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FIRST BDS
ANATOMY

# Comprehensive Anatomy Notes for First-Year BDS Students

I've compiled these high-quality, concise notes tailored for first-year Bachelor of Dental Surgery (BDS) students. Drawing from standard curricula like those from Indian universities (e.g., Rajasthan University of Health Sciences), these notes emphasize general human anatomy, embryology, histology, and dental anatomy—core subjects in your first year. The focus is on head and neck regions due to their clinical relevance in dentistry, while providing an overview of systemic anatomy for foundational understanding. Use these alongside textbooks like BD Chaurasia's Human Anatomy (Head & Neck volume) and Wheeler's Dental Anatomy for best results.

## Goals and Objectives of Studying Anatomy in BDS
**Goals**: Gain insight into the functional anatomy of the head and neck, histology, genetics, and embryological development of clinically relevant structures. This builds a foundation for clinical dentistry, understanding disease, injury, and procedures like injections or imaging.

**Knowledge & Understanding**:
- Normal body structures for clinical exams.
- Anatomical basis of diseases.
- Microscopic tissues and nervous system for lesion localization.
- Embryology: Critical stages, teratogens, mutations.
- Sectional anatomy for radiographs (e.g., CT, MRI).
- Cardio-pulmonary resuscitation anatomy.

**Skills**:
- Locate structures, identify tissues under microscope.
- Interpret imaging and detect congenital abnormalities.

**Integration**: Combine with physiology, biochemistry, and clinical subjects. Total hours: ~890 theory, ~4835 practical (dissections, histology slides, models).

## Syllabus Overview
1. **General Anatomy**: Terms, body systems outline.
2. **Regional Anatomy**: Head/neck osteology (dental focus), thoracic/abdominal/pelvic organs, injection sites.
3. **Embryology**: General and systemic (head/neck focus).
4. **Histology**: Cells, tissues, glands, organs (e.g., salivary glands, teeth).
5. **Medical Genetics**: Mitosis, meiosis, inheritance.

## Section 1: General Anatomy - Building Blocks
Start with basics to understand body organization.

- **Introduction to Terms**: Anatomical position (standing, palms forward). Planes: Sagittal (divides left/right), Coronal (front/back), Transverse (upper/lower). Terms: Proximal (near trunk), Distal (away), Superior/Inferior, Anterior/Posterior.
- **The Cell**: Basic unit; components include nucleus (DNA), cytoplasm, organelles (mitochondria for energy). Types: Epithelial, connective.
- **Tissues**: Four types:
- **Epithelium**: Covering/lining (simple squamous for diffusion, stratified for protection).
- **Connective**: Support (loose for cushioning, dense for strength; includes blood, bone, cartilage).
- **Muscle**: Movement (skeletal voluntary, smooth involuntary, cardiac).
- **Nervous**: Impulse transmission (neurons, glial cells).
- **Histology Basics**: Study under microscope. Key for BDS: Salivary glands (serous/mucous/mixed), lymphoid tissue, skin. Organs: Tooth (enamel, dentin), lip, tongue, palate, esophagus.

*(Visualization Tip: Draw a cell diagram with labeled organelles; practice histology slides of epithelium vs. connective tissue.)*

## Section 2: Embryology - Development of Head & Neck
Focus on craniofacial development; anomalies are common in dentistry (e.g., clefts).

- **General Embryology**: Fertilization, implantation. Bilaminar/trilaminar disc, neural crest (forms craniofacial structures), notochord.
- **Pharyngeal Arches**: Six arches (1-6); derivatives:
- Arch 1: Mandible, muscles of mastication (trigeminal nerve).
- Arch 2: Hyoid, facial muscles (facial nerve).
- Arches 3-6: Larynx, pharynx.
- **Development of Face**: From frontonasal process and arches; anomalies: Cleft lip (failure of fusion).
- **Development of Palate**: Primary (frontonasal) + secondary (palatine shelves fuse); cleft palate if unfused.
- **Development of Tongue**: From arches 1-4; anterior 2/3 (lingual swellings), posterior 1/3 (hypobranchial eminence). Anomalies: Ankyloglossia (tongue-tie).
- **Thyroid Gland**: From foramen cecum; descends. Anomalies: Thyroglossal cyst, ectopic thyroid.
- **Tooth Development**: Initiation (bud stage), morphogenesis (cap/bell), histogenesis (enamel/dentin formation).

| Stage | Key Events | Anomalies |
|-------|------------|-----------|
| **Bud** | Ectoderm invaginates | Anodontia |
| **Cap** | Enamel organ forms | Gemination |
| **Bell** | Differentiation (ameloblasts/odontoblasts) | Enamel hypoplasia |

*(Clinical Note: Teratogens like alcohol can cause facial dysmorphologies.)*

## Section 3: Gross Anatomy - Focus on Head & Neck
Emphasize dental relevance (e.g., nerves for anesthesia).

- **Osteology**: Skull bones (mandible, maxilla, hyoid). Foramina: Mental (inferior alveolar nerve), Infraorbital.
- **Neck Triangles**:
- **Carotid Triangle**: Boundaries (sternocleidomastoid, omohyoid, digastric); contents (carotid arteries, internal jugular vein, vagus nerve).
- **Posterior Triangle**: Boundaries (sternocleidomastoid, trapezius, clavicle); contents (subclavian vessels, brachial plexus).
- **Salivary Glands**:
- **Parotid**: Largest; duct (Stensen's) opens opposite upper 2nd molar. Innervation: Glossopharyngeal.
- **Submandibular**: Duct (Wharton's) under tongue. Relations: Hyoglossus muscle.
- **Tongue**: Muscles (intrinsic/extrinsic), papillae. Arteries: Lingual. Lymphatics: Tip to submental, posterior to deep cervical.
- **Pharynx & Larynx**: Pharynx muscles (constrictors); larynx cartilages (thyroid, cricoid), muscles (cricothyroid).
- **Systemic Overview**: Brief on thorax (heart, lungs), abdomen (organs), limbs (injection sites like deltoid for IM).

*(Diagram Tip: Sketch carotid sheath contents; label nerves/vessels.)*

## Section 4: Dental Anatomy & Histology
Specific to teeth and oral structures.

- **Terminology**: Midline divides arches; quadrants (4 total). Occlusion: Tooth contact. Dentition: Primary (20 teeth, deciduous), Permanent (32, succedaneous except molars).
- **Tooth Structure**:
- **Crown**: Anatomical (enamel-covered), Clinical (visible).
- **Root**: Anatomical (cementum-covered), Clinical (hidden).
- Tissues: Enamel (hardest, acellular), Dentin (bulk, sensitive), Cementum (root covering), Pulp (nerves/vessels).
- Junctions: CEJ (cemento-enamel), DEJ (dentino-enamel).
- **Surfaces**: Facial (labial/buccal), Lingual/Palatal, Proximal (mesial/distal), Incisal/Occlusal.
- **Numbering Systems**:
- **Zsigmondy-Palmer**: Grid for quadrants.
- **FDI**: Two digits (quadrant + tooth, e.g., 11 = upper right central incisor).
- **Universal**: Numbers 1-32 for permanent.
- **Supporting Structures**: Alveolar process/bone, Periodontal ligament, Gingiva.

| Tooth Type | Number (Permanent) | Function |
|------------|---------------------|----------|
| Incisors | 8 | Cutting |
| Canines | 4 | Tearing |
| Premolars | 8 | Grinding |
| Molars | 12 | Crushing |

*(Histology Note: Tooth - Ameloblasts form enamel; odontoblasts dentin.)*

## Key Facts and Revision Tips
- Skull has 22 bones; mandible is movable.
- Neural crest cells are crucial for head/neck.
- Common Anomalies: Cleft lip/palate (1 in 700 births), thyroglossal cysts.
- Exam Questions: Draw/label tongue development; describe parotid gland; explain cleft palate basis.

!

PHYSIOLOGY

DENTAL ANATOMY +

HISTOLOGY

SECOND BDS

PHARMACOLOGY

ANTI VIRAL DRUG

## VIRUS:

Virus are the smallest infective agents, consisting essentially of nucleic acid (either RNA or
DNA) enclosed in a protein coat or capsid.

Some important examples of viruses and the diseases they cause are as follows:

DNA VIRUSES:
 Pox Viruses (smallpox)
 Herpes viruses (chickenpox, herpes etc)
 Adenoviruses (sore throat, conjunctivitis)
 Hepadnaviruses (serum hepatitis)
 Papillomaviruses (warts)

RNA VIRUSES:
 Orthomyxoviruses (influenza)
 Paramyxoviruses (measles, mumps)
 Rhabdoviruses (rabies)
 Picornaviruses (colds, meningitis, poliomyelitis)
 Retroviruses (AIDS, T-cell leukemia)
 Arenaviruses (meningitis, Lassa fever)
 Arboviruses (arthropod-borne encephalitis, yellow fever)

*(Insert Diagram: Structure of a Virus - Lipoprotein envelope, Nucleic acid core, Coat (capsid), Capsomere (the morphological protein units of the coat))*

---

## LIFE CYCLE OF VIRUSES:

Lytic versus lysogenic life cycles:
 In the lytic stage, many viral particles are made and copies are sent back into
the environment.
 A virus is found in this phase when conditions are favorable, i.e. when
bacteria is "growing like crazy"
 In the lysogenic phase there is no pathology. Under certain conditions the
lysogenic lifestyle can switch to a lytic lifestyle.
 A virus is found at this stage under harsh conditions.

*(Insert Diagram: Life Cycle of Viruses - Showing steps like Attachment, Penetration, Uncoating, Early transcription, Synthesis of viral mRNA, Late translation, Assembly, and Release)*

---

*(Insert Diagram: Lytic and Lysogenic Cycles)*

**Lytic:**
The virus attaches to bacteria (host)
The virus inserts its DNA into the bacteria
The virus takes over the cell's machinery
The virus reproduces itself and self-assembles.
The host cell is destroyed

**Lysogenic:**
The virus is a prophage at this stage.
The virus binds to bacteria (host)
The virus inserts its DNA into the bacteria
The viral DNA gets incorporated into the cell's chromosome
Viral DNA is replicated along with chromosomal material

---

## CLASSIFICATION OF ANTIVIRAL DRUGS:

1. According to stages of viral replication:

A. Inhibition of free extracellular viruses:
Eg.: Gammaglobulins

B. Inhibition of penetration of viruses into the cells:
Eg.: Amanthadine, Disoxaril, Rimantidine

C. Inhibition of intracellular viral synthesis:

I. Inhibition of transcription of the viral genome:
a. DNA polymerase inhibitors:
Eg.: Aciclovir, Famciclovir, Ganciclovir, Ribavirin, Forscarnet

b. Reverse transcriptase inhibitors:
Eg.: Zidovudine, Didanosine, Zalcitabine

II. Post-translation event inhibitors:
Eg.: Protease inhibitors: Saquinavir, Ritonavir, Indinavir, Nelfinavir.

III. Inhibition of early protein synthesis:
Eg.: Guanidine, Hydroxybenzylbenz-imidazole

IV. Inhibition of nucleic acid synthesis:
Eg.: Rebavirin, Idoxouridine, Cytarabin, Vidarabin, Trifluridin, Forscarnet,
Acyclovir,Zidovudine, Ganciclovir etc.

D. Inhibition of assembly:
Eg.: Methesazone

E. Miscellaneous agent:
Eg.: Interferon

*(Insert Diagram: Sites of Action of Antiviral Drugs in Viral Replication Cycle)*

2. According to viral specific action:

A. Anti-herpes virus agents
Eg.: Acyclovir, Valacyclovir, Famciclovir, Penciclovir, Ganciclovir, Cidofovir, Foscarnet
Trifluridine, Idoxuridine , Vidarabine

B. Anti-influenza viruses:
Eg.: Amantadine, Rimantadine, Oseltamivir, Zanamivir

C. Anti-retroviruses:

I. Nucleoside reverse transcriptase inhibitors:
Eg.: Zidovudine, Stavudine, Didanosine, Zalcitabine, Lumivudine, Abacavir

II. Non nucleoside reverse transcriptase inhibitors:
Eg.: Nevirapine, Efavirenz, Delavirdine

III. Protease inhibitors:
Eg.: Saquinavir, Indinavir, Ritonavir, Nelfinavir, Amprenavir, Lopinavir

D. Non selective anti-viral agents:
Eg.: Ribavirin, lamivudine, Fomiversen, Imiquimod, Interferon – α etc.

*(Insert Diagram: Classification According to Viral Specific Action - Showing Blocked by various inhibitors like gamma-globulins, amantadine, etc.)*

---

## ACYCLOVIR:

 A widely used antiviral with main implications in the treatment of herpes
 Seen as a “new age” in antiviral therapy, Gertrude Elion, its creator, was given the
Nobel prize for medicine in 1988
 It is a nucleoside analogue and prevents viral replication in infected cells
 Extremely selective and low in toxicity

Structure:
• Purine Mimic
• Similarity to 2`-deoxyguanosine: lack of 3` hydroxyl

*(Insert Diagram: Chemical Structures of Acyclovir and 2'-deoxyguanosine)*

Mechanism of action:

Acyclovir
↓ Herpes virus specific thymidine kinase
Acyclovir Monophosphate
↓ Cellular kinases
Acyclovir triphosphate

Inhibits herpes virus DNA Polymerase competitively
Gets incorporated in viral DNA and stops lengthening of DNA strands.
The terminated DNA Inhibits DNA-polymerase irreversibly

*(Insert Diagram: Mechanism Flowchart for Acyclovir Activation and Action)*

Step 1: Activation:

*(Insert Diagram: Phosphorylation steps from Acyclovir to Acyclovir triphosphate)*

Step 2: Incorporation into growing DNA chain:

*(Insert Diagram: Normal vs Acyclovir incorporation in DNA chain, showing inhibition)*

Antiviral spectrum:
 Effective against the following:
1. Herpes simplex virus type I (HSV-1)
2. Herpes simplex virus type II (HSV-2)
3. Varicella zoster virus (VZV)
4. Epstein-Barr virus (EBV)
5. Cytomegalovirus (CMV) -- least activity

Pharmacokinetics:
 Poor oral absorption and is only 15 - 20% (lipophilic) and unaffected by food
 Good CSF penetration
 Excreted unchanged in urine – glomerular filtration and active tubular secretion
(peritoneal and hemodyalysis)
 Half-life: 2-3 Hrs only
 Good corneal penetration
 Bioavailability can be improved by design of suitable prodrugs
 Valaciclovir – ester prodrug of acyclovir
 Famciclovir: ester prodrug of gunine analogue

*(Insert Diagram: Prodrug Conversion for Valacyclovir and Famciclovir)*

Therapeutic Uses:
1. Genital Herpes simplex: HSV -II
 Primary disease: Ointment – Oral - IV
 Recurrent disease: Oral – IV (5 mg/kg q8 hrly)
(Suppressive oral therapy 400 mg BD)

2. Mucocutaneous H. simplex: Type - I
 Acyclvir cream
 Oral or IV in immunocompromized patients

3. H. simplex encephalitis: type – 1
 10 to 20 mg/kg/8hr X 10 days

4. H. simplex keratitis

5. H. zoster

6. Chicken pox

*(Insert Diagram: Photos of Herpes Lesions - Genital, Oral, and Skin Rash)*

 Resistance:
 Resistance to acyclovir can develop in HSV or VZV through alteration in
either the viral thymidine kinase or the DNA polymerase
 Immunocompromised hosts
 foscarnet, cidofovir, and trifluridine (acyclovir resistant strain)

 ADRs:
 Oral: Nausea, diarrhea, and headache
 IV: Rashes, sweating and emesis and fall in BP
 Reversible renal dysfunction due to crystalline nephropathy
 Neurologic toxicity (eg, tremors, delirium, seizures)
 No Teratogenicity
 10 years therapy

---

## NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTIS):

 Drugs used against retrovirus – HIV
 Useful in prolonging and improving quality of life
 Do not cure the infection
 Zidovudine (AZT)
 Abacavir (ABC)
 Lamivudine (3TC)
 Didanosine (ddI)
 Zalcitabine (ddC)
 Stavudine (d4T)

Mechanism of action:
 When HIV infects a cell, reverse transcriptase copies the viral single stranded RNA
genome into a double-stranded viral DNA
 The viral DNA is then integrated into the host chromosomal DNA
 Then, host cellular processes start transcribing viral RNA and mRNA to reproduce the
virus
 Regulatory and structural proteins are produced under the direction of viral mRNA
 Zidovudine inhibits viral reverse transcriptase (RNA dependent DNA polymerase)
 Zidovudine prevents infection of new cell by HIV, but not effective on already
infected host chromosomes

*(Insert Diagram: HIV Replication Cycle Showing Reverse Transcription Step)*

 Resistance:
 Point mutation altering reverse transcriptase enzyme

 Kinetics:
 Bioavailability – 60-80%.
 t1/2 – 1 hour, intracellular half-life of the active triphosphate is 3 hours.
 Conc. in CSF – 65% of that in plasma, crosses placenta and excreted in milk
 Metabolism – Most of the drug is metabolized to inactive glucuronide in the
liver, only 20% of the active form is excreted in the urine

 Unwanted effects:
 Blood dyscrasias – Anaemia and Neutropenia
 G.I disturbances – Nausea, vomiting, abdominal pain
 Myopathy, Paraesthesia, Myalgia
 Skin rash, Insomnia, Fever, Headaches, Abnormalities of liver function

 Drug Interaction:
 Paracetamol – AZT toxicity and azoles – inhibits AZT metabolism

 Uses:
 HIV infection in combination with other drugs – minimum 2 other (3TC and
NVP)

---

## NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS (NNRTI):

Eg: Nevirapine (NVP), Efavirenz (EFZ), Delavirdine (DLV)

Mechanism of action:
 Direct inhibitor of reverse transcriptase without intracellular phosphorylation
 NNRTIs bind to the Reverse transcriptase near the catalytic site and cause its
denaturation
 More potent on HIV-1 than Zidovudine but not HIV-2
 Cross resistance among themselves but not with others

 Kinetics:
 Administered Orally.
 Plasma half-life – 20 min.
 Conc. in CSF – 45% of that in plasma.
 Metabolism – Metabolized in the liver and metabolite is excreted in the urine
(CYP3A4)
 Nevirapine can prevent mother-to-baby transmission of HIV if given to the
parturient mother and the neonate

 Unwanted effects:
 Skin rash(17%)
 Fever
 Headaches
 Lethargy.
 If not monitored carefully: Stevens-Johnson syndrome or Toxic epidermal
necrolysis.
 Fulminant hepatitis (occasionally)

 Dose: 200 mg/day

---

## RETROVIRAL PROTEASE INHIBITORS (PIS):

Eg.: Saquinavir (SQV), Nelfinavir (NFV), Indinavir (IDV), Ritonavir (RTV), Lopinavir and
Amprenavir (AMP)

Mechanism of action:
 In last stage of HIV growth cycle viral polyproteins are formed and then become
immature budding particles
 Protease is responsible for cleaving these precursor molecules to produce the final
structural proteins of the mature virion core
 PIs bind to these proteins and inhibit formation of structural proteins
 All given orally
 CSF levels – negligible with Saquinavir & highest with Indinavir (76% of plasma
conc.)
 They are used in combination with Reverse transcriptase inhibitors
 ADRs: CYP3A4 isoenzyme
 G.I disturbances
 Metabolic abnormalities, e.g. insulin resistance, High blood sugar & Hyperlipidaemia
 Altered distribution of fat (some fat wasting, some fat accumulation)
 ↑ conc. of liver enzymes with Ritonavir & Indinavir
 Parasthesias around the mouth, in hands & feet with Ritonavir & Amprenavir
 Renal stones (with Indinavir)
 Stevens-Johnson syndrome (with Amprenavir)

SAQUINAVIR (SQV):
 Oral formulation hard gel capsules – poor bioavailability (4%)
 Replaced in clinical use by a soft gel capsule formulation
 Administered after fatty meal
 Large volume of distribution but is 98% protein-bound
 The elimination half-life is 12 hours
 Excreted primarily in faeces
 High first pass metabolism
 ADRs include GIT disturbances – nausea, diarrhoea, abdominal discomfort and
dyspepsia

HIV TREATMENT:

HAART (Highly Active Antiretroviral Therapy)
 Aggressive therapy aimed at supressing plasma viral load
 Combination treatment is essential
 Combination treatment → HAART

2 NRTIs + 1 NNRTI (Z+L+Efavirenz) OR
2 NRTIs + 1 or 2 Protease inhibitors (Z+L+lopinavir)

WHO Recommendations for a First Line Regimen in Adults and Adolescents:

*(Insert Table: WHO Recommendations - Drugs like d4T+3TC+NVP, etc., with use in women/childbearing age, pregnant, available as FDC)*

---

## ANTI-INFLUENZA DRUGS:

Eg.: Amantadine, Oseltamivir, Peramivir, Rimantadine, Zanamivir

 Tricyclic amine unrelated to any nucleic acid precursor

Amantadine - Approved by FDA in 1976 to treat influenza A (not influenza B)

 Mechanism:
 Inhibits the un-coating of the viral genome
 Specifically targets a protein called M2 (an ion channel)
 Inactive against influenza B, which lacks M2

 Pharmacokinetics:
 Well absorbed orally; crosses BBB
 90% excreted unchanged ; no reports of metabolic products

 Side effects:
 Low toxicity at therapeutic levels; some CNS side effects (scary hallucinations

 Doses: 100 mg BD or 200 mg OD

Osetalmivir (Tamiflu), Zanamivir:
 Broad spectrum – Influenza A, B and avian influenza
 Oseltamivir is a prodrug that is activated in the gut and liver to O. carboxylate
 MOA: Neuraminidase inhibitor (important for viral replication and release)
 Not further metabolized and excreted in kidney
 Half life: 6-8 Hrs
 ADRs: Nausea and vomiting
 Used in both prophylaxis and treatment
 Dose: 75 mg BD for 5 days

---

## Interferone α:

 Interferon has broad spectrum anti-viral activity (DNA viruses):
 herpes simplex 1 and 2; herpes zoster
 human papillomavirus (genital warts)

 (RNA viruses):
 Influenza, chronic hepatitis, common cold
 Breast cancer. lung cancer
 Karposi’s sarcoma (cancer associated with AIDS)

 Pharmacokinetics:
 Not orally bioavailable
 Topically routes: intramuscular, subcutaneous, topical (nasal spray)

 Mechanism of action:
 Binds to cell surface receptors
 Induces expression of translation inhibitory protein (TIP)
 TIP binds to ribosome, inhibits host expression of viral proteins

 Available as vials for injection

 ADRs: Flue like symptoms, neurotoxicity, myelosuppression etc

*(Insert Diagram: Sites of Action of Interferons in Viral Replication - Showing inhibition at reverse transcriptase, integrase, protease, etc.)

THIRD BDS

FINAL BDS

Detailed Notes on Odontogenic Cysts

## Introduction and Definition
Odontogenic cysts are closed, epithelium-lined pathological cavities that arise from the remnants of odontogenic (tooth-forming) epithelium within the jaws. They are typically filled with fluid or semi-fluid material and can occur in the maxilla or mandible. These cysts are common in oral pathology, often discovered incidentally during routine dental radiographic examinations. They account for a significant portion of jaw lesions and can lead to bone expansion, tooth displacement, or secondary infections if untreated. The epithelium originates from sources such as the rests of Malassez (from Hertwig's epithelial root sheath), rests of Serres (from dental lamina), or reduced enamel epithelium.

Odontogenic cysts are distinct from non-odontogenic cysts (e.g., nasopalatine duct cyst) and odontogenic tumors, though some overlap in presentation requires careful differentiation. They are generally benign but can exhibit aggressive behavior, particularly in certain types like odontogenic keratocysts.

## Classification
Historically, odontogenic cysts were classified as inflammatory (arising from inflammatory stimuli) or developmental (arising from epithelial remnants without inflammation). However, the 2022 World Health Organization (WHO) classification of head and neck tumors simplifies this by listing odontogenic cysts without formal subdivision into inflammatory or developmental categories, emphasizing their odontogenic origin and histological features. This represents a shift from the 2017 WHO classification, where odontogenic keratocyst was reclassified as a tumor (keratocystic odontogenic tumor) due to its aggressive nature and genetic associations, but in 2022, it was reverted to a cyst category. Calcifying odontogenic cyst remains a cyst, not a tumor, and orthokeratinized odontogenic cyst is retained as a distinct entity.

The 2022 WHO classification includes the following odontogenic cysts:

| Category (Informal, for Educational Purposes) | Specific Types |
|-----------------------------------------------|---------------|
| Inflammatory | - Radicular (periapical) cyst - Residual cyst - Paradental cyst - Buccal bifurcation cyst |
| Developmental | - Dentigerous cyst - Odontogenic keratocyst (OKC) - Lateral periodontal cyst (including botryoid variant) - Gingival cyst - Glandular odontogenic cyst - Calcifying odontogenic cyst - Orthokeratinized odontogenic cyst - Eruption cyst (soft tissue variant of dentigerous) |

This table is for illustrative purposes; the official WHO list does not use subcategories but groups them under "odontogenic cysts."

## Major Types of Odontogenic Cysts
Below is a detailed description of the most common and clinically significant types, organized by informal category for clarity. Each includes etiology, clinical features, radiographic features, histopathology, differential diagnosis, treatment, and prognosis.

### Inflammatory Odontogenic Cysts

#### 1. Radicular (Periapical) Cyst
- **Etiology**: Arises from epithelial rests of Malassez stimulated by inflammation from a non-vital tooth, often due to dental caries, trauma, or pulp necrosis. It is the most common odontogenic cyst (accounting for ~50-70% of cases).
- **Clinical Features**: Often asymptomatic; may present with pain, swelling, or sinus tract if infected. Occurs in adults (30-50 years), slight male predominance, associated with carious or traumatized teeth.
- **Radiographic Features**: Well-circumscribed, unilocular radiolucency at the root apex, <1 cm typically but can enlarge; corticated borders, may cause root resorption or cortical expansion. On MRI: High T2 signal, variable T1, enhancing walls.
- **Histopathology**: Non-keratinized stratified squamous epithelium lining; fibrous wall with chronic inflammation, cholesterol clefts, Rushton bodies, and dystrophic calcifications possible.
- **Differential Diagnosis**: Granuloma, abscess, other inflammatory cysts; distinguish from dentigerous cyst by tooth vitality and location.
- **Treatment**: Endodontic therapy (root canal), apicoectomy, or extraction with curettage. Marsupialization for large lesions.
- **Prognosis**: Excellent with proper treatment; recurrence rare unless incomplete removal.

#### 2. Residual Cyst
- **Etiology**: Persists after incomplete removal of a radicular cyst following tooth extraction.
- **Clinical Features**: Asymptomatic, incidental finding in edentulous areas; similar demographics to radicular cyst.
- **Radiographic Features**: Unilocular radiolucency not associated with a tooth, well-demarcated.
- **Histopathology**: Identical to radicular cyst.
- **Differential Diagnosis**: Residual infection, other cysts like OKC.
- **Treatment**: Surgical enucleation.
- **Prognosis**: Good, low recurrence.

#### 3. Paradental Cyst
- **Etiology**: Inflammatory response at the crown or root of partially erupted teeth, often molars, due to pericoronitis.
- **Clinical Features**: Gingival swelling, purulent discharge, deep pockets; young patients (20-30 years).
- **Radiographic Features**: Pericoronal or lateral radiolucency, unilocular, associated with erupted tooth.
- **Histopathology**: Inflamed squamous epithelium, similar to radicular.
- **Differential Diagnosis**: Dentigerous cyst, buccal bifurcation cyst.
- **Treatment**: Extraction of involved tooth and enucleation.
- **Prognosis**: Favorable.

#### 4. Buccal Bifurcation Cyst
- **Etiology**: Inflammatory, arising from buccal periodontium at mandibular molar bifurcation.
- **Clinical Features**: Tipping of molar, lingual root displacement; children/adolescents.
- **Radiographic Features**: Well-circumscribed lytic lesion at bifurcation.
- **Histopathology**: Non-specific inflamed epithelium.
- **Differential Diagnosis**: Lateral periodontal cyst, OKC.
- **Treatment**: Extraction or enucleation.
- **Prognosis**: Excellent.

### Developmental Odontogenic Cysts

#### 1. Dentigerous Cyst
- **Etiology**: Fluid accumulation between reduced enamel epithelium and crown of unerupted tooth, preventing eruption; associated with impacted teeth (e.g., third molars, canines).
- **Clinical Features**: Asymptomatic unless infected; buccal expansion; peaks in 20-40 years, male predominance.
- **Radiographic Features**: Unilocular radiolucency enclosing crown of unerupted tooth; well-corticated, may displace structures. MRI: High T2, thin enhancing wall; thick wall suggests ameloblastoma.
- **Histopathology**: Thin non-keratinized squamous lining, no palisading; may have mucous metaplasia or cholesterol clefts.
- **Differential Diagnosis**: OKC, unicystic ameloblastoma, hyperplastic follicle (follicular space <3-4 mm).
- **Treatment**: Enucleation with tooth removal; marsupialization for large lesions to preserve teeth.
- **Prognosis**: Good, but monitor for rare malignant transformation.

#### 2. Odontogenic Keratocyst (OKC)
- **Etiology**: From dental lamina remnants (rests of Serres); associated with PTCH1 mutations in Gorlin syndrome (nevoid basal cell carcinoma syndrome).
- **Clinical Features**: Asymptomatic or with pain/swelling; posterior mandible common; bimodal age (20s and 60s), male predilection.
- **Radiographic Features**: Uni- or multilocular radiolucency, anterior-posterior expansion, minimal buccal/lingual growth; may involve sinuses.
- **Histopathology**: Parakeratinized stratified squamous epithelium with palisaded basal layer, corrugated surface; daughter cysts possible.
- **Differential Diagnosis**: Ameloblastoma, dentigerous cyst; genetic testing for syndromic cases.
- **Treatment**: Enucleation with curettage or peripheral ostectomy; resection for recurrent/large lesions; chemical cauterization (Carnoy's solution).
- **Prognosis**: Aggressive with 20-30% recurrence; long-term follow-up needed.

#### 3. Lateral Periodontal Cyst
- **Etiology**: From rests of Serres along lateral root surface.
- **Clinical Features**: Asymptomatic, vital teeth; mandibular premolar-canine region; 40-60 years.
- **Radiographic Features**: Small unilocular radiolucency lateral to root.
- **Histopathology**: Thin squamous or cuboidal lining; botryoid variant multilocular.
- **Differential Diagnosis**: Gingival cyst, radicular cyst.
- **Treatment**: Enucleation.
- **Prognosis**: Excellent, rare recurrence.

#### 4. Glandular Odontogenic Cyst
- **Etiology**: Rare, from rests of Serres or Malassez; aggressive behavior.
- **Clinical Features**: Tooth mobility, cortical perforation; mean age 46, slight male predominance.
- **Radiographic Features**: Multilocular radiolucency, destructive.
- **Histopathology**: Squamous lining with glandular/mucous cells, cilia.
- **Differential Diagnosis**: Mucoepidermoid carcinoma, botryoid cyst.
- **Treatment**: Enucleation or resection.
- **Prognosis**: Recurrence up to 30%; monitor.

#### 5. Calcifying Odontogenic Cyst
- **Etiology**: From odontogenic epithelium; may have neoplastic potential.
- **Clinical Features**: Asymptomatic swelling; anterior jaws.
- **Radiographic Features**: Mixed radio-opaque/lucent lesion with calcifications.
- **Histopathology**: Ameloblastoma-like epithelium with ghost cells and calcifications.
- **Differential Diagnosis**: Calcifying epithelial odontogenic tumor.
- **Treatment**: Enucleation.
- **Prognosis**: Good, low recurrence.

#### 6. Orthokeratinized Odontogenic Cyst
- **Etiology**: From rests of Serres; distinct from OKC.
- **Clinical Features**: Associated with impacted teeth; 20-40 years, males.
- **Radiographic Features**: Unilocular radiolucency, dentigerous-like.
- **Histopathology**: Orthokeratinized lining, no palisading.
- **Differential Diagnosis**: OKC, dentigerous cyst.
- **Treatment**: Enucleation.
- **Prognosis**: Better than OKC, low recurrence.

#### 7. Eruption Cyst
- **Etiology**: Fluid/blood in follicular space during eruption; soft tissue variant of dentigerous.
- **Clinical Features**: Bluish gingival swelling in children.
- **Radiographic Features**: Rarely needed; superficial.
- **Histopathology**: Similar to dentigerous.
- **Differential Diagnosis**: Hematoma, gingival cyst.
- **Treatment**: Often self-resolving; incision if needed.
- **Prognosis**: Excellent.

#### 8. Gingival Cyst
- **Etiology**: From rests of Serres in gingiva.
- **Clinical Features**: Small nodules in adults or infants (Gingival cyst of newborn).
- **Radiographic Features**: None, soft tissue.
- **Histopathology**: Squamous lining.
- **Differential Diagnosis**: Mucocele.
- **Treatment**: Excision.
- **Prognosis**: Excellent.

## General Diagnosis
Diagnosis involves clinical history, examination, radiography (panoramic, CT, MRI for complex cases), and histopathology from biopsy or enucleation. Aspiration may yield fluid for cytology. Vitality testing distinguishes inflammatory from developmental cysts.

## Complications
- Bone expansion/fracture
- Infection
- Tooth displacement/loss
- Rare malignant transformation (e.g., in dentigerous or OKC)

## Key Takeaways for Students
- Always correlate clinical, radiographic, and histologic findings.
- OKC requires vigilant follow-up due to recurrence risk.
- Refer to 2022 WHO for updated nomenclature to avoid diagnostic errors.
- Multidisciplinary approach (dentist, oral surgeon, pathologist) is essential.

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