Chronic Periodontitis

Chronic periodontitis is the most common form of periodontitis13; Box 5.3 includes the characteristics of this form of
periodontitis. Chronic periodontitis is most prevalent in adults, but it can also be observed in children. Different classiication
schemes have confirmed or discarded the age range of more than 35 years to separate chronic versus aggressive
periodontitis. According to the existing deinition, persons younger than 35 years may exhibit a rate of progression of disease
consistent with the deinition of chronic periodontitis. Nonetheless, epidemiologic evidence supports the suggestion that
persons younger than 25 years at disease onset are likely to exhibit aggressive periodontitis. Intraoral radiographs along with
periodontal charting records are of paramount importance to the documentation of disease onset and rate of progression.
Chronic periodontitis is associated with the accumulation of plaque and calculus. It generally has a slow to moderate rate of
disease progression, but periods of more rapid destruction may also be observed. Increases in the rate of disease progression
may be caused by the impact of local, systemic, or environmental factors that may inluence the normal host–bacteria
interaction. Local factors may inluence plaque accumulation (Box 5.4), whereas systemic diseases (e.g., diabetes mellitus,
HIV) may inluence the host’s defenses, and environmental factors (e.g., cigarette smoking, stress) may influence the
response of the host to plaque accumulation. Chronic periodontitis may occur as a localized disease in which less than 30%
of evaluated teeth demonstrate attachment and bone loss, or it may occur as generalized when more than 30% of teeth are
affected.
Chronic periodontitis can be further classiied on the basis of its extent and severity. The severity of disease has
been traditionally determined as either slight/mild (1 to 2 mm of loss; Fig. 5.15), moderate (3 to 4 mm of loss; Fig. 5.16), or
severe (_5 mm of loss; Fig. 5.17) on the basis of the amount of clinical attachment loss (see Box 5.3). Clinical attachment
levels provide important beneits over probing depth alone to monitor disease progression using the CEJ as a ixed reference
point. In fact, probing depth levels only have poor to moderate sensitivity for predicting attachment level changes overtime.
Nonetheless, clinical experience has revealed that oftentimes measurement of clinical attachment levels in practice may
prove to be erroneous. The most common error occurs in the case of sites without gingival recession, whereby the location of
the gingival margin is coronal to the CEJ. If the clinician in such a case only records the probing depth without charting the
location of the CEJ (often charted as “positive recession” in electronic periodontal charts), the resulting attachment levels
will be erroneously recorded as being equal to the probing depth. To prevent such an overestimate of disease, it has been
suggested that clinicians consider that mild periodontitis be associated with probing depths of <4 mm, moderate periodontitis
with probing depths of 5 to 6 mm, and severe periodontitis with probing depths of _7 mm. However, probing depths alone
should not be used to classify periodontitis without simultaneous consideration of clinical attachment levels and radiographic
bone loss.

STILLMAN’S CLEFT AND MCCALL FESTOONED

The term Stillman cleft has been used to describe a speciic type of gingival recession that consists of a narrow,
triangularshaped gingival recession. As the recession progresses apically, the cleft becomes broader, thereby exposing the
cementum of the root surface. When the lesion reaches the mucogingival junction, the apical border of oral mucosa is
usually inlamed because of the difficulty in maintaining adequate plaque control at this site. The term McCall festoon has
been used to describe a rolled, thickened band of gingiva that is usually seen adjacent to the cuspids when recession
approaches the mucogingival junction. Initially,
Stillman clefts and McCall festoons were attributed to traumatic occlusion, and the recommended treatment was occlusal
adjustment. However, this association was never proved, and the indentations
merely represent peculiar inlammatory changes of the marginal gingiva

Bone Loss and Patterns of Bone Destruction, 316

Bone Destruction Caused by Trauma

From Occlusion
Another cause of periodontal bone destruction is trauma from occlusion, which can occur in the absence or presence of
inflammation (see Chapter 25). In the absence of inlammation, the changes caused by trauma
from occlusion vary from increased compression and tension of the periodontal ligament and increased osteoclasis of
alveolar bone to necrosis of the periodontal ligament and bone and the resorption of bone and tooth structure. These changes
are reversible in that they can be repaired if the offending forces are removed. However, persistent trauma from occlusion
results in funnel-shaped widening of the crestal portion of the periodontal ligament with resorption of the adjacent bone. 33
These changes, which may cause the bony crest to have an angular shape, represent adaptation of the periodontal tissues
aimed at “cushioning” increased occlusal forces; however, the modiied bone shape may weaken tooth support and cause
tooth mobility. When it is combined with inlammation, trauma from occlusion may aggravate the bone destruction caused by
the inlammation33 and results in bizarre bone patterns.

Furcation involvements have been classiied as grades I through IV according to the amount of tissue destruction. Grade I
involves incipient bone loss; grade II involves partial bone loss (cul-de-sac); and grade III involves total bone loss with a
through-and-through opening of the furcation, but the opening of the furcation is not visible due to the gingiva, which covers
the oriice. Grade IV is to grade III but includes gingival recession that exposes the furcation to view. (See Chapter 64 for
further discussion on furcation classiication.)

Trauma From Occlusion (Chapter 25)

Trauma from occlusion is deined as microscopic alterations of periodontal structures in the area of the periodontal
ligament that become manifest clinically in the elevation of tooth mobility. As mentioned earlier, an inherent “margin of
safety” that is common to all tissues permits some variation in occlusion without adversely affecting the periodontium.
However, when occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. 43,44 The resultant injury is
termed trauma from occlusion, which is also known
as occlusal trauma.
Thus trauma from occlusion refers to the tissue injury rather than the occlusal force. An occlusion that produces
such an injury is called a traumatic occlusion.2 Excessive occlusal forces may also disrupt the function of the masticatory
musculature and cause painful spasms, injure the temporomandibular joints, or produce excessive tooth wear. However, the
term trauma from occlusion is generally used in connection with injury in the periodontium.
Traumatic occlusal relationships are referred to by such terms as occlusal disharmony, functional imbalance, and
occlusal dystrophy.
Acute trauma from occlusion refers to periodontal changes associated with an abrupt occlusal impact such as that
produced by biting on a hard object (e.g., an olive pit). In addition, 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.
Chronic trauma from occlusion refers to periodontal changes associated with 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. Chronic trauma from occlusion is more common
than the acute form and of greater clinical significance.

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.
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.

Clinical and Radiographic Signs of Trauma From Occlusion Alone

The most common clinical sign of trauma to the periodontium is increased tooth mobility. During the injury stage of trauma
from occlusion, the destruction of periodontal ibers occurs, which increas es tooth mobility. During the inal stage, the
accommodation of the periodontium to increased forces entails a widening of the periodontal ligament, which also leads to
increased tooth mobility. Although this tooth mobility is greater than the so-called normal mobility, it cannot be considered
pathologic, because it is an adaptation and not a disease process. If it does become progressively worse, it can then be
considered pathologic.
Other causes of increased tooth mobility include advanced bone loss, inlammation of the periodontal ligament of periodontal
or periapical origin, and some systemic causes (e.g., pregnancy). The destruction of surrounding alveolar bone, such as
occurs with osteomyelitis or jaw tumors, may also increase tooth mobility.

Radiographic signs of trauma from occlusion may include the following:

1. Increased width of the periodontal space, often with thickening of the lamina dura along the lateral aspect of the root, in
the apical region, and in bifurcation areas. These changes do not necessarily indicate destructive changes, because they may
result from thickening and strengthening of the periodontal ligament and alveolar bone, thereby constituting a favorable
response to increased occlusal forces.
2. A vertical rather than horizontal destruction of the interdental septum.
3. Radiolucency and condensation of the alveolar bone.
4. Root resorption.
In summary, trauma from occlusion does not initiate gingivitis or periodontal pockets, but it may constitute an additional risk
factor for the progression and severity of the disease. An understanding of the effect of trauma from occlusion on the
periodontium is useful during the clinical management of periodontal problems

Trauma From Occlusion

Trauma from occlusion can produce radiographically detectable changes in the thickness of the lamina dura,
morphology of the alveolar crest, width of the PDL space, and density of the surrounding cancellous bone.5
Traumatic lesions manifest more clearly in faciolingual aspects because mesiodistally, the tooth has added stability provided
by the contact areas with adjacent teeth. Therefore slight variations in the proximal surfaces may indicate greater changes in
the facial and lingual aspects.
The radiographic changes listed next are not pathognomonic for trauma from occlusion and must be interpreted in
combination with clinical indings, particularly tooth mobility, presence of wear facets, pocket depth, and analysis of occlusal
contacts and habits.
The injury phase of trauma from occlusion produces a loss of the lamina dura that may be noted in apices,
furcations, and marginal areas. This loss of lamina dura results in widening of the PDL space (Fig. 33.23). The repair phase
of trauma from occlusion results in an attempt to strengthen the periodontal structures to better support the increased loads.
Radiographically, this is manifested by a widening of the PDL space, which may be generalized or localized. Although
microscopic measurements have determined normal variations in the PDL space width along the root surface, these are
generally not detected radiographically. Thus, when seen on radiographs, variations in PDL space width suggest that the
tooth is being subjected to increased forces. Successful attempts to reinforce the periodontal structures by widening the PDL
space can be accompanied by increased width of the lamina dura and sometimes by condensation of the perialveolar
cancellous bone. More advanced traumatic lesions may result in deep angular bone loss, which, when combined with
mgairnal inlammation, may lead to intrabony pocket formation. In terminal stages, these lesions extend around the root apex,
producing a wide, radiolucent periapical image (cavernous lesions).
Root resorption may also result from excessive forces on the periodontium, particularly those caused by
orthodontic appliances. Although trauma from occlusion produces many areas of root resorption, these areas are usually of a
magnitude insuficient to be detected radiographically.

Radiographic Appearance of Periodontal Disease Periodontitis

Radiographic changes in periodontitis follow the pathophysiology of periodontal tissue destruction and include the
following:
1. Fuzziness and disruption of lamina dura crestal cortication continuity is the earliest radiographic change in periodontitis
(Fig. 33.12A–B) and results from bone resorption activated by extension of gingival inlammation into the periodontal bone.
Depicting these early changes depends greatly on the radiographic technique, as well as on anatomic variations (thickness
and density of interdental bone, position of adjoining teeth). No correlation has been found between crestal lamina dura in
radiographs and the presence or absence of clinical inlammation, bleeding on probing, periodontal pockets, or loss of
attachment.16 Therefore
it can be concluded that the presence of an intact crestal lamina dura may be an indicator of periodontal health, whereas its
absence lacks diagnostic relevance.1,3
2. Continued periodontal bone loss and widening of the periodontal space results in a wedge-shaped radiolucency at the
mesial or distal aspect of the crest (Fig. 33.12B). The apex of the area is pointed in the direction of the root.
3. Subsequently, the destructive process extends across the alveolar crest, thus reducing the height of the interdental bone.
As increased osteoclastic activity results in increased bone resorption along the endosteal margins of the medullary spaces,
the remaining interdental bone can appear partially eroded (Fig. 33.12C).
4. The height of the interdental septum is progressively reduced by the extension of inlammation and the resorption of bone
(Fig. 33.12D).
5. Frequently a radiopaque horizontal line can be observed across the roots of a tooth. This opaque line demarcates the
portion of the root where the labial or lingual bony plate has been partially or completely destroyed from the remaining
bone-supported portion

Periodontal Examination and Diagnosis, 378

Mobility is scored according to the ease and extent of tooth movement according
to the Miller Index46 as follows:
• Mobility no. 1: irst distinguishable sign of movement greater than “normal”
• Mobility no. 2: movement of the crown up to 1 mm in any direction
• Mobility no. 3: movement of the crown more than 1 mm in any direction or vertical depression or rotation of the crown in
its socket
Physiologic mobility is movement up to 0.2 mm horizontally and 0.02 mm axially. Mobility beyond the physiologic range is
termed abnormal or pathologi

Currently, the severity of chronic periodontitis is characterized on a three-tier system based on clinical attachment loss
(CAL): slight = 1 or 2 mm CAL, moderate = 3 or 4 mm CAL, and severe ≥5 mm CAL.

Clinical Risk Assessment, 410

Determination of Prognosis, 413

A prognosis is a prediction of the probable course, duration, and outcome of a disease based on a general knowledge of the
pathogenesis of the disease and the presence of risk factors for the disease. It
One scheme25,34 assigns the following classiications:
Good prognosis: Control of etiologic factors and adequate periodontal support ensure the tooth will be easy to maintain by
the patient and clinician.
Fair prognosis: Approximately 25% attachment loss or grade I furcation invasion (location and depth allow proper
maintenance with good patient compliance).
Poor prognosis: 50% attachment loss, grade II furcation invasion (location and depth make maintenance possible but
dificult).
Questionable prognosis: >50% attachment loss, poor crown-to-root ratio, poor root form, grade II furcation invasion
(location and depth make access dificult) or grade III furcation invasion; mobility no. 2 or no. 3; root proximity.
Hopeless prognosis: Inadequate attachment to maintain health, comfort, and function

In contrast to schemes based on tooth mortality, Kwok and Caton25 proposed a scheme based on “the probability of obtaining
stability of the periodontal supporting apparatus.” This scheme is based on the probability of disease progression as related
to local and systemic factors (see Box 35.1). Although some of these factors may affect disease progression more than
others, consideration of each factor is important in assigning a prognosis. This scheme is as follows:
Favorable prognosis: Comprehensive periodontal treatment and maintenance will stabilize the status of the tooth. Future
loss of periodontal support is unlikely.
Questionable prognosis: Local or systemic factors inluencing the periodontal status of the tooth may or may not be
controllable. If controlled, the periodontal status can be stabilized with comprehensive periodontal treatment. If not, future
periodontal breakdown may occur.
Unfavorable prognosis: Local or systemic factors inluencing the periodontal status cannot be controlled. Comprehensive
periodont al treatment and maintenance are unlikely to prevent future periodontal breakdown.
Hopeless prognosis: The tooth must be extracted. Because periodontal stability is assessed on a regular basis using clinical
measures, it may be more useful in making treatment decisions and prognosis predictions than in trying to determine the
likelihood that the tooth will be lost.

The Treatment Plan, 426

Occlusal Evaluation and Therapy, 574
Excursive movement: Any movement of the mandible away from maximum intercuspation.
Guidance: The pattern of opposing tooth contact during excursive movements of the mandible.
Initial contact in centric relation: The irst occlusal contact in the centric relation closure arc.
Interference: Any occlusal contact in the centric relation closure arc or in any excursion that prevents the remaining
occlusal surfaces from achieving stable contact or functioning harmoniously or that encourages masticatory system
disharmony; also called an occlusal discrepancy.
Lateral excursion: Movement of the mandible laterally to the right or to left from maximal intercuspation.
Maximal intercuspation: Position of the mandible when there is maximal interdigitation and occlusal contact between the
maxillary and mandibular teeth; also called centric occlusion and intercuspal position.
Nonworking side: The side of either arch that corresponds with the side of the mandible moving toward the midline during
a lateral excursion; also called the balancing side.
Protrusion: Movement of the mandible anteriorly from maximal intercuspation.
Retrusion: Movement of the mandible posteriorly relative to a more anterior position.
Working side: The side of either dental arch that corresponds with the side of the mandible moving away from the midline
during a lateral excursion.

Occlusal Adjustment
As teeth tighten from consistent use of the appliance, occlusal interferences may become more evident, and greater
discrepancy between the initial dental contact and maximal intercuspation may be observed. Interferences with harmonious
excursive movement of the mandible may also become more obvious. When the clinician conirms that the interferences
correlate with a greater than expecte loss of attachment, direct intervention in the patient’s occlusion is considered. With the
patient’s full understanding and consent, occlusal adjustment or selective reshaping of the occluding surfaces of the teeth can
reduce the magnitude of occlusal interferences or direct the forces to be more compatible with the long axes of the affected
teeth.
Clinical analysis of the occlusion should be combined with a detailed analysis of diagnostic casts mounted in
centric relation on an adjustable articulator. Accurately mounted duplicate models can be used to accomplish a trial occlusal
adjustment to determine safety and eficacy for a patient. 10,28 Scheduling patients so that they leave their appliances on
overnight and in place until they are seated in the dental chair allows assessment of their teeth at maximal irmnes s, when
interferences are most readily identiiable. Teeth usually progressively tighten with continued compliance with the appliance
and repeated careful occlusal adjustment. Other methods that can be employed to alter occlusal relationships include
orthodontics and restorative dentistry. Provisional restoration of teeth is another method of improving occlusal contacts and
stability, and it often simpliies the process of occlusal adjustment and inal restoration.