
Age 8:
Anterior IOPA's: 8
Posterior IOPA's: 4
Bitewings: 2
Total Films: 14
Age 8 (another entry):
Anterior IOPA's: 8
Posterior IOPA's: 8
Bitewings: 2
Total Films: 20
Summary of Total Films by Type
Anterior IOPA's:
Age 2: 2
Age 8: 8
Age 8 (another entry): 8
Total Anterior IOPA's: 18
Posterior IOPA's:
Age 2: 4
Age 8: 4
Age 8 (another entry): 8
Total Posterior IOPA's: 16
Bitewings:
Age 2: 2
Age 8: 2
Age 8 (another entry): 2
Total Bitewings: 6
Overall Total Films
Total Films for Age 2: 12
Total Films for Age 8 (first entry): 14
Total Films for Age 8 (second entry): 20
Grand Total Films: 12 + 14 + 20 = 46
Necrotizing Ulcerative Gingivitis (NUG)
PeriodontologyNecrotizing Ulcerative Gingivitis (NUG)
Necrotizing Ulcerative Gingivitis (NUG), also known as Vincent's disease or
trench mouth, is a severe form of periodontal disease characterized by the
sudden onset of symptoms and specific clinical features.
Etiology and Predisposing Factors
Sudden Onset: NUG is characterized by a rapid onset of
symptoms, often following debilitating diseases or acute respiratory
infections.
Lifestyle Factors: Changes in living habits, such as
prolonged work without adequate rest, poor nutrition, tobacco use, and
psychological stress, are frequently noted in patient histories .
Smoking: Smoking has been identified as a significant
predisposing factor for NUG/NDP .
Immune Compromise: Conditions that compromise the
immune system, such as poor oral hygiene, smoking, and emotional stress, are
major contributors to the development of NUG .
Clinical Presentation
Symptoms: NUG presents with:
Punched-out, crater-like depressions at the crest of interdental
papillae.
Marginal gingival involvement, with rare extension to attached
gingiva and oral mucosa.
Grey, pseudomembranous slough covering the lesions.
Spontaneous bleeding upon slight stimulation of the gingiva.
Fetid odor and increased salivation.
Microbiology
Mixed Bacterial Infection: NUG is caused by a complex
of anaerobic bacteria, often referred to as the fusospirochetal complex,
which includes:
Treponema vincentii
Treponema denticola
Treponema macrodentium
Fusobacterium nucleatum
Prevotella intermedia
Porphyromonas gingivalis
Treatment
Control of Acute Phase:
Clean the wound with an antibacterial agent.
Irrigate the lesion with warm water and 5% vol/vol hydrogen
peroxide.
Prescribe oxygen-releasing mouthwash (e.g., hydrogen peroxide DPF,
sodium perborate DPF) to be used thrice daily.
Administer oral metronidazole for 3 to 5 days. If sensitive to
metronidazole, prescribe penicillin; if sensitive to both, consider
erythromycin or clindamycin.
Use 2% chlorhexidine in select cases for a short duration.
Management of Residual Condition:
Remove predisposing local factors (e.g., overhangs).
Perform supra- and subgingival scaling.
Consider gingivoplasty to correct any residual gingival deformities.
Exchange of gases in Lungs
PhysiologyExchange of gases takes place in Lungs
A person with an average ventilation rate of 7.5 L/min will breathe in and out 10,800 liters of gas each day
From this gas the person will take in about 420 liters of oxygen (19 moles/day) and will give out about 340 liters of carbon dioxide (15 moles/day)
The ratio of CO2 expired/O2 inspired is called the respiratory quotient (RQ)
RQ = CO2 out/O2 in = 340/420 = 0.81
In cellular respiration of glucose CO2 out = O2 in; RQ = 1
The overall RQ is less than 1 because our diet is a mixture of carbohydrates and fat; the RQ for metabolizing fat is only 0.7
All of the exchange of gas takes place in the lungs
The lungs also give off large amounts of heat and water vapor
Red blood cell cycle
PhysiologyRed blood cell cycle:
RBCs enter the blood at a rate of about 2 million cells per second. The stimulus for erythropoiesis is the hormone erythropoietin, secreted mostly by the kidney. RBCs require Vitamin B12, folic acid, and iron. The lifespan of RBC averages 120 days. Aged and damaged red cells are disposed of in the spleen and liver by macrophages. The globin is digested and the amino acids released into the blood for protein manufacture; the heme is toxic and cannot be reused, so it is made into bilirubin and removed from the blood by the liver to be excreted in the bile. The red bile pigment bilirubin oxidizes into the green pigment biliverdin and together they give bile and feces their characteristic color. Iron is picked up by a globulin protein (apotransferrin) to be transported as transferrin and then stored, mostly in the liver, as hemosiderin or ferritin. Ferritin is short term iron storage in constant equilibrium with plasma iron carried by transferrin. Hemosiderin is long term iron storage, forming dense granules visible in liver and other cells which are difficult for the body to mobilize.
Some iron is lost from the blood due to hemorrhage, menstruation, etc. and must be replaced from the diet. On average men need to replace about 1 mg of iron per day, women need 2 mg. Apotransferrin (transferrin without the iron) is present in GI lining cells and is also released in the bile. It picks up iron from the GI tract and stimulates receptors on the lining cells which absorb it by pinocytosis. Once through the mucosal cell iron is carried in blood as transferrin to the liver and marrow. Iron leaves the transferrin molecule to bind to ferritin in these tissues. Most excess iron will not be absorbed due to saturation of ferritin, reduction of apotransferrin, and an inhibitory process in the lining tissue.
Erythropoietin Mechanism:
Myeloid (blood producing) tissue is found in the red bone marrow located in the spongy bone. As a person ages much of this marrow becomes fatty and ceases production. But it retains stem cells and can be called on to regenerate and produce blood cells later in an emergency. RBCs enter the blood at a rate of about 2 million cells per second. The stimulus for erythropoiesis is the hormone erythropoietin, secreted mostly by the kidney. This hormone triggers more of the pleuripotential stem cells (hemocytoblasts) to follow the pathway to red blood cells and to divide more rapidly.
It takes from 3 to 5 days for development of a reticulocyte from a hemocytoblast. Reticulocytes, immature rbc, move into the circulation and develop over a 1 to 2 day period into mature erythrocytes. About 1 to 2 % of rbc in the circulation are reticulocytes, and the exact percentage is a measure of the rate of erythropoiesis.