NEET MDS Synopsis
Bones of the Face
Anatomy
-> Most of the facial skeleton is formed by nine bones: four paired (nasal, zygomatic, maxilla, and palatine) and one unpaired (mandible).
-> The calvaria of the new-born infant is large compared with the relatively small fascial skeleton.
-> This results from the small size of the jaws and the almost complete absence of the maxillary and other paranasal sinuses in the new-born skull.
-> These sinuses form large spaces in the adult facial skeleton. As the teeth and sinuses develop during infancy and childhood, the facial bones enlarge.
-> The growth of the maxillae between the ages of 6 and 12 years accounts for the vertical elongation of the child’s face.
The Nasal Bones
-> These bones may be felt easily because they form the bridge of the nose.
-> The right and left nasal bones articulate with each other at the internasal suture.
-> They also articulate with the frontal bones, the maxillae, and the ethmoid bones.
-> The mobility of the anteroinferior portion of the nose, supported only by cartilages, serves as a partial protection against injure (e.g., a punch in the nose). However, a hard blow to the anterosuperior bony portion of the nose may fracture the nasal bones (broken nose).
-> Often the bones are displaced sideways and/or posteriorly.
The Maxillae
-> The skeleton of the face between the mouth and the eyes is formed by the two maxillae.
-> They surround the anterior nasal apertures and are united in the medial plane at the intermaxillary suture to form the maxilla (upper jaw).
-> This suture is also visible in the hard palate, where the palatine processes of the maxillae unite.
-> Each adult maxilla consists of: a hollow body that contains a large maxillary sinus; a zygomatic process that articulates with its mate on the other side to form most of the hard palate; and alveolar processes that form sockets for the maxillary (upper) teeth.
-> The maxillae also articulate with the vomer, lacrimal, sphenoid, and palatine bones.
-> The body of the maxilla has a nasal surface that contributes to the lateral wall of the nasal cavity; an orbital surface that forms most of the floor of the orbit; an infratemporal surface that forms the anterior wall of the infratemporal fossa; and an anterior surface that faces partly anteriorly and partly anterolaterally and is covered buy facial muscles.
-> The relatively large infraorbital foramen, which faces inferomedially, is located about 1 cm inferior to the infraorbital margin; it transmits the infraorbital nerve and vessels.
-> The incisive fossa is a shallow concavity overlying the roots of the incisor teeth, just a shallow concavity overlying the roots of the incisor teeth, just inferior to the nasal cavity. This fossa is the injection site for anaesthesia of the maxillary incisor teeth.
-> If infected maxillary teeth are removed, the bone of the alveolar processes of the maxillae begins to be reabsorbed. As a result, the maxilla becomes smaller and the shape of the face changes.
-> Owing to absorption of the alveolar processes, there is a marked reduction in the height of the lower face, which produces deep creases in the facial skin that pass posteriorly from the corners of the mouth.
The Mandible
-> This is a U-shaped bone and forms the skeleton of the lower jaw and the inferior part of the face. It is the largest and strongest facial bone.
-> The mandibular (lower) teeth project superiorly from their sockets in the alveolar processes.
-> The mandible (L. mandere, to masticate) consists of two parts: a horizontal part called the body, and two vertical oblong parts, called rami.
-> Each ramus ascends almost vertically from the posterior aspect of the body.
-> The superior part of the ramus has two processes: a posterior condylar process with a head or condyle and a neck, and a sharp anterior coronoid process.
-> The condylar process is separated from the coronoid process by the mandibular notch, which forms the concave superior border of the mandible.
-> Viewed from the superior aspect, the mandible is horseshoe-shaped, whereas each half is L-shaped when viewed laterally.
-> The rami and body meet posteriorly at the angle of the mandible.
-> Inferior to the second premolar tooth on each side of the mandible is a mental foramen (L. mentum, chin) for transmission of the mental vessels and the mental nerve.
-> In the anatomical position, the rami of the mandible are almost vertical, except in infants and in edentulous (toothless) adults.
-> On the internal aspect of the ramus, there is a large mandibular foramen.
-> It is the oblong entrance to the mandibular canal that transmits the inferior alveolar vessels and nerve to the roots of the mandibular teeth.
-> Branches of these vessels and the mental nerve emerge from the mandibular canal at the mental foramen.
-> Running inferiorly and slightly anteriorly on the internal surface of the mandible from the mandibular foramen is a small mylohyoid groove (sulcus), which indicates the course taken by the mylohyoid nerve and vessels.
-> These structures arise from the inferior alveolar nerve and vessels, just before they enter the mandibular foramen.
-> The internal surface of the mandible is divided into two areas by the mylohyoid line, which commences posterior to the third molar tooth. -> Just superior to the anterior end of the mylohyoid line are two small, sharp mental spines (genial tubercles), which serve as attachments for the genioglssus muscles.
The Zygomatic Bones
-> The prominences of the cheeks (L. mala), the anterolateral rims and much of the infraorbital margins of the orbits, are formed by the zygomatic bones (malar bones, cheekbones).
-> They articulate with the frontal, maxilla, sphenoid, and temporal bones.
-> The frontal process of the zygomatic bone passes superiorly, where it forms the lateral border of the orbit (eye socket) and articulates with the frontal bone at the lateral edge of the supraorbital margin.
-> The zygomatic bones articulate medially with the greater wings of the sphenoid bone. The site of their articulation may be observed on the lateral wall of the orbit.
-> On the anterolateral aspect of the zygomatic bone near the infraorbital margin is a small zygomaticofacial foramen for the nerve and vessels of the same name.
-> The posterior surface of the zygomatic bone near the base of its frontal process is pierced by a small zygomaticotemporal foramen for the nerve of the same name.
-> The zygomaticofacial and zygomaticotemporal nerves, leaving the orbit through the previously named foramina, enter the zygomatic bone through small zygomaticoorbital foramina that pierces it orbital surface.
-> The temporal process of the zygomatic bone unites with the zygomatic process of the temporal bone to form the zygomatic arch.
-> This arch can be easily palpated on the side of the head, posterior to the zygomatic prominence (malar eminence) at the inferior boundary of the temporal fossa (temple).
-> The zygomatic arches form one of the useful landmarks for determining the location of the pterion. These arches are especially prominent in emaciated persons.
-> A horizontal plane passing medially from the zygomatic arch separates the temporal fossa superiorly from the infratemporal fossa inferiorly.
Other Bones
There are several other, very important bones in the skull, including the palatine bone, ethmoid bone, vomer, inferior concha and the ossicles of the ear (malleus, incus and stapes). These, however, are covered to greater detail where they are relevant in the head (e.g., ethmoid bone with the orbit and nasal cavity).
Gout
General Pathology
Gout
This is a disorder caused by the tissue accumulation of excessive amounts of uric acid, an end product of purine metabolism. It is marked by recurrent episodes of acute arthritis, sometimes accompanied by the formation of large crystalline aggregates called tophi & chronic joint deformity. All of these are the result of precipitation of monosodium urate crystals from supersaturated body fluids. Not all individuals with hyperuricemia develop gout; this indicates that influences besides hyperuricemia contribute to the pathogenesis. Gout is divided into primary (90%) and secondary forms (10%).
Primary gout designates cases in whom the basic cause is unknown or when it is due to an inborn metabolic defect that causes hyperuricemia.
In secondary gout the cause of the hyperuricemia is known.
Pathologic features
The major morphologic manifestations of gout are
1. Acute arthritis
2. Chronic tophaceous arthritis
3. Tophi in various sites, and
4. Gouty nephropathy
Acute arthritis
- The synovium is edematous and congested,
- There is an intense infiltration of the synovium & synovial fluid by neutrophils.
- Long, slender, needle-shaped monosodium urate crystals are frequently found in the cytoplasm of the neutrophils as well as in small clusters in the synovium.
Chronic tophaceous arthritis:
- This evolves from repetitive precipitation of urate crystals during acute attacks. The urates can heavily encrust the articular surfaces and form visible deposits in the synovium.
- The synovium becomes hyperplastic, fibrotic, and thickened by inflammatory cells, forming a pannus that destroys the underlying cartilage, and leading to erosions of subjacent bone.
- In severe cases, fibrous or bony ankylosis occurs, resulting in loss of joint function.
Tophi
These are the pathognomonic hallmarks of gout.
- Tophi can appear in the articular cartilage, periarticular ligaments, tendons, and soft tissues, including the ear lobes. Superficial tophi can lead to large ulcerations of the overlying skin.
- Microscopically, they are formed by large aggregations of urate crystals surrounded by an intense inflammatory reaction of lymphocytes, macrophages, and foreign-body giant cells, attempting to engulf the masses of crystals.
Gouty nephropathy
- This refers to the renal complications associated with urate deposition including medullary tophi, intratubular precipitations and renal calculi. Secondary complications such as pyelonephritis can occur, especially when there is urinary obstruction.
Pathogenesis
- Although the cause of excessive uric acid biosynthesis in primary gout is unknown in most cases, rare patients have identifiable enzymatic defects or deficiencies that are associated with excess production of uric acid.
- In secondary gout, hyperuricemia can be caused by increased urate production (e.g., rapid cell lysis during chemotherapy for lymphoma or leukemia) or decreased excretion (chronic renal failure), or both. Reduced renal excretion may also be caused by drugs such as thiazide diuretics, because of their effects on uric acid tubular transport.
- Whatever the cause, increased levels of uric acid in the blood and other body fluids (e.g., synovium) lead to the precipitation of monosodium urate crystals. The precipitated crystals are chemotactic to neutrophils & macrophages through activation of complement components C3a and C5a fragments. This leads to a local accumulation of neutrophils and macrophages in the joints and synovial membranes to phagocytize the crystals. The activated neutrophils liberate destructive lysosomal enzymes. Macrophages participate in joint injury by secreting a variety of proinflammatory mediators such as IL-1, IL-6, and TNF. While intensifying the inflammatory response, these cytokines can also directly activate synovial cells and cartilage cells to release proteases (e.g., collagenases) that cause tissue injury.
- Repeated bouts of acute arthritis, however, can lead to the permanent damage seen in chronic tophaceous arthritis.
b Pseudogout (chondrocalcinosis) (Calcium pyrophosphate crystal deposition disease). Pseudogout typically first occurs in the age 50 years or older. It involves enzymes that lead to accumulation and eventual crystallization of pyrophosphate with calcium. The pathology in pseudogout involves the recruitment and activation of inflammatory cells, and is reminiscent of gout. The knees, followed by the wrists, elbows,
shoulders, and ankles, are most commonly affected. Approximately 50% of patients experience significant joint damage.
Infectious Arthritis can cause rapid joint destruction and permanent deformities. Microorganisms can lodge in joints during hematogenous dissemination, by direct inoculation or by contiguous spread from osteomyelitis or a soft tissue abscess.
Suppurative Arthritis is a subtype of infectious arthritis in which the bacteria seed the joint during episodes of bacteremia. Haemophilus influenzae predominates in children under age 2 years, S. aureus is the main causative agent in older children and adults, and gonococcus is prevalent during late adolescence and young adulthood.
There is sudden onset of pain, redness, and swelling of the joint with fever, leukocytosis, and elevated ESR. In 90% of nongonococcal suppurative arthritis, the infection involves only a single joint-usually the knee. Joint aspiration is typically purulent, and allows identification of the causal agent.
Twin Block appliance
OrthodonticsTwin Block appliance is a removable functional orthodontic
device designed to correct malocclusion by positioning the lower jaw forward. It
consists of two interlocking bite blocks, one for the upper jaw and one for the
lower jaw, which work together to align the teeth and improve jaw relationships.
Features of the Twin Block Appliance
Design: The Twin Block consists of two separate
components that fit over the upper and lower teeth, promoting forward
movement of the lower jaw.
Functionality: It utilizes the natural bite forces to
gradually shift the lower jaw into a more favorable position, addressing
issues like overbites and jaw misalignments.
Material: Typically made from acrylic, the appliance is
custom-fitted to ensure comfort and effectiveness during treatment.
Treatment Process
Initial Consultation:
A comprehensive evaluation is conducted, including X-rays and
impressions to assess the alignment of teeth and jaws.
Fitting the Appliance:
Once ready, the Twin Block is fitted and adjusted to the patient's
mouth. Initial discomfort may occur but usually subsides quickly.
Active Treatment Phase:
Patients typically wear the appliance full-time for about 12 to 18
months, with regular check-ups for adjustments.
Retention Phase:
After active treatment, a retainer may be required to maintain the
new jaw position while the bone stabilizes.
Benefits of the Twin Block Appliance
Non-Surgical Solution: Offers a less invasive
alternative to surgical options for correcting jaw misalignments.
Improved Functionality: Enhances chewing, speaking, and
overall jaw function by aligning the upper and lower jaws.
Facial Aesthetics: Contributes to a more balanced facial
profile, boosting self-esteem and confidence.
Faster Results: Compared to traditional braces, the Twin
Block can provide quicker corrections, especially in growing patients.
Care and Maintenance
Oral Hygiene: Patients should maintain good oral hygiene
by brushing and flossing regularly, especially around the appliance.
Food Restrictions: Avoid hard, sticky, or chewy foods
that could damage the appliance.
Regular Check-Ups: Attend scheduled appointments to
ensure the appliance is functioning correctly and to make necessary
adjustments.
Regulation of glomerular filtration
Physiology
Regulation of glomerular filtration :
1. Extrinsic regulation :
- Neural regulation : sympathetic and parasympathetic nervous system which causes vasoconstriction or vasodilation respectively .
- Humoral regulation : Vasoactive substances may affect the GFR , vasoconstrictive substances like endothelin ,Angiotensin II , Norepinephrine , prostaglandine F2 may constrict the afferent arteriole and thus decrease GFR , while the vasodilative agents like dopamine , NO , ANP , Prostaglandines E2 may dilate the afferent arteriole and thus increase the filtration rate .
2. Intrinsic regulation :
- Myogenic theory ( as in the intrinsic regulation of cardiac output) .
- Tubuloglomerular feedback: occurs by cells of the juxtaglomerular apparatus that is composed of specific cells of the distal tubules when it passes between afferent and efferent arterioles ( macula densa cells ) , these cells sense changes in flow inside the tubules and inform specific cells in the afferent arteriole (granular cells ) , the later secrete vasoactive substances that affect the diameter of the afferent arteriole.
Hemorrhage
Oral and Maxillofacial SurgeryTypes of Hemorrhage
Hemorrhage, or excessive bleeding, can occur during and after surgical
procedures. Understanding the different types of hemorrhage is crucial for
effective management and prevention of complications. The three main types of
hemorrhage are primary, reactionary, and secondary hemorrhage.
1. Primary Hemorrhage
Definition: Primary hemorrhage refers to bleeding that
occurs at the time of surgery.
Causes:
Injury to blood vessels during the surgical procedure.
Inadequate hemostasis (control of bleeding) during the operation.
Management:
Immediate control of bleeding through direct pressure,
cauterization, or ligation of blood vessels.
Use of hemostatic agents or sutures to secure bleeding vessels.
Clinical Significance: Prompt recognition and
management of primary hemorrhage are essential to prevent significant blood
loss and ensure patient safety during surgery.
2. Reactionary Hemorrhage
Definition: Reactionary hemorrhage occurs within a few
hours after surgery, typically when the initial vasoconstriction of damaged
blood vessels subsides.
Causes:
The natural response of blood vessels to constrict after injury may
initially control bleeding. However, as the vasoconstriction diminishes,
previously damaged vessels may begin to bleed again.
Movement or changes in position of the patient can also contribute
to the reopening of previously clamped vessels.
Management:
Monitoring the patient closely in the immediate postoperative period
for signs of bleeding.
If reactionary hemorrhage occurs, surgical intervention may be
necessary to identify and control the source of bleeding.
Clinical Significance: Awareness of the potential for
reactionary hemorrhage is important for postoperative care, as it can lead
to complications if not addressed promptly.
3. Secondary Hemorrhage
Definition: Secondary hemorrhage refers to bleeding
that occurs up to 14 days postoperatively, often as a result of infection or
necrosis of tissue.
Causes:
Infection at the surgical site can lead to tissue breakdown and
erosion of blood vessels, resulting in bleeding.
Sloughing of necrotic tissue may also expose blood vessels that were
previously protected.
Management:
Careful monitoring for signs of infection, such as increased pain,
swelling, or discharge from the surgical site.
Surgical intervention may be required to control bleeding and
address the underlying infection.
Antibiotic therapy may be necessary to treat the infection and
prevent further complications.
Clinical Significance: Secondary hemorrhage can be a
serious complication, as it may indicate underlying issues such as infection
or inadequate healing. Early recognition and management are crucial to
prevent significant blood loss and promote recovery.
Anti-Infective and Anticariogenic Agents
PedodonticsAnti-Infective and Anticariogenic Agents in Human Milk
Human milk is not only a source of nutrition for infants but also contains
various bioactive components that provide anti-infective and anticariogenic
properties. These components play a crucial role in protecting infants from
infections and promoting oral health. Below are the key agents found in human
milk:
1. Immunoglobulins
Secretory IgA: The predominant immunoglobulin in human
milk, secretory IgA plays a vital role in mucosal immunity by preventing the
attachment of pathogens to mucosal surfaces.
IgG and IgM: These immunoglobulins also contribute to
the immune defense, with IgG providing systemic immunity and IgM being
involved in the initial immune response.
2. Cellular Elements
Lymphoid Cells: These cells are part of the immune
system and help in the recognition and response to pathogens.
Polymorphonuclear Leukocytes (Polymorphs): These white
blood cells are essential for the innate immune response, helping to engulf
and destroy pathogens.
Macrophages: These cells play a critical role in
phagocytosis and the immune response, helping to clear infections.
Plasma Cells: These cells produce antibodies,
contributing to the immune defense.
3. Complement System
C3 and C4 Complement Proteins: These components of the
complement system have opsonic and chemotactic activities, enhancing the
ability of immune cells to recognize and eliminate pathogens. They promote
inflammation and attract immune cells to sites of infection.
4. Unsaturated Lactoferrin and Transferrin
Lactoferrin: This iron-binding protein has
antimicrobial properties, inhibiting the growth of bacteria and fungi by
depriving them of iron.
Transferrin: Similar to lactoferrin, transferrin also
binds iron and plays a role in iron metabolism and immune function.
5. Lysozyme
Function: Lysozyme is an enzyme that breaks down
bacterial cell walls, providing antibacterial activity. It helps protect the
infant from bacterial infections.
6. Lactoperoxidase
Function: This enzyme produces reactive oxygen species
that have antimicrobial effects, contributing to the overall antibacterial
properties of human milk.
7. Specific Inhibitors (Non-Immunoglobulins)
Antiviral and Antistaphylococcal Factors: Human milk
contains specific factors that inhibit viral infections and the growth of
Staphylococcus bacteria, providing additional protection against infections.
8. Growth Factors for Lactobacillus Bifidus
Function: Human milk contains growth factors that
promote the growth of beneficial bacteria such as Lactobacillus bifidus,
which plays a role in maintaining gut health and preventing pathogenic
infections.
9. Para-Aminobenzoic Acid (PABA)
Function: PABA may provide some protection against
malaria, highlighting the potential role of human milk in offering broader
protective effects against various infections.
Acid Etching on Enamel
Conservative DentistryEffects of Acid Etching on Enamel
Acid etching is a critical step in various dental procedures, particularly in
the bonding of restorative materials to tooth structure. This process modifies
the enamel surface to enhance adhesion and improve the effectiveness of dental
materials. Below are the key effects of acid etching on enamel:
1. Removal of Pellicle
Pellicle Removal: Acid etching effectively removes the
acquired pellicle, a thin film of proteins and glycoproteins that forms on
the enamel surface after tooth cleaning.
Exposure of Inorganic Crystalline Component: By
removing the pellicle, the underlying inorganic crystalline structure of the
enamel is exposed, allowing for better interaction with bonding agents.
2. Creation of a Porous Layer
Porous Layer Formation: Acid etching creates a porous
layer on the enamel surface.
Depth of Pores: The depth of these pores typically
ranges from 5 to 10 micrometers (µm), depending on the concentration and
duration of the acid application.
Increased Surface Area: The formation of these pores
increases the surface area available for bonding, enhancing the mechanical
retention of restorative materials.
3. Increased Wettability
Wettability Improvement: Acid etching increases the
wettability of the enamel surface.
Significance: Improved wettability allows bonding
agents to spread more easily over the etched surface, facilitating better
adhesion and reducing the risk of voids or gaps.
4. Increased Surface Energy
Surface Energy Elevation: The etching process raises
the surface energy of the enamel.
Impact on Bonding: Higher surface energy enhances the
ability of bonding agents to adhere to the enamel, promoting a stronger bond
between the tooth structure and the restorative material.
The Parathyroid Glands
Physiology
The Parathyroid Glands
The parathyroid glands are 4 tiny structures embedded in the rear surface of the thyroid gland. They secrete parathyroid hormone (PTH) a polypeptide of 84 amino acids. PTH increases the concentration of Ca2+ in the blood in three ways. PTH promotes
release of Ca2+ from the huge reservoir in the bones. (99% of the calcium in the body is incorporated in our bones.)
reabsorption of Ca2+ from the fluid in the tubules in the kidneys
absorption of Ca2+ from the contents of the intestine (this action is mediated by calcitriol, the active form of vitamin D.)
PTH also regulates the level of phosphate in the blood. Secretion of PTH reduces the efficiency with which phosphate is reclaimed in the proximal tubules of the kidney causing a drop in the phosphate concentration of the blood.
Hyperparathyroidism
Elevate the level of PTH causing a rise in the level of blood Ca2+ .Calcium may be withdrawn from the bones that they become brittle and break.
Patients with this disorder have high levels of Ca2+ in their blood and excrete small amounts of Ca2+ in their urine. This causes hyperparathyroidism.
Hypoparathyroidism
This disorder have low levels of Ca2+ in their blood and excrete large amounts of Ca2+ in their urine.