Bruxism, Clenching, and Occlusal Neurosis

Trauma From Occlusion

When occlusal forces exceeds the adaptive capacity of tissues, tissue injury results which is called as trauma from occlusion or occlusal trauma.Orban and Glickman et al (1968)

Trauma from Occlusion is defined as “damage in the periodontium caused by stress on the teeth produced directly or indirectly by the teeth of the opposing jaw”.

Classification of Trauma from Occlusion

Depending on Mode of Onset

Acute trauma from occlusion
Chronic trauma from occlusion

Read And Learn More: Periodontics Question And Answers

Depending on Capacity of Periodontium to Resist Occlusal Forces

Primary trauma from occlusion
Secondary trauma from occlusion

Trauma from Occlusion Clinical Features

Presence of hypermobility of tooth is the most common clinical sign.
Presence of tooth migration
Presence of tenderness of tooth while chewing or percussion.
Presence of tenderness in muscles of mastication.
Temporomandibular dysfunction is seen.
Presence of chipped enamel or crown/root fractures.
Wear facets are seen beyond the level of age of patient’s and diet consistency.
Presence of fremitus.
In severe cases, periodontal abscess formation and cemental tears are seen.

Histopathological Features or Tissue Response to Increased Occlusal Forces

The response of tissues is explained under three stages, i.e.

Stage 1—Injury
Stage 2—Repair
Stage 3—Adaptive remodeling of periodontium.

Trauma from Occlusion Stage : Injury

Tissue injury occurs due to excessive occlusal forces.
Body then attempts to repair the injury and restore the periodontium.
This may occur if the forces are diminished or if the tooth drift away from them.
If the offending force is chronic, the periodontium is remodeled to cushion its impact. The ligament is widened at the expense of the bone, which results in angular bone defects without periodontal pockets, and the tooth becomes loose.
Slightly excessive pressure stimulates the resorption of alveolar bone along with the resultant widening of the periodontal ligament space.
Slightly excessive tension leads to elongation of periodontal ligament fibers and apposition of alveolar bone.
In areas of increased pressure, blood vessels are numerous and reduced in size; in areas of increased tension, they get enlarged.
Greater pressure leads to the gradation of changes inside periodontal ligament, starting with compression of the fibers, which produces areas of hyalinization.
Subsequent injury to firoblasts and other connective tissue cells leads to necrosis of areas of the ligament.
Vascular changes are also seen within 30 minutes, impairment and stasis of blood flw occur at 2 to 3 hours, blood vessels appear to be packed with erythrocytes, which start to fragment; and between 1 and 7 days, disintegration of the blood vessel walls and release of the contents into the surrounding tissue occur.
In addition there is increased resorption of alveolar bone and resorption of the tooth surface occurs.
Severe tension leads to widening of periodontal ligament, thrombosis, hemorrhage, tearing of the periodontal ligament, and resorption of alveolar bone.
Pressure, which is severe enough to force the root against bone leads to necrosis of the periodontal ligament and bone.
Bone gets resorbed from viable periodontal ligament adjacent to necrotic areas and from marrow spaces, this process is known as undermining resorption.

Trauma from Occlusion Stage 2: Repair

Repair goes on constantly inside the normal periodontium, and trauma from occlusion stimulates increased reparative activity.
Damaged tissues are removed, and new connective tissue cells and fibers, bone, and cementum are formed in an attempt to restore the injured periodontium.
Forces remain traumatic only as long as damage produced exceeds the reparative capacity of tissues.
When bone gets resorbed by excessive occlusal forces, the body attempts to reinforce the thinned bony trabeculae with new bone. This attmpt to compensate for lost bone is known as buttressing bone formation which is an important feature of the reparative process associated with trauma from occlusion.
This buttessing bone formation also occurs when bone is destroyed by inflmmation or osteolytic tumors.
Buttessing bone formation occurs within the jaw known as central buttessing and on the bone surface known as peripheral buttessing.
During central buttessing, the endosteal cells deposit new bone, which restores the bony trabeculae and reduces the size of the marrow spaces.
Peripheral butterssing occurs on the facial and lingual surfaces of the alveolar plate.
Depending on its severity, peripheral butterssing may produce a shelf like thickening of the alveolar margin, which is referred to as lipping or a pronounced bulge in the contour of the facial and lingual bone.

Trauma from Occlusion Stage 3: Adaptive Remodeling of Periodontium

If repair process cannot keep pace with the destruction produced by the occlusion, the periodontium is remodeled in an effort to create a structural relationship in which the forces are no longer injurious to tissues.
This result in a widened periodontal ligament, which is funnel shaped at the crest, and angular defects in the bone, with no pocket formation. The involved teeth become loose.
Increased vascularization has also been observed.
Injury phase demonstrates an increase in areas of resorption and a decrease in bone formation, whereas the repair phase shows decreased resorption and increased bone formation.
After adaptive remodeling of the periodontium, resorption and formation return to normal.

Trauma From Occlusion Radiographic Features

There is increased width of the periodontal space, often with thickening of lamina dura along the lateral aspect of the root, in apical region, and in bifurcation areas.
A vertical rather than horizontal destruction of the interdental septum.
Radiolucency and condensation of the alveolar bone.
Presence of root resorption.

Role of Trauma from Occlusion in Pathogenesis of Periodontal Disease

The role of trauma from occlusion in pathogenesis of periodontal disease is explained by:

Glickman’s Concept

He claimed that the pathway of spread of plaque associated gingival lesion can be changed, if forces of an abnormal magnitude are acting on teeth harboring subgingival plaque. He explained, teeth which are nontraumatized exhibit suprabony pockets and horizontal bone loss, whereas teeth with trauma exhibits, angular bony defects and infrabony pockets:

According to him periodontal structures are divided into two parts:

Zone of irritation.
Zone of co-destruction.

Zone of Irritation

This zone includes marginal and interdental gingiva. Sof tissue of this zone is bordered by hard tissue i.e. tooth is only on one side and is not affcted by forces of occlusion. This means that gingival inflmmation cannot be induced by trauma from occlusion but is the result of irritation from microbial plaque.
The plaque-associated lesion at a non-traumatized tooth propagates in apical direction by first involving the alveolar bone and later the periodontal ligament area. The progression of this lesion results in an even (horizontal) bone destruction

Zone of Co-destruction

This includes the periodontal ligament, the root, cementum and alveolar bone and is coronally demarcated by the transseptal (interdental) and the dentoalveolar collagen 0.fiber bundles.
The tissue in this zone may become the seat of a lesion caused by trauma from occlusion.
The spread of the inflammatory lesion from the zone of irritation directly down into the periodontal ligament (i.e. not via the interdental bone) may hereby be facilitated.
This alteration of the normal pathway of spread of the plaque-associated inflammatory lesion results in the development of angular bony defects.
According to Glickman (1967), trauma from occlusion is the significant causative agent in situations where angular bony defects combined with infrabony pockets are found at one or the several teeth.

Waerhaug’s Concept

The loss of periodontium, according to Waerhaug, was result of inflammatory lesions associated with subgingival plaque. He concluded that angular defects occur when subgingival plaque of one tooth has reached more apical level than microbiota on neighboring tooth, and when volume of alveolar bone surrounding roots is comparatively large.

In conclusion, four possibilities can occur when a tooth with gingival inflmmation is expressed to trauma.

Trauma from occlusion may alter pathway of extension of gingival inflmmation to underlying tissues inflmmation may proceed to PDL rather than to alveolar bone and resulting bone loss will be angular with infrabony pockets.
It may favor the environment for formation of attchment of plaque and calculus and may be responsible for development of deeper lesions.
Supragingival plaque can become subgingival, if the tooth is tilted orthodontically migrates into an edentulous area, resulting in transformation of suprabony pocket into an infrabony pockets.
Increase tooth mobility associated with trauma to periodontium may have pumping effct of plaque metabolites increasing their diffusion.