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Cementogenesis - Formation of Cementum

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1. Definition

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2. What is Cementum? (Quick Review)

• 65% inorganic (hydroxyapatite) - similar to bone
• Contains the highest concentration of fluoride of any mineralized tissue in the body
• Avascular (unlike bone)
• Produced by cementoblasts

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3. Pre-requisite: Role of Hertwig's Epithelial Root Sheath (HERS)

1. At the completion of crown formation, the inner and outer enamel epithelium at the cervical loop proliferate apically
2. They fuse together to form a two-layered collar of cells - this is Hertwig's Epithelial Root Sheath (HERS)
3. HERS grows apically, molding and determining the shape, number, and length of the roots
4. HERS induces the adjacent ectomesenchymal cells (dental papilla) to differentiate into odontoblasts, which then lay down root dentin
5. Once root dentin is deposited, HERS breaks up and disintegrates (due to penetration by blood vessels from the dental follicle)
6. The fragmented epithelial remnants of HERS persist in the periodontal ligament as the Rests of Malassez (clinically important - can give rise to radicular cysts and certain odontogenic tumors)
7. The disintegration of HERS exposes the newly formed root dentin surface to the dental follicle cells - this is the trigger for cementogenesis

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4. Source of Cementoblasts

Cementoblasts are derived from the ectomesenchyme of the dental follicle (dental sac), NOT from epithelium.

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5. Steps of Cementogenesis (Mechanism)

Step 1 - Cementoblast Differentiation

• Dental follicle cells adjacent to the exposed root dentin surface differentiate into large, cuboidal cementoblasts
• These cells resemble osteoblasts in morphology and function

Step 2 - Secretion of Cementoid (Precementum)

• Cementoblasts secrete an unmineralized organic matrix called cementoid (also called precementum)
• This matrix consists of:
  • Type I collagen (intrinsic fibers)
  • Non-collagenous proteins: osteopontin, bone sialoprotein, osteocalcin
  • Proteoglycans

Step 3 - Mineralization

• The cementoid matrix undergoes mineralization by deposition of hydroxyapatite crystals
• Mineralization front advances away from the dentin surface
• A thin layer of unmineralized cementoid is always maintained at the outer surface (between the mineralizing front and the cementoblasts) - this is the precementum zone

Step 4 - Formation of Two Types of Cementum (see below)

Step 5 - Cementoblast Fate

• Some cementoblasts get entrapped within the mineralizing matrix and become cementocytes (cellular cementum)
• Others remain on the surface and continue secretion
• Cementocytes reside in spaces called lacunae and extend processes through canaliculi - analogous to osteocytes in bone, but the canaliculi do NOT form an interconnecting network (unlike bone)

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6. Types of Cementum Formed

A. Acellular (Primary) Cementum

B. Cellular (Secondary) Cementum

Memory tip: "ACellular = Absent cells; Cellular = Contains cells"

1. Acellular afibrillar cementum - no cells, no collagen fibers (found at CEJ, over enamel)
2. Acellular extrinsic fiber cementum (AEFC) - only Sharpey's fibers, most important for attachment
3. Cellular mixed fiber cementum (CMFC) - cementocytes + both fiber types (apical region)
4. Cellular intrinsic fiber cementum (CIFC) - only cementocytes + intrinsic collagen
5. Intermediate cementum - thin, acellular sheath around entire root

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7. Sharpey's Fibers - The Attachment Mechanism

• The principal fibers of the periodontal ligament (PDL) are type I collagen bundles secreted by PDL fibroblasts
• One end embeds into the alveolar bone, the other end embeds into cementum - these embedded portions are Sharpey's fibers
• During cementogenesis, the mineralizing cementum engulfs these fiber bundles, anchoring the tooth to the bone
• Sharpey's fibers within cementum are mineralized; those within the PDL are not mineralized
• This arrangement forms the gomphosis joint - a fibrous joint unique to teeth

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8. Sequence Summary: CEJ to Apex

Crown complete → HERS forms → Root dentin deposited → HERS breaks up 
→ Rests of Malassez left behind → Dental follicle cells exposed to dentin 
→ Differentiate into cementoblasts → Secrete cementoid → Mineralization 
→ Acellular cementum (cervical) + Cellular cementum (apical) formed 
→ Sharpey's fibers embedded → PDL anchors tooth to bone

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9. Comparison: Cementum vs Bone vs Dentin

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10. Clinical Relevance (Know for Exams)

1. Orthodontic movement: Alveolar bone is resorbed and redeposited during tooth movement, but cementum is NOT resorbed - this is why teeth can be moved orthodontically without damaging root attachment
2. Rests of Malassez: HERS remnants in the PDL - can give rise to periapical (radicular) cysts due to inflammatory stimulation
3. Hypercementosis: Excessive cementum deposition around the root (associated with Paget's disease, periapical inflammation)
4. Ankylosis: Fusion of cementum directly to alveolar bone (no PDL space) - complicates tooth extraction
5. Root sensitivity: Exposure of cementum at the cervical region (due to gingival recession) - cementum is thin here and dentinal tubules may be exposed
6. Cementoma/Cemento-ossifying fibroma: Benign lesions involving cementum-like deposits

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11. Key Terms Summary

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Deglutition (Swallowing)

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1. Definition

"Swallowing is a complicated mechanism, principally because the pharynx subserves both respiration and swallowing." - Guyton & Hall Textbook of Medical Physiology

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2. Stages of Deglutition

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Stage 1: Oral (Voluntary) Stage

A. Oral Preparatory Phase

• Food is received in the mouth and mixed with saliva
• Mastication (chewing) reduces food to a manageable size
• The tongue, buccal musculature, and teeth work together to form a cohesive bolus
• The soft palate is lowered to seal off the nasopharynx initially, directing the bolus toward the oropharynx

B. Oral Transport Phase

• The tongue voluntarily squeezes and rolls the bolus posteriorly
• The tongue tip elevates against the hard palate and presses backward in a wave-like motion
• The bolus is pushed through the oropharyngeal isthmus into the pharynx
• Once the bolus reaches the tonsillar pillars and posterior pharyngeal wall, swallowing becomes automatic and cannot be stopped

Key point for dentistry: This stage is why tongue posture, palatal vault shape, and missing teeth directly affect swallowing efficiency.

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Stage 2: Pharyngeal Stage (Involuntary Reflex)

Trigger

• The bolus stimulates epithelial swallowing receptor areas around the pharyngeal opening, especially on the tonsillar pillars
• Afferent impulses travel via CN V (trigeminal) and CN IX (glossopharyngeal) to the medulla oblongata (tractus solitarius)
• The swallowing/deglutition center in the reticular formation of the medulla and lower pons coordinates the reflex

Five Sequential Protective Events (must happen in order):

• Soft palate is pulled upward by the levator and tensor veli palatini muscles
• Closes off the posterior nares → prevents food reflux into the nasal cavity

• Palatopharyngeal folds are pulled medially toward each other
• Forms a narrow sagittal slit through which the bolus must pass
• Acts as a selective filter - adequately chewed food passes; large objects are impeded
• This entire process takes < 1 second

• Vocal cords strongly approximate (adduct) - this is the PRIMARY airway protector
• The larynx is pulled upward and anteriorly by the suprahyoid and thyrohyoid muscles
• The hyoid bone moves anteriorly
• This upward movement causes the epiglottis to swing backward (tilt) over the laryngeal inlet
• The result: three-tiered airway closure - aryepiglottic folds, ventricular folds, and true vocal folds all close
• Vocal fold adduction during swallowing averages ~2.3 seconds

• The upward-forward movement of the larynx pulls open the UES (pharyngoesophageal sphincter)
• The UES = upper 3-4 cm of esophageal muscular wall, normally tonically contracted
• It relaxes to allow the bolus to enter the esophagus
• There is a transient negative pressure in the cricopharyngeal sphincter as the bolus passes

• A peristaltic wave sweeps from the superior pharynx downward through the middle and inferior pharynx
• This propels the bolus into the upper esophagus
• Entire pharyngeal stage: less than 2 seconds

Respiration is Temporarily Halted

• The swallowing center inhibits the respiratory center of the medulla
• Breathing is interrupted at any point in the respiratory cycle for < 6 seconds
• This prevents aspiration

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Stage 3: Esophageal Stage (Involuntary)

A. Primary Peristalsis

• A continuation of the pharyngeal peristaltic wave into the esophagus
• Travels the entire length of the esophagus in 8-10 seconds
• In an upright person, gravity assists - bolus may reach the stomach in 5-8 seconds even before the wave arrives

B. Secondary Peristalsis

• Occurs if primary peristalsis fails to clear all food from the esophagus
• Initiated by distension of the esophagus by retained food
• Continues until the esophagus is completely emptied
• Involves the intrinsic myenteric plexus of the esophagus

Muscular Composition of the Esophagus

Even if vagal input is cut, the myenteric plexus alone can sustain secondary peristalsis after a few days.

Receptive Relaxation of the Stomach

• As the peristaltic wave approaches the stomach, a wave of relaxation precedes it
• The stomach and proximal duodenum relax ahead of the bolus - this is "receptive relaxation"
• Mediated by myenteric inhibitory neurons

Lower Esophageal Sphincter (LES / Gastroesophageal Sphincter)

• Located 3 cm above the esophagogastric junction
• Normally tonically contracted at ~30 mmHg intraluminal pressure
• As the peristaltic wave arrives, receptive relaxation of the LES occurs → bolus enters the stomach
• Between swallows, the LES prevents gastroesophageal reflux (GERD)
• Failure to relax = Achalasia

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3. Neural Control Summary

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4. Dental Relevance of Deglutition

1. Tongue thrust swallowing (infantile swallowing pattern): The tongue pushes forward against the teeth during swallowing instead of pressing the palate. If this persists beyond age 4, it causes open bite and proclination of anterior teeth - a major concern in orthodontics
2. Edentulous patients: Loss of teeth impairs the oral preparatory phase; inadequate bolus formation increases choking risk
3. Xerostomia (dry mouth): Reduced saliva makes bolus formation difficult - impairs oral stage of swallowing
4. Palatal defects (cleft palate): Incompetent soft palate closure → nasal regurgitation during swallowing
5. Dysphagia: Difficulty swallowing; can result from oral cancer, post-radiation changes, neurological lesions
6. TMJ disorders: Can impair mastication and thus the oral preparatory phase

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5. Quick Comparison: Oral vs Pharyngeal vs Esophageal Stage

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6. Key Terms

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