NEET MDS Synopsis
Full Mucoperiosteal Flap Design in Periradicular Surgery
EndodonticsA full mucoperiosteal flap is a critical component in periradicular surgery,
allowing access to the underlying bone and root structures for effective
treatment. This flap design includes the surface mucosa, submucosa, and
periosteum, providing adequate visibility and access to the surgical site.
Here’s a detailed overview of the flap design, its types, and considerations in
periradicular surgery.
Key Components of Full Mucoperiosteal Flap
Surface Mucosa:
The outermost layer that is reflected during the flap procedure.
Submucosa:
The layer beneath the mucosa that contains connective tissue and
blood vessels.
Periosteum:
A dense layer of vascular connective tissue that covers the outer
surface of bones, providing a source of blood supply during healing.
Flap Design Types
Two-Sided (Triangular) Flap:
Description: Created with a horizontal
intrasulcular incision and a vertical relieving incision.
Indications: Commonly used for anterior teeth.
Advantages: Provides good access while preserving
the interdental papilla.
Drawbacks: May be challenging to re-approximate the
tissue.
Three-Sided (Rectangular) Flap:
Description: Involves a horizontal intrasulcular
incision and two vertical relieving incisions.
Indications: Used for posterior teeth.
Advantages: Increases surgical access to the root
surface.
Drawbacks: Difficult to re-approximate the tissue
and may lead to scarring.
Envelope Flap:
Description: A horizontal intrasulcular incision
without vertical relieving incisions.
Indications: Provides access to the buccal aspect
of the tooth.
Advantages: Minimally invasive and preserves more
tissue.
Drawbacks: Limited access to the root surface.
Surgical Procedure Steps
Local Anesthesia:
Administer local anesthesia to ensure patient comfort during the
procedure.
Incision:
Make a horizontal intrasulcular incision along the gingival margin,
followed by vertical relieving incisions as needed.
Flap Reflection:
Carefully reflect the flap to expose the underlying bone and root
structures.
Bone Removal and Curettage:
Remove any bone or granulation tissue as necessary to access the
root surface.
Apicectomy and Retrograde Filling:
Perform apicectomy if indicated and prepare the root end for
retrograde filling.
Flap Re-approximation:
Re-approximate the flap and secure it with sutures to promote
healing.
Postoperative Care:
Provide instructions for postoperative care, including the use of
ice packs and gauze to control bleeding.
Considerations
Haemostasis:
Achieving and maintaining haemostasis is crucial for optimal
visualization and healing. Techniques include the use of local
anesthetics with vasoconstrictors and topical hemostatic agents.
Tissue Preservation:
Care should be taken to preserve as much tissue as possible to
enhance healing and minimize scarring.
Postoperative Monitoring:
Monitor the surgical site for signs of infection or complications
during the healing process.
Limited Mucoperiosteal Flap Design in Periradicular Surgery
Limited mucoperiosteal flaps are essential in periradicular surgery,
particularly for accessing the root surfaces while minimizing trauma to the
surrounding tissues. This flap design is characterized by specific incisions and
techniques that aim to enhance surgical visibility and access while promoting
better healing outcomes.
Limited Mucoperiosteal Flaps
Definition: Limited mucoperiosteal flaps involve
incisions that do not include marginal or interdental tissues, focusing on
preserving the integrity of the surrounding soft tissues.
Purpose: These flaps are designed to provide access to
the root surfaces for procedures such as apicoectomy, root resection, or
treatment of periapical lesions.
Types of Limited Mucoperiosteal Flaps
Submarginal Horizontal Incision
Description: A horizontal incision made in the
attached gingiva, avoiding the marginal gingiva.
Advantages: Preserves the marginal tissue, reducing
the risk of gingival recession and scarring.
Semilunar Flap
Description: A curved incision that begins in the
alveolar mucosa, dips into the attached gingiva, and returns to the
alveolar mucosa.
Advantages: Provides access while minimizing trauma
to the marginal tissue; however, it has poor healing potential and may
lead to scarring.
Scalloped (Ochsenbein-Luebke) Flap
Description: Similar to the rectangular flap but
with a scalloped horizontal incision in the attached gingiva.
Advantages: Follows the contour of the gingival
margins, preserving aesthetics but is also prone to delayed healing and
scarring.
Surgical Technique
Incision: The flap is initiated with a careful incision
in the attached gingiva, ensuring that the marginal tissue remains intact.
Reflection: The flap is gently reflected to expose the
underlying bone and root surfaces, allowing for the necessary surgical
procedures.
Irrigation and Closure: After the procedure, the area
should be well-irrigated to prevent infection, and the flap is
re-approximated and sutured in place.
Clinical Considerations
Healing Potential: Limited mucoperiosteal flaps
generally have better healing potential compared to full mucoperiosteal
flaps, as they preserve more of the surrounding tissue.
Aesthetic Outcomes: These flaps are particularly
beneficial in aesthetic zones, as they minimize the risk of visible scarring
and gingival recession.
Postoperative Care: Proper postoperative care,
including the use of ice packs and digital pressure on gauze, is essential
to control bleeding and promote healing.
Drawbacks
Limited Access: While these flaps minimize trauma, they
may provide limited access to the root surfaces, which can be a disadvantage
in complex cases.
Healing Complications: Although they generally promote
better healing, there is still a risk of complications such as delayed
healing or scarring, particularly with semilunar and scalloped designs.
Conclusion
Limited mucoperiosteal flap designs are valuable in periradicular surgery,
offering a balance between surgical access and preservation of surrounding
tissues. Understanding the various types of flaps and their applications can
significantly enhance the outcomes of endodontic surgical procedures. Proper
technique and postoperative care are crucial for achieving optimal healing and
aesthetic results.
Other coxibs
Pharmacology
Valdecoxib
used in the treatment of osteoarthritis, acute pain conditions, and dysmenorrhoea
Etoricoxib new COX-2 selective inhibitor
Lamotrigine
Pharmacology
Lamotrigine (Lamictal): newer; broad spectrum (for most seizure types)
Mechanism: ↓ reactivation of Na channels (↑ refractory period, blocks high frequency cell firing)
Side effects: dizziness, ataxia, fatigue, nausea, no significant drug interactions
Classification of Cementum
Dental Anatomy
Classification of Cementum
Embryologically
Primary and secondary
2. According to cellular component
Acellular: Thin, Amorphous, First layer to seal the dentin tubules
Cellular: Thick, Better structure, Apical surface
Layers of cellular and acellular cementum alternate (randomly)
3. Based on the origin of the collagenous matrix
Extrinsic
Intrinsic
Mixed
4. Combined classification
a. Primary acellular intinsic fiber cementum
b. Primary acellualar extrinsic fiber cementum
c. Secondary cellular intrinsic fiber cementum
d. Secondary cellular mixed fiber cementum
e. Acellular afibrillar cementum
5. Depending on the location and patterning
Intermediate and mixed stratified cementum
Participating Cells
Cementoblasts
Active
Cells are round, plump with basophilic cytoplasm (rough endoplasmic reticulum)
Inactive
Cells have little cytoplasm
Cementocytes
Cementocyte lacuna
cementocyte canaliculus
Cells have fewer organelles compared to cementoblasts. They are found in lacunae and have numerous processes toward the periodontal ligament. Eventually they die due to avascularity
Cementicles
a) free
b) attached
c) embedded
INNATE (NON-SPECIFIC) IMMUNITY
General Microbiology
INNATE (NON-SPECIFIC) IMMUNITY
The elements of the innate (non-specific) immune system include anatomical barriers, secretory molecules and cellular components.
Among the mechanical anatomical barriers are the skin and internal epithelial layers, the movement of the intestines and the oscillation of broncho-pulmonary cilia.
Associated with these protective surfaces are chemical and biological agents.
A. Anatomical barriers to infections
1. Mechanical factors
The epithelial surfaces form a physical barrier that is very impermeable to most infectious agents. Thus, the skin acts as our first line of defense against invading organisms. The desquamation of skin epithelium also helps remove bacteria and other infectious agents that have adhered to the epithelial surfaces.
2. Chemical factors
Fatty acids in sweat inhibit the growth of bacteria. Lysozyme and phospholipase found in tears, saliva and nasal secretions can breakdown the cell wall of bacteria and destabilize bacterial membranes. The low pH of sweat and gastric secretions prevents growth of bacteria. Defensins (low molecular weight proteins) found in the lung and gastrointestinal tract have antimicrobial activity. Surfactants in the lung act as opsonins (substances that promote phagocytosis of particles by phagocytic cells).
3. Biological factors
The normal flora of the skin and in the gastrointestinal tract can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.
B. Humoral barriers to infection
Humoral factors play an important role in inflammation, which is characterized by edema and the recruitment of phagocytic cells. These humoral factors are found in serum or they are formed at the site of infection.
1. Complement system – The complement system is the major humoral non-specific defense mechanism (see complement chapter). Once activated complement can lead to increased vascular permeability, recruitment of phagocytic cells, and lysis and opsonization of bacteria.
2. Coagulation system – Depending on the severity of the tissue injury, the coagulation system may or may not be activated. Some products of the coagulation system can contribute to the non-specific defenses because of their ability to increase vascular permeability and act as chemotactic agents for phagocytic cells. In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysin, a protein produced by platelets during coagulation can lyse many Gram positive bacteria by acting as a cationic detergent.
3. Lactoferrin and transferrin – By binding iron, an essential nutrient for bacteria, these proteins limit bacterial growth.
4. Interferons – Interferons are proteins that can limit virus replication in cells.
5. Lysozyme – Lysozyme breaks down the cell wall of bacteria.
6. Interleukin -1 – Il-1 induces fever and the production of acute phase proteins, some of which are antimicrobial because they can opsonize bacteria.
C. Cellular barriers to infection
Part of the inflammatory response is the recruitment of polymorphonuclear eosinophiles and macrophages to sites of infection. These cells are the main line of defense in the non-specific immune system.
1. Neutrophils – Polymorphonuclear cells are recruited to the site of infection where they phagocytose invading organisms and kill them intracellularly. In addition, PMNs contribute to collateral tissue damage that occurs during inflammation.
2. Macrophages – Tissue macrophages and newly recruited monocytes , which differentiate into macrophages, also function in phagocytosis and intracellular killing of microorganisms. In addition, macrophages are capable of extracellular killing of infected or altered self target cells. Furthermore, macrophages contribute to tissue repair and act as antigen-presenting cells, which are required for the induction of specific immune responses.
3. Natural killer (NK) and lymphokine activated killer (LAK) cells – NK and LAK cells can nonspecifically kill virus infected and tumor cells. These cells are not part of the inflammatory response but they are important in nonspecific immunity to viral infections and tumor surveillance.
4. Eosinophils – Eosinophils have proteins in granules that are effective in killing certain parasites.
Physiology
PhysiologyPhysiology - science that describes how organisms FUNCTION and survive in continually changing environments
Muscle pathology
General Pathology
Muscle pathology
1. Myasthenia gravis
a. An autoimmune disease caused by autoantibodies to acetylcholine receptors at the neuromuscular junctions.
b. Characterized by muscle weakness or the inability to maintain long durations of muscle contractions; this worsens during exercise but recovers after rest.
c. Affects various muscle groups, including:
(1) Eyes—diplopia, ptosis.
(2) Neck—dysphagia, problems swallowing or speaking.
(3) Extremities—arms and legs.
d. Treatment: cholinesterase inhibitors(neostigmine), anti-immune therapy.
2. Muscle tumors
a. Rhabdomyoma—benign tumor of skeletal muscle.
b. Leiomyoma
(1) Benign tumor of smooth muscle.
(2) Most common tumor found in women.
(3) Usually affects the uterus, although it can occur anywhere.
c. Rhabdomyosarcoma
(1) Malignant tumor of skeletal muscle.
(2) Most common sarcoma found in children.
(3) Usually affects head and neck region—orbit, nasal cavity, and nasopharynx.
The Sliding Filament mechanism of muscle contraction
PhysiologyThe Sliding Filament mechanism of muscle contraction.
When a muscle contracts the light I bands disappear and the dark A bands move closer together. This is due to the sliding of the actin and myosin myofilaments against one another. The Z-lines pull together and the sarcomere shortens
The thick myosin bands are not single myosin proteins but are made of multiple myosin molecules. Each myosin molecule is composed of two parts: the globular "head" and the elongated "tail". They are arranged to form the thick bands.
It is the myosin heads which form crossbridges that attach to binding sites on the actin molecules and then swivel to bring the Z-lines together
Likewise the thin bands are not single actin molecules. Actin is composed of globular proteins (G actin units) arranged to form a double coil (double alpha helix) which produces the thin filament. Each thin myofilament is wrapped by a tropomyosin protein, which in turn is connected to the troponin complex.
The tropomyosin-troponin combination blocks the active sites on the actin molecules preventing crossbridge formation. The troponin complex consists of three components: TnT, the part which attaches to tropomyosin, TnI, an inhibitory portion which attaches to actin, and TnC which binds calcium ions. When excess calcium ions are released they bind to the TnC causing the troponin-tropomyosin complex to move, releasing the blockage on the active sites. As soon as this happens the myosin heads bind to these active sites.