Acute and Chronic Trauma

Trauma from occlusion may be acute or chronic. Acute trauma from occlusion results from an abrupt occlusal impact such as that produced by biting on a hard object (e.g., olive pit). Restorations or prosthetic appliances that interfere with or alter the direction of occlusal forces on the teeth may also induce acute trauma.

Acute trauma results in tooth pain, sensitivity to percussion, and increased tooth mobility. If the force is dissipated by a shift in the position of the tooth or by the wearing away or correction of the restoration, then the injury heals, and the symptoms subside. Otherwise, periodontal injury may worsen and develop into necrosis accompanied by periodontal abscess formation, or it may persist as a symptom-free chronic condition. Acute trauma can also produce cementum tears (Figure 22-2) (see Chapter 2).

Chronic trauma from occlusion is more common than the acute form, and it is of greater clinical significance. It most often develops from gradual changes in occlusion produced by tooth wear, drifting movement, and extrusion of the teeth in combination with parafunctional habits (e.g., bruxism, clenching) rather than as a sequela of acute periodontal trauma (see Chapter 20). The features of chronic trauma from occlusion and their significance are discussed in the following sections.

The criterion that determines if an occlusion is traumatic is whether it produces periodontal injury; this criterion is not how the teeth occlude. Any occlusion that produces periodontal injury is traumatic. Malocclusion is not necessary to produce trauma; periodontal injury may occur when the occlusion appears normal. The dentition may be anatomically and aesthetically acceptable but functionally injurious. Similarly, not all malocclusions are necessarily injurious to the periodontium. Traumatic occlusal relationships are referred to by such terms as occlusal disharmony, functional imbalance, and occlusal dystrophy. These terms refer to the effect of the occlusion on the periodontium rather than to the position of the teeth. Because trauma from occlusion refers to the tissue injury rather than the occlusion, an increased occlusal force is not traumatic if the periodontium can accommodate it.

Primary and Secondary Trauma from Occlusion

Trauma from occlusion may be caused by alterations in occlusal forces, a reduced capacity of the periodontium to withstand occlusal forces, or both. When trauma from occlusion is the result of alterations in occlusal forces, it is called primary trauma from occlusion. When it results from the reduced ability of the tissues to resist the occlusal forces, it is known as secondary trauma from occlusion.

Primary trauma from occlusion occurs if trauma from occlusion is considered the primary etiologic factor in periodontal destruction and if the only local alteration to which a tooth is subjected is a result of occlusion. Examples include periodontal injury produced around teeth with a previously healthy periodontium after the following: (1) the insertion of a “high filling”; (2) the insertion of a prosthetic replacement that creates excessive forces on abutment and antagonistic teeth; (3) the drifting movement or extrusion of the teeth into spaces created by unreplaced missing teeth; or (4) the orthodontic movement of teeth into functionally unacceptable positions. Most studies of the effect of trauma from occlusion involving experimental animals have examined the primary type of trauma. Changes produced by primary trauma do not alter the level of connective tissue attachment and do not initiate pocket formation. This is probably because the supracrestal gingival fibers are not affected and therefore prevent the apical migration of the junctional epithelium.⁴⁸

Secondary trauma from occlusion occurs when the adaptive capacity of the tissues to withstand occlusal forces is impaired by bone loss that results from marginal inflammation. This reduces the periodontal attachment area and alters the leverage on the remaining tissues. The periodontium becomes more vulnerable to injury, and previously well-tolerated occlusal forces become traumatic.

Figure 22-3 depicts three different situations on which excessive occlusal forces can be superimposed:

The first case is an example of primary trauma from occlusion, whereas the last two represent secondary trauma from occlusion. The effects of trauma from occlusion in these different situations are analyzed in the following discussion.

It has been found in experimental animals that systemic disorders can reduce tissue resistance and that previously tolerable forces may become excessive.21,51,61 This could theoretically represent another mechanism by which tissue resistance to increased forces is lowered, thereby resulting in secondary trauma from occlusion.

Stage I: Injury

Tissue injury is produced by excessive occlusal forces. The body then attempts to repair the injury and restore the periodontium. This can occur if the forces are diminished or if the tooth drifts away from them. If the offending force is chronic, however, 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.

Under the forces of occlusion, a tooth rotates around a fulcrum or axis of rotation, which in single-rooted teeth is located in the junction between the middle third and the apical third of the clinical root and in multirooted teeth in the middle of the interradicular bone (Figure 22-4). This creates areas of pressure and tension on opposite sides of the fulcrum. Different lesions are produced by different degrees of pressure and tension. If jiggling forces are exerted, these different lesions may coexist in the same area.

The areas of the periodontium that are most susceptible to injury from excessive occlusal forces are the furcations.²²

Injury to the periodontium produces a temporary depression in mitotic activity, in the rate of proliferation and differentiation of fibroblasts,⁶² in collagen formation, and in bone formation.^29,58,60,62 These return to normal levels after the dissipation of the forces.

Stage II: Repair

Repair occurs constantly in the normal periodontium, and trauma from occlusion stimulates increased reparative activity.

The damaged tissues are removed, and new connective tissue cells and fibers, bone, and cementum are formed in an attempt to restore the injured periodontium (Figure 22-5). Forces remain traumatic only as long as the damage produced exceeds the reparative capacity of the tissues.

When bone is resorbed by excessive occlusal forces, the body attempts to reinforce the thinned bony trabeculae with new bone (Figure 22-6). This attempt to compensate for lost bone is called buttressing bone formation, and it is an important feature of the reparative process associated with trauma from occlusion.¹⁶ It also occurs when bone is destroyed by inflammation or osteolytic tumors.

Buttressing bone formation occurs within the jaw (central buttressing) and on the bone surface (peripheral buttressing). During central buttressing, the endosteal cells deposit new bone, which restores the bony trabeculae and reduces the size of the marrow spaces. Peripheral buttressing occurs on the facial and lingual surfaces of the alveolar plate. Depending on its severity, peripheral buttressing may produce a shelflike thickening of the alveolar margin, which is referred to as lipping (Figure 22-7), or a pronounced bulge in the contour of the facial and lingual bone^8,16 (see Chapter 14).

Cartilage-like material sometimes develops in the periodontal ligament space as an aftermath of the trauma.¹³ The formation of crystals from erythrocytes has also been demonstrated.⁵⁷

Stage III: Adaptive Remodeling of the Periodontium

If the repair process cannot keep pace with the destruction caused by the occlusion, the periodontium is remodeled in an effort to create a structural relationship in which the forces are no longer injurious to the tissues.¹⁸ This results 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.⁶⁷ Increased vascularization has also been reported.⁹

The three stages in the evolution of traumatic lesions have been differentiated histometrically by the relative amounts of periodontal bone surface undergoing resorption or formation5,8 (Figure 22-8). The injury phase shows an increase in areas of resorption and a decrease in bone formation, whereas the repair phase demonstrates decreased resorption and increased bone formation. After adaptive remodeling of the periodontium, resorption and formation return to normal.