TRAUMA FROM OCCLUSION

Post Graduate Theory Examination Answer (50 Marks)

1. DEFINITION AND TERMINOLOGY (4 marks)

• Carranza / Glossary of Periodontic Terms (American Academy of Periodontology - AAP, 1986): "An injury to the attachment apparatus as a result of excessive occlusal force." The resultant injury is termed trauma from occlusion. Thus, trauma from occlusion refers to tissue injury, not the occlusal force itself. An occlusion that produces such injury is called a traumatic occlusion. (Carranza's Clinical Periodontology, 10th ed., Chapter 29)
• World Health Organization (WHO), 1978: "Damage in the periodontium caused by stress on the teeth produced directly or indirectly by the teeth of the opposing jaw." (Lindhe 5th ed., Chapter 14; TFO Periobasic, Chapter 35)
• Stillman (1917): "A condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position." (Lindhe 5th ed., Chapter 14)

Historical Terminology

2. ETIOLOGY (5 marks)

2.1 Precipitating Factors

Types of Occlusal Forces (TFO Periobasic)

• Normal physiological forces: Exerted during chewing and swallowing; rarely exceed 80 N; beneficial for maintaining PDL and alveolar bone health.
• Impact forces: High magnitude, short duration; exceed the viscoelastic buffer capacity of the PDL.
• Continuous forces: Low magnitude, long duration (as in orthodontic treatment); cause directional bone remodeling.
• Jiggling forces: Intermittent, multidirectional forces (as from premature contacts, high crowns/fillings); most deleterious - cause widening of the alveolus and increased tooth mobility.

2.2 Predisposing Factors

• Long axis orientation of teeth relative to forces
• Morphological characteristics of roots - short, conical, slender, or fused roots are more vulnerable
• Morphology of the alveolar process - quality and quantity of alveolar bone

• Local factors such as bacterial plaque leading to alveolar bone loss
• Fabrication of long-span bridges overloading abutment teeth
• Injudicious bone resection during periodontal or oral surgery
• Parafunctional habits (bruxism, clenching) - resulting from neurosis or sleep-disordered breathing
• Food impaction, overhanging fillings, poorly contoured crowns and bridges, ill-fitting partial dentures

3. CLASSIFICATION OF TRAUMA FROM OCCLUSION (6 marks)

3.1 Based on Duration

3.2 Based on Periodontal Status

• No alteration in connective tissue attachment level
• Does not initiate pocket formation
• Supracrestal gingival fibers remain unaffected, preventing apical migration of junctional epithelium
• Changes are reversible when the excessive forces are removed (Carranza 10th ed., Chapter 29; Lindhe 5th ed., Chapter 14)

Key Note: All teeth suffering from secondary TFO histologically show signs of primary TFO (i.e., secondary TFO never occurs without manifestations of primary TFO). (TFO Periobasic)

4. PATHOGENESIS: STAGES OF TISSUE RESPONSE TO EXCESSIVE OCCLUSAL FORCES (8 marks)

Stage I: Injury

• In single-rooted teeth: Located at the junction of the middle and apical thirds of the clinical root
• In multi-rooted teeth: Located near the furcation area

• Pressure side: Bone resorption, widening of PDL space; blood vessels compressed
• Tension side: Elongation of PDL fibers; blood vessels enlarged
• Slow remodeling of the alveolar socket occurs

• Compression of PDL produces areas of hyalinization
• Areas of necrosis in PDL due to excessive trauma to fibers and cells
• Vascular changes within 30 minutes: impairment and stasis of blood flow
• Within 2-3 hours: blood vessels packed with erythrocytes that begin to fragment
• Within 1-7 days: disintegration of blood vessel walls and dispersal of fragmented products (TFO Periobasic)

• Thrombosis, hemorrhage, tearing of PDL
• Hyalinization: First sign is pyknotic nuclei, then areas of acellularity (cell-free zones)
• Resolution of hyalinized area involves macrophages, foreign body giant cells, and osteoclasts from adjacent undamaged areas, which invade and remove necrotic tissue - process known as undermining resorption
• Temporary reduction in mitotic activity of fibroblasts (reducing proliferation rate) and osteoblasts (reducing bone formation rate)

• Pressure zone: Transient hemorrhage, edema, thrombosis, followed by increased vascular permeability, PDL fiber disorganization, collagen destruction, increased osteoclasts, bone resorption - resulting in widening of PDL space
• Tension zone: Stretched PDL, widened PDL space, newly formed bone alongside preexisting alveolar bone

Stage II: Repair

• Central buttressing: Endosteal cells deposit bone on trabecular walls, reducing marrow space and strengthening bone; occurs within the jaw
• Peripheral buttressing: Shelf-like thickening of bone on the facial or lingual surface of alveolar bone - sometimes referred to as "lipping"; occurs on bone surface (Carranza 10th ed., Chapter 29; TFO Periobasic, Chapter 35)

Stage III: Adaptive Remodeling of the Periodontium

• Thickened PDL, funnel-shaped at the crest
• Angular/vertical bone defects without pocket formation
• Tooth mobility (looseness)
• Increased vascularization of the involved area
• No apical migration of the junctional epithelium (no pocket formation in the absence of inflammation)

• Injury phase: Increase in resorption, decrease in bone formation
• Repair phase: Decreased resorption, increased bone formation
• Adaptive remodeling: Resorption and formation return to normal (Carranza 10th ed.)

5. THEORIES ON THE INTERACTION OF TFO AND PLAQUE-INDUCED PERIODONTAL DISEASE (8 marks)

5.1 Glickman's Concept / Theory of Co-Destruction (1963, 1965)

• Consists of marginal and interdental gingiva
• Bordered by hard tissue (tooth) on only one side
• Unaffected by occlusal forces (blood supply not affected even when PDL vessels are obliterated)
• Gingival inflammation is the result of irritation from microbial plaque alone
• Plaque-associated lesion results in horizontal bone loss

• Consists of the trans-septal/alveolar crest fibers, PDL, cementum, and alveolar bone
• Coronally demarcated by trans-septal and dentoalveolar collagen fiber bundles
• This zone may become the seat of a lesion caused by TFO

1. From the inflammatory lesion produced by plaque (from the zone of irritation)
2. From trauma-induced changes in the zone of co-destruction

5.2 Waerhaug's Concept

• Angular bony defects and infrabony pockets occurred with equal frequency in teeth with TFO and in teeth without TFO
• Reduction in alveolar crestal height was related to the presence of subgingival plaque (ranging 0.5-2.7 mm, mean 1.63 mm from the alveolar crest)
• Loss of attachment and bone are the result of inflammation induced by subgingival plaque, not occlusal trauma
• Teeth with narrow interproximal bone develop horizontal defects; teeth with wide interproximal bone are more likely to develop angular/vertical defects

5.3 Additional Theories on TFO-Inflammation Interaction

• TFO may alter the pathway of extension of gingival inflammation - reduced collagen density and increased leukocytes, osteoclasts, and blood vessels in the coronal portion of increasingly mobile teeth may allow inflammation to proceed to the PDL rather than to bone, resulting in angular bone loss and intrabony pockets
• Trauma-induced areas of root resorption uncovered by apical migration may offer a favorable environment for subgingival plaque formation and deeper lesions
• Supragingival plaque can become subgingival if the tooth is tilted orthodontically or migrates, transforming a suprabony pocket into an intrabony pocket
• Increased mobility of traumatically loosened teeth may have a pumping effect on plaque metabolites, increasing their diffusion

6. ANIMAL STUDIES (5 marks)

Rochester Group (Polson and Co-workers) - Squirrel Monkeys

• Mesial-distal compression forces (orthodontic type) imposed on experimental teeth
• Experimental duration: up to 10 weeks
• Conclusions:
  • TFO alone could not cause attachment loss
  • Gingival inflammation is not initiated by occlusal trauma
  • In the absence of inflammation, TFO results in increased mobility, widened PDL, loss of crestal bone height, but no attachment loss
  • Excessive jiggling forces in the presence of inflammation did NOT cause accelerated attachment loss in squirrel monkeys
  • Adaptive changes in response to occlusal trauma can be largely reversible if inflammation is controlled

Gothenburg Group (Lindhe and Co-workers) - Beagle Dogs

• Buccal-lingual jiggling forces using cap splints and orthodontic appliances imposed on experimental teeth
• Experimental duration: up to 1 year
• Severe plaque-induced gingival inflammation induced
• Conclusions (Lindhe & Svanberg 1974; Lindhe & Ericsson 1976):
  • Occlusal trauma could accelerate the progression of periodontal disease when present with plaque
  • Found evidence of accelerated attachment loss when occlusal trauma was present in the presence of inflammation
  • Treating gingival inflammation in the presence of continuing mobility or jiggling trauma results in decreased mobility and increased bone density, but no change in attachment level or alveolar bone level
  • When excessive occlusal forces are removed, loss of bone density is reversible, except in the presence of periodontitis

7. CLINICAL AND RADIOGRAPHIC SIGNS AND SYMPTOMS OF TFO (5 marks)

Clinical Signs

1. Tooth Mobility: The earliest and most common sign of TFO. Widening of PDL space and angular bone loss during adaptive response are the main causes.
   • Miller's Index (1938) for tooth mobility:
     • Class 0: Normal physiologic movement when force is applied
     • Class I: Mobility greater than physiologic
     • Class II: Tooth can be moved up to 1 mm or more in a lateral direction (buccolingual or mesiodistal); inability to depress the tooth vertically (apicocoronally)
     • Class III: Tooth can be moved 1 mm or more laterally; also ability to depress the tooth vertically
2. Fremitus: Vibratory pattern or movement of teeth when in contacting positions. Classified as:
   • Class I: Mild vibration or movements detected
   • Class II: Easily palpable vibration, but no visible movements
   • Class III: Movements visible with the naked eye
3. Tooth Migration: Tooth moves away from excessive occlusal forces; loss of interproximal contacts and migration from stable position.
4. Wear Facets/Wear Patterns: Shiny, irregular areas on occlusal/incisal surfaces from bruxism; presence in areas of interference.
5. Abfraction (especially in premolars): Caused by lateral deflection. On the traction side, enamel cannot resist and presents with early fractures/cracks in the cervical portion, leading to loss of tooth structure. Wear facets and abfraction appear before gingival recession (V-shaped recession). (TFO Periobasic)
6. V-shaped or Angled Gingival Recessions: TFO may promote V-shaped or angled gingival recession; researchers are divided on this association.
7. Buccal Bone Dehiscence: A very small amount of bone resorption in the cervical area (particularly thin buccal cortex over canine and premolar areas) may result in V-shaped bone dehiscence detectable by Cone Beam Computed Tomography (CBCT).
8. Fractured teeth

Symptoms

• Persistent discomfort on eating
• Thermal sensitivity: Occlusal trauma causes changes in vascular supply of the pulp, leading to increased blood pressure in the pulp and thermal sensitivity
• Muscle hypertonicity: Tired jaws, especially in the morning and at end of day, due to occlusal interferences causing muscle spasm

Radiographic Signs

1. Thickening of the lamina dura along lateral aspect of root, in the apical region, and in bifurcation areas (may indicate strengthening response)
2. Irregular widening of the PDL space (increased width of periodontal space) - most characteristic finding
3. Vertical/angular bone loss rather than horizontal destruction of the interdental septum
4. Bone sclerosis in the periapical area or interdental bone crest (radiolucency and condensation of alveolar bone)
5. Inflammatory root resorption - more common in advanced stages
6. Furcation involvement (TFO Periobasic; Carranza 10th ed.)

8. REVERSIBILITY OF TFO (2 marks)

• It does not always correct itself and is therefore not always temporary or of limited clinical significance
• The injurious force must be relieved for repair to occur
• The presence of inflammation in the periodontium as a result of plaque accumulation may impair reversibility of traumatic lesions
• When bone is resorbed by TFO and the excessive forces are eliminated, loss of bone density is reversible, except in the presence of periodontitis (Carranza 10th ed.; TFO Periobasic)

9. TFO AROUND IMPLANTS (2 marks)

10. CURRENT UNDERSTANDING OF TFO (3 marks)

1. There is presently no evidence that TFO can cause gingivitis or periodontitis or accelerate the progression of gingivitis to periodontitis.
2. TFO does not cause pockets or induce gingival inflammation.
3. In the absence of inflammation, TFO results in adaptation (widened PDL, increased mobility) that is largely reversible.
4. In the presence of inflammation, TFO can act as a co-destructive factor, amplifying (not causing) the rate of progression of existing periodontal disease.
5. Occlusal trauma can amplify localized loss of attachment from inflammatory bone damage (Nunn & Harrel, 2001 - confirmed in Newman 14th ed.).
6. Correction of occlusal abnormalities is not a substitution for conventional methods of resolving plaque-induced inflammation.
7. Elimination of both inflammation and TFO is essential for complete periodontal health.

Key Fact (Newman 14th ed.): "Occlusal trauma can amplify (not cause) localized loss of attachment from inflammatory bone damage." The role of occlusal trauma is tooth specific.

11. TREATMENT OF TRAUMA FROM OCCLUSION (2 marks)

A. Occlusal Adjustment (Coronoplasty)

• Indications (1989 World Workshop in Periodontics): To reduce traumatic forces to teeth exhibiting increasing mobility/fremitus; discomfort during occlusal contact; as adjunctive therapy to reduce parafunctional habit damage; reshaping teeth contributing to soft tissue injury; adjusting marginal ridges causing food impaction; in conjunction with restorative, orthodontic, or orthognathic treatment
• Contraindications: Prophylactic adjustment without evidence of TFO signs/symptoms; as primary treatment of microbial-induced periodontal disease; without pre-treatment study and patient education

B. Management of Parafunctional Habits

• Correct diagnosis of bruxism (history + clinical findings)
• Night guard (occlusal appliance) to prevent nocturnal grinding; also promotes masticatory muscle relaxation

C. Splinting

• Indications: Stabilize teeth with increasing mobility not responding to occlusal adjustment and periodontal treatment; teeth with advanced mobility interfering with normal function; stabilize teeth post-orthodontic movement; prevent tipping/drifting of teeth
• Contraindications: When inflammatory periodontal disease has not been addressed; when occlusal adjustment has not been previously addressed
• Types: Composite resin splint (with or without fiber meshwork), wire splint with composite resin

D. Orthodontic Tooth Movement

E. Occlusal Reconstruction

F. Extraction of Selected Teeth

SUMMARY TABLE: Key Distinctions

CONCLUSION

ABBREVIATIONS USED:

• TFO = Trauma from Occlusion
• PDL = Periodontal Ligament
• WHO = World Health Organization
• AAP = American Academy of Periodontology
• ICP = Intercuspal Position
• CBCT = Cone Beam Computed Tomography
• RANKL = Receptor Activator of Nuclear Factor Kappa-B Ligand
• IL = Interleukin
• TMJ = Temporomandibular Joint
• CEJ = Cementoenamel Junction
• N = Newton (unit of force)

REFERENCES (from uploaded materials):

1. Newman MG, Takei HH, Klokkevold PR, et al. Newman and Carranza's Clinical Periodontology and Implantology, 14th ed. Elsevier, 2023 (Chapter 35).
2. Newman MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology, 10th ed. Saunders, 2006 (Chapter 29).
3. Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry, 5th ed. Blackwell Munksgaard, 2008 (Chapter 14 - Lindhe, Nyman & Ericsson; Chapter 15 - Lang & Berglundh).
4. Rose LF, Genco RJ, Mealey BL, Cohen DW. Periodontics: Medicine, Surgery and Implants. Elsevier Mosby (Chapter 29 - Rosenberg & Evian).
5. Bathla SC. Periodontics Revisited (Periobasic). Jaypee Brothers (Chapter 35 - Trauma from Occlusion).

Answer Structure at a Glance