NEET MDS Synopsis
Periodontal Medications
PeriodontologyPeriodontal Medications and Their Uses
Periodontal medications play a crucial role in the management of periodontal
diseases, aiding in the treatment of infections, inflammation, and tissue
regeneration. Understanding the various types of medications and their specific
uses is essential for effective periodontal therapy.
Types of Periodontal Medications
Antibiotics:
Uses:
Used to treat bacterial infections associated with periodontal
disease.
Commonly prescribed antibiotics include amoxicillin,
metronidazole, and doxycycline.
Mechanism:
They help reduce the bacterial load in periodontal pockets,
promoting healing and reducing inflammation.
Antimicrobial Agents:
Chlorhexidine:
Uses: A topical antiseptic used as a mouth
rinse to reduce plaque and gingivitis.
Mechanism: It disrupts bacterial cell membranes
and inhibits bacterial growth.
Tetracycline:
Uses: Can be used topically in periodontal
pockets to reduce bacteria.
Mechanism: Inhibits protein synthesis in
bacteria, reducing their ability to cause infection.
Anti-Inflammatory Medications:
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs):
Uses: Used to manage pain and inflammation
associated with periodontal disease.
Examples: Ibuprofen and naproxen.
Corticosteroids:
Uses: May be used in severe cases to reduce
inflammation.
Mechanism: Suppress the immune response and
reduce inflammation.
Local Delivery Systems:
Doxycycline Gel (Atridox):
Uses: A biodegradable gel that releases
doxycycline directly into periodontal pockets.
Mechanism: Provides localized antibiotic
therapy to reduce bacteria and inflammation.
Minocycline Microspheres (Arestin):
Uses: A localized antibiotic treatment that is
placed directly into periodontal pockets.
Mechanism: Releases minocycline over time to
combat infection.
Regenerative Agents:
Bone Grafts and Guided Tissue Regeneration (GTR) Materials:
Uses: Used in surgical procedures to promote
the regeneration of lost periodontal tissues.
Mechanism: Provide a scaffold for new tissue
growth and prevent the ingrowth of epithelium into the defect.
Desensitizing Agents:
Fluoride Varnishes:
Uses: Applied to sensitive areas to reduce
sensitivity and promote remineralization.
Mechanism: Strengthens enamel and reduces
sensitivity by occluding dentinal tubules.
Clinical Significance of Periodontal Medications
Management of Periodontal Disease:
Medications are essential in controlling infections and
inflammation, which are critical for the successful treatment of
periodontal diseases.
Adjunct to Non-Surgical Therapy:
Periodontal medications can enhance the effectiveness of
non-surgical treatments, such as scaling and root planing, by reducing
bacterial load and inflammation.
Surgical Interventions:
In surgical procedures, medications can aid in healing and
regeneration, improving outcomes for patients undergoing periodontal
surgery.
Patient Compliance:
Educating patients about the importance of medications in their
treatment plan can improve compliance and overall treatment success.
Antiplatelet Drugs
Pharmacology
Antiplatelet Drugs
Aspirin/ASA
- Works on Cyclo-oxygenase (AA -> thromboxane)
- Low dose (80-160 mg/day) irreversibly inhibits plt COX, and they can’t make new COX b/c they have no nucleus
- Some inhibition of endothelial COX but not much, therefore prostacyclin (anti-coag) synthesis isn’t affected much
- Benefit is greater after thrombolysis
- SE is bleeding
- Prophylaxis for MI or TIA (80mg/day), higher doses for post-MI/TIA (160-325mg/day)
- Contraindications (bleeding risk): Vit. K def., Hemophilia, Hypoprothombinemia, pregnancy & childbirth
Clopidogrel/Plavix
- ADP antagonist
- Competes with ADP for P2Y receptor (prevents lowering of cAMP)
- Less incidence of neutropenia/thrombocytopenia
- Used in combo with ASA
Ticlopidine
- ADP antagonist, prodrug
- Often used in combo with ASA (synergistic)
- May cause severe neutropenia (1%)
Dipyridamole
- phosphodiesterase inhibitor (prevents cAMP breakdown)
GpIIb-IIIa inhibitors
- Eptifibatide, Abciximab, Tirofiban
- Block the receptor for fibrinogen blocking plt Aggregation
Heparin (& derivatives)
- Stimulates natural anticoags (antithrombin)
Heparin
- Monitor using aPTT (add negative charges)
- Negatively charged, therefore cannot cross membranes (given IM, IV, parentally)
- Good for pregnancy
- Eliminated by RES & macrophages
- Potentiates AT III (in the plasma) – inhibits IIa, Xa, IXa and VIIa
- Toxicity – hemorrhage
- Antidote – protamine sulfate (1mg for every 100 units of heparin)
Heparin-Induced Thrombocytopenia (HIT) – occurs 5-10 days after, stop heparin immediately; use alternatives lepirudin/danaparoid
- Good for PE and DVT and during pregnancy
LMWH – better bioavailability, can be given subcut. w/o lab monitoring as outpatient, less risk of bleeding
- More expensive, not good in renal failure, not for pregnancy
- DOES NOT inhibit IIa (but inhibit Xa)
- Good for DVT, PE and UA
Danaparoid – promotes inhibition of Xa by AT (for HIT)
Lepirudin – direct thrombin inhibitor (for HIT)
Coumarin (Oral) anticoags
Warfarin
- Monitored using PT (add tissue factor)
- Inhibit Vit. K Epoxide reductase in liver
-Prevents carboxylation of Vit.K dependent factors
-Takes 4-5 days to get effective (carboxylated fx’s in plasma need to be cleared before inactive ones take over)
-Small volume of distribution, steep dose-response curve (small therapeutic window)
-Teratogenic
- For DVT and PE, prosthetic heart valves or Afib, MI
-Metabolized by CYP1A and CYP2C9
-Efficacy measured by INR, pt’s PT time divided by PT time in pooled plasma
- INR = (PTpt/PTref)^ISI (target is 2.0 – 3.0)
- Warfarin overdose
- Give Excess Vit.K, goes through a diff enzyme that isn’t inhibited by warfarin (Diaphorase)
Fibrinolytics (lyse formed thrombi)
Streptokinase – turns plasminogen -> plasmin
-Plasmin breaks down fibrin (lysis of formed clot) Dissolves clots post-MI/DVT/PE
- SE – bleeding (systemic plasminogen activation), allergy, hTN, fever
- Streptokinase has an additive effect with ASA
Tissue plasminogen activator (tPA) – acts on fibrin and circulating plasminogen -> plasmin
- Less systemic plasmin
- Same indications as streptokinase
- More expensive
Direct Pulp Capping
EndodonticsDirect pulp capping is a minimally invasive endodontic procedure used to
preserve the vitality of the tooth's pulp when it is exposed due to caries or
trauma. The goal is to induce a biological response that leads to the formation
of dentin-bridge to seal the pulp and prevent further infection.
Indications:
- Cariously exposed pulp that is asymptomatic and has no evidence of
irreversible pulpitis.
- Recent traumatic exposure of the pulp with no signs of necrosis or infection.
- Presence of a thin layer of residual dentin over the pulp.
Contraindications:
- Signs of irreversible pulpitis or pulpal necrosis.
- Presence of a deep carious lesion that may lead to pulpal exposure during
restoration.
- Large pulp exposures or when the pulp is exposed for an extended period.
- Immunocompromised patients or those with poor oral hygiene.
Procedure:
1. Local anesthesia: Numb the tooth and surrounding tissue to ensure patient
comfort.
2. Caries removal: Carefully remove caries and any infected dentin using a
high-speed handpiece with water spray to prevent pulp exposure.
3. Hemostasis: Apply a mild hemostatic agent if necessary to control bleeding.
4. Pulp conditioning: Apply a calcium hydroxide paste or a bioactive material to
the exposed pulp for a brief period.
5. Application of the capping material: Place a bioactive material, such as
mineral trioxide aggregate (MTA), calcium silicate, or a glass ionomer cement,
directly over the pulp.
6. Restoration: Seal the tooth with a temporary restoration material and place a
final restoration (usually a composite resin) to protect the pulp from further
trauma.
7. Follow-up: Monitor the tooth for signs of pain, swelling, or discoloration.
If these symptoms occur, a root canal treatment may be necessary.
Advantages:
- Preservation of pulp vitality.
- Reduced need for root canal treatment.
- Faster healing and less post-operative sensitivity.
- Conservative approach, maintaining more natural tooth structure.
Disadvantages:
- Limited success in deep or prolonged exposures.
- Higher risk of failure in certain cases, such as extensive caries or pulp
exposure.
- Requires careful technique to avoid further pulp damage.
Maxillary Third Permanent Molar
Dental Anatomy
Maxillary Third Permanent Molar
They are the teeth most often congenitally missing
Facial: The crown is usually shorter in both axial and mesiodistal dimensions. Two buccal roots are present, but in most cases they are fused. The mesial buccal cusp is larger than the distal buccal cusp.
Lingual: In most thirds, there is just one large lingual cusp. In some cases there is a poorly developed distolingual cusp and a lingual groove. The lingual root is often fused to the to buccal cusps.
Proximal: The outline of the crown is rounded; it is often described as bulbous in dental literature. Technically, the mesial surface is the only 'proximal' surface. The distal surface does not contact another tooth.
Occlusal: The crown of this tooth is the smallest of the maxillary molars. The outline of the occlusal surface can be described as heart-shaped. The mesial lingual cusp is the largest, the mesial buccal is second in size, and the distal buccal cusp is the smallest.
Root Surface:-The root may have from one to as many as eight divisions. These divisions are usually fused and very often curved distally.
Age changes in the dentition
Dental Anatomy
Age changes in the dentition
I. After the teeth have reached full occlusion, microscopic tooth movements occur to compensate for wear at the contact area (Mesial Drift) and occlusal surfaces (by Deposition of cementum at the root apex)
2. Attrition of incisal ridges and cusp tips may be so severe that dentin may become exposed and intrinsically stained
3. Secondary dentin may be formed in response to dental caries, trauma, and aging and result in decreased pulp size and tooth sensation
Anchorage
OrthodonticsAnchorage in orthodontics refers to the resistance to unwanted tooth movement
during orthodontic treatment. It is a critical concept that helps orthodontists
achieve desired tooth movements while preventing adjacent teeth or the entire
dental arch from shifting. Proper anchorage is essential for effective treatment
planning and execution, especially in complex cases where multiple teeth need to
be moved simultaneously.
Types of Anchorage
Absolute Anchorage:
Definition: This type of anchorage prevents any
movement of the anchorage unit (the teeth or structures providing
support) during treatment.
Application: Used when significant movement of
other teeth is required, such as in cases of molar distalization or when
correcting severe malocclusions.
Methods:
Temporary Anchorage Devices (TADs): Small
screws or plates that are temporarily placed in the bone to provide
stable anchorage.
Extraoral Appliances: Devices like headgear
that anchor to the skull or neck to prevent movement of certain
teeth.
Relative Anchorage:
Definition: This type allows for some movement of
the anchorage unit while still providing enough resistance to achieve
the desired tooth movement.
Application: Commonly used in cases where some
teeth need to be moved while others serve as anchors.
Methods:
Brackets and Bands: Teeth can be used as
anchors, but they may move slightly during treatment.
Class II or Class III Elastics: These can be
used to create a force system that allows for some movement of the
anchorage unit.
Functional Anchorage:
Definition: This type utilizes the functional
relationships between teeth and the surrounding structures to achieve
desired movements.
Application: Often used in conjunction with
functional appliances that guide jaw growth and tooth positioning.
Methods:
Functional Appliances: Such as the Herbst or
Bionator, which reposition the mandible and influence the growth of
the maxilla.
Factors Influencing Anchorage
Tooth Position: The position and root morphology of the
anchorage teeth can affect their ability to resist movement.
Bone Quality: The density and health of the surrounding
bone can influence the effectiveness of anchorage.
Force Magnitude and Direction: The amount and direction
of forces applied during treatment can impact the stability of anchorage.
Patient Compliance: Adherence to wearing appliances as
prescribed is crucial for maintaining effective anchorage.
Clinical Considerations
Treatment Planning: Proper assessment of anchorage
needs is essential during the treatment planning phase. Orthodontists must
determine the type of anchorage required based on the specific movements
needed.
Monitoring Progress: Throughout treatment,
orthodontists should monitor the anchorage unit to ensure it remains stable
and that desired tooth movements are occurring as planned.
Adjustments: If unwanted movement of the anchorage unit
occurs, adjustments may be necessary, such as changing the force system or
utilizing additional anchorage methods.
Lichen planus
General Pathology
Lichen planus is an itchy, violaceous, flat-topped papule highlighted by white dots or lines called Wickham's striae.
- lichen planus may occur in the oral mucosa, where it has a fine white net-like appearance.
- increased epidermal proliferation; ? immunologic; initiated by epidermal injury from drugs, viruses, or topical agents.
- characteristic histologic features include:
- hyperkeratosis
- absence of parakeratosis
- prominent stratum granulosum
- an irregular "saw toothed" accentuation of the rete pegs.
- dermal-epidermal junction obscured by a band-like infiltrate of lymphocytes.
- It is generally self-limiting and resolves spontaneously 1 to 2 years after onset; however, the oral lesions may persist for years.