What is Occlusal Trauma?

Occlusal trauma refers to the injury resulting in tissue changes within the attachment apparatus as a result of occlusal force(s) (Glossary of Periodontal Terms, 2001). The culprit of this type of histologically diagnosed lesion is the occlusal traumatism (Glossary of Periodontal Terms, 2001) (or traumatogenic occlusion). Occlusal trauma will arise when the occlusal load is sufficiently high that the periodontium cannot withstand and distribute the force without unaltered position and stability of the involved teeth.

Occlusal trauma can be further classified in:

• Primary occlusal trauma: damage around a tooth with a normal, healthy and non-inflamed periodontium caused by excessive and non-physiological forces.
• Secondary occlusal trauma: damage around a tooth with a reduced height of the periodontium, caused by normal or excessive and non-physiological forces.

Signs of occlusal trauma are: fremitus, pulpal and/or periodontal sensitivity, abnormal tooth mobility, enamel wear, tooth fracture, widening of the periodontal ligament.

The Role of Occlusion on the Initiation of Periodontal Disease

Glickman & Smulow 1965 found that trauma doesn’t cause gingival inflammation or periodontal pockets. If gingival inflammation extends beyond gingival margin and transeptal fibers, trauma combined with inflammation acts as a “Co-destructive” factor and results in more sever bone loss than that seen with periodontitis alone. They believed that excessive occlusal forces associated with tension and pressure alter the pathway of inflammation and induce an oblique arrangement of transeptal fibers (rather than perpendicular) resulting in specific destructive patterns like angular/vertical infrabony defects.

Using a similar study design, Waerhaug in 1979 found no evidence that traumatic forces act as co-factor in causation of angular defects. According to Waerhaug, loss of attachment and bone resorption around teeth is the result of inflammation induced by bacterial plaque. In his research the author found that a plaque forefront approximated bone for a distance ranging from 0.5 to 2.7mm. The most coronal periodontal fibers could be found at 0.2 to 1.8mm from plaque. Noticing that bone resorption was always present when the plaque forefront was 0.5mm or closer to the bone, he hypothesized that angular defects occur when the apical extent of plaque on adjacent teeth is at different levels on two neighboring teeth. These two studies (Glickman 1965 and Waerhaug 1979) have a major weakness; both used autopsy material to draw their conclusions. This type of investigation is not able to prove the cause effect relationship between occlusal traumatism and periodontal destruction. Therefore other investigators decided to further study the issue.

The effect of occlusal forces on periodontal attachment levels has been well-studied in animal models. I will briefly summarize the studies the brought light on the role of occlusal trauma on initiation of periodontal disease.

Single episode of trauma: Polson and Zander 1983 found that a single episode of trauma results in damage to the periodontium consisting in ischemia, necrosis, undermining resorption, widening of the periodontal ligament space. However, this lesion was totally reversible and the periodontium healed with no loss of connective tissue attachment or bone (the gold standard to measure periodontal destruction).

Jiggling-type of trauma: the effect of jiggling-type of trauma has been studied on healthy periodontium and on healthy but reduced periodontium.

Neither single nor repeated episodes of trauma produce loss of connective tissue attachment

On healthy periodontium: Polson 1976 (I and II) examining histologically interproximal areas of mandibular bicuspids of monkeys jiggled mesiodistally for 10 weeks found an area of compression (acellular, necrotic area paired with bone resorption) and an area of tension (highly cellular and vascular) followed by intense osteoclastic-mediated resorptive activity of the adjacent alveolar bone. The alveolar bone changes consisted in loss of height and density, with large marrow spaces surrounded by vascular and cellular connective tissue, however these changes were reversible after interruption of the jiggling. No initiation of loss of attachment was detected.

 Jiggling trauma can cause loss in height of crestal bone, and a considerable loss in volume. This damage to the bony support is totally reversible once trauma is halted.

On reduced but healthy periodontium: Perrier and Polson 1982 studying the effect of progressive and increasing tooth hypermobility upon a periodontium reduced by marginal periodontitis where the inflammatory lesion had been resolved, found that an existing inflammation in the gingival tissues will not be converted to a destructive periodontitis as a result of tooth mobility. Progressive and increased mobility represents an adaptation to accomodate the forces and is without effect upon the level of connective tissue attachment which will be maintained by control gingival inflammation. In dogs Lindhe and Ericsson 1976 found that after resolving inflammation oral hygiene, scaling and root planing and modified Widman flap, healing also occurred in cases where jiggling forces were acting on hypermobile teeth. Healing occurred when the test teeth were still in “traumatic phase” (widened periodontal ligament, increase vascularity, increased tooth mobility, increased osteoclastic activity). No connective tissue attachment loss occurred, jiggling and tooth hypermobility had no detrimental effect on healing after periodontal surgery.

In conclusion: Jiggling trauma can cause loss in height of crestal bone, and a considerable loss in volume. This damage to the bony support is totally reversible once trauma is halted. Neither single nor repeated episodes of trauma produce loss of connective tissue attachment.

Traumatic lesions and their sequelae will not cause periodontal pocket formation.

The Role of Occlusion on the Progression of Periodontal Disease

Here comes Part 2. In this section I will discuss the role of occlusion in progression of periodontal disease. This one is shorter and easy to read.

Single episode of trauma + periodontal disease

Polson 1974, in monkeys, found that at the time of trauma an area of acellularity in the PDL subjacent the area of inflammatory infiltration associated with periodontitis was present. At 2 weeks the area was repopulated by cells, bone resorption created a widened PDL space, osteoid tissue showed that repair was occurring. At 8 weeks the tissues were similar to controlateral areas that had periodontitis but did not receive the single trauma. No CT attachment or bone loss.

Jiggling-type of trauma + periodontal disease

Meitner 1975 found loss of alveolar bone and widening of PDL space but no loss of connective tissue attachment. Polson in 1983 found greater loss of bone in presence of periodontitis with intrabony defects and trauma but no increased loss of CT attachment.Angular defects were not related to presence or absence of trauma, location of plaque may be the principal factor in determining pattern of bone loss (horizontal if on adjacent surfaces and vertical if on isolated surfaces).

Lindhe and Svanberg 1974 found that after 6 months of trauma plus periodontitis there was a dramatic change in alveolar bone morphology at crestal and apical locations, and greater loss of CT attachment when trauma was present.

The difference between studies from Rochester and Gothenburg might be due to the different model (Monkey vs Dog), the difference in forces applied during trauma (low forces vs high forces) and the duration of trauma (short-term vs long-term).

A single episode of trauma + periodontal disease does not enhance marginal periodontitis.
Jiggling trauma + periodontal disease enhance bone loss and might alter CT attachment levels.

The Role of Occlusion on the Response to Periodontal Disease Therapy

Does occlusal trauma (and therefore mobility) affect the outcome of our therapy?

The influence of occlusal traumatism on response to periodontal therapy (surgical on non-surgical) has been evaluated in a limited number of clinical trials. Probably one of the major difficulties is to clinically assess which tooth might present occlusal trauma. In fact, not every mobile tooth suffers from occlusal trauma, but certainly every tooth with a sustained occlusal trauma lesion will become mobile.

Animal studies

Polson 1979 found that when tooth mobility is due only to periodontitis, after resolution of inflammation (removal of plaque and calculus) a marked reduction of mobility occurred. However, there was no gain in attachment or coronal bone gain.
When tooth mobility is due to periodontitis + trauma if:

• Jiggling trauma was discontinued, but periodontitis persisted (Polson 1976 II), no decrease in tooth hypermobility, no change in clinical attachment level (CAL), no changes in bone morphology occurred. Periodontitis seems to be the one to inhibit alveolar bone regeneration and not trauma.
• Jiggling trauma and periodontitis (both) were resolved (Kantor 1976, Polson 1983) mobility decreased, bone density increased, but there were no changes in CAL.

Human studies

As previously said, in a clinical study it is difficult (if not impossible) to know if a tooth is suffering from occlusal trauma. Therefore most of the studies used other criteria, such as: mobility, occlusal wear or parafunction, to assess the link between periodontal disease and occlusal traumatism.

Philstrom 1986: Teeth with signs of traumatism (widened periodontal ligament and functional mobility) had deeper probing depth (PD), more CAL loss and less radiographic bone support, whereas teeth with no evidence of traumatism had no significant differences in PD, CAL or bone loss.
Ismail 1990 in the Tecumseh study found that mobility is a risk marker for loss of periodontal attachment.
Neiderud 1992 examining PD at mobile/nonmobile teeth found that mobility can lower resistance to probing (this could explain some of the findings of previous studies).
Jin and Cao 1992 reported no difference in PD and CAL between teeth with and without abnormal occlusal contacts.
Nunn and Harrel 2001 found that teeth with no initial (or treated) occlusal discrepancies were 60% less likely to worsen in overall clinical condition compared to teeth with untreated occlusal discrepancies.
Cortellini 2001 in a randomized clinical trial on regeneration of infrabony defect found that mobility was associated with reduced gain of clinical attachment and reduced bone fill. However, the main objective of the study was another and the influence of occlusion was evaluated as secondary outcome.

In conclusion:

Occlusal discrepancies are quite common in general population and do not require any adjustment. Ramfjord and Ash in 1981 stated that:

The need for adjustment should be based on a definite diagnosis of a traumatic lesion rather than the location of some occlusal interferences which may be of no significance.

Occlusion should not be adjusted as a preventive measure. When evident traumatic lesions are present clinically and/or radiographically it might be appropriate to adjust the occlusion. Another “biological” rationale for occlusal adjustment could be: stabilization of blood clot, increasing mobility despite of therapy, or mobility not compatible with masticatory function.