Periodontal Disease

Periodontal diseases are biofilm-initiated inflammatory conditions that impact susceptible individuals.⁶ Gingivitis, the first stage of periodontal disease, is defined as “gingival inflammation without loss of connective tissue attachment.”⁷ Periodontitis is defined as follows:

The presence of gingival inflammation at sites where there has been a pathological detachment of collagen fibers from cementum and the junctional epithelium has migrated apically.⁷ In addition, inflammatory events associated with connective tissue attachment loss also lead to the resorption of coronal portions of tooth-supporting alveolar bone.

Similar definitions are associated with periimplant mucositis and periimplantitis, respectively. The disease process is disrupted and controlled by host resistance through therapy or natural defenses.⁸

The organization and activity of biofilm are important because biofilm is the first component of periodontal disease targeted in therapy. Biofilm is a complex community of microorganisms protected by a secreted extracellular polymeric substance. As it becomes more mature, the microbes use a molecular communication, quorum sensing, to create a highly organized and adaptable infrastructure. The various microbes within the biofilm behave so as to preserve the entire community and become a living organism.⁹

As the biofilm responds to its environment, its adaptation provides resistance to such factors as ultraviolet (UV) light, bacteriophages, biocides, antibiotics, immune system responses, and environmental stresses.¹⁰ Manor et al.¹¹ found that biofilm penetrates epithelium and underlying connective tissue, possibly to a depth of 500 microns (µ; or micrometers, µm). Biofilm has been observed penetrating tissues along the path of capillaries. Through various means, including stimulating the host’s inflammatory pathways, biofilm may control transudate production to supply its nourishment.¹² This demonstrates the parasitic nature of biofilm in tissue.

As the body responds to biofilm invasion, proinflammatory cytokines, prostanoids, and proteolytic enzymes are synthesized and released. Fluids increase within the tissues, circulation becomes stagnant, swelling occurs, and metabolic products become backlogged. Enzymes such as collagenase, gellatinase, elastase, and fibrinolysin,³ so instrumental in the initial healing stage, remain at the site, destroying the developing strands of healing matrix needed to form connective tissue. The inflamed tissue is unable to progress from the granulation phase of healing into the remodeling phase because of the continued insult with pathogenic activities and further biofilm proliferation.¹³ The site is now a biofilm-infested chronic wound¹⁴ and, without treatment, will most likely progress, creating localized destruction and impacting systemic health.

All the following terms used throughout this chapter refer to treating the soft tissue wall of the periodontal pocket:

Nonsurgical periodontal therapy

Sulcular debridement

Active phase I periodontal infection therapy

Laser decontamination refers specifically to reducing the biofilm of the pocket, usually meaning what is contained within diseased tissue.

Laser coagulation refers specifically to sealing of capillaries and lymphatics after laser decontamination within the tissue wall.

Benefits of Laser Therapy

The advantages of lasers affect the bacteria directly and support the body’s healing response. Incorporating lasers into conventional therapies helps accomplish treatment objectives. Conventional nonsurgical periodontal therapy addresses debriding the area of bacteria, endotoxins, and hard deposits from the tooth structure to restore gingival health.⁸ Instrumentation is focused on the tooth structure and most often accomplished through manual and power scaling. In the future, lasers will also be used for root debridement.

As of this writing, the U.S. Food and Drug Administration (FDA) has not yet cleared laser-assisted removal of deposits and biofilm from tooth structure. However, Aoki et al.¹⁵ determined that deposits and biofilm are more thoroughly removed and that a more biocompatible surface is created for reattachment with an erbium (Er) laser versus conventional methods.¹⁶ The alexandrite laser also has been in development for selective removal of calculus from the root structure.¹⁷ The carbon dioxide (CO₂) laser has been shown to increase adherence of fibroblasts to root surfaces, and the fibroblast adherence is superior to conventional techniques both in quantity of fibroblasts attached and in the quality of the attachment.¹⁸

Regardless of the instrument used, it is essential that contaminants are thoroughly removed from the tooth structure in any periodontal therapy. Current laser-assisted methods address the biofilm of the tissue wall, supplementing conventional methods that address the tooth structure. It is critical to note that laser treatment is an addition to, not a replacement for, conventional periodontal therapy.

Both in vitro and in vivo studies show that lasers are bactericidal.^19–22 Although not specific to certain bacteria, the argon (Ar), neodymium-doped yttrium-aluminum-garnet (Nd:YAG), and diode lasers have strong absorption in darkly pigmented bacteria, causing a direct, increased effect on the red and orange–complex bacteria associated with periodontitis.²³ The CO₂ laser also has excellent bactericidal properties.^24,25 Both CO₂ and erbium lasers act on pathogens by heating intracellular fluids, causing the microbes to collapse.^26,27 The absorption of laser energy by tissues produces a photothermal effect. With the appropriate parameters, most nonsporulating bacteria, including anaerobes, are readily deactivated at 50° C.^28,29

In laser-assisted active phase I periodontal infection therapy, the diseased biofilm-infested tissues of periodontal pockets are debrided. Working within the recommended parameters of 60° C,³⁰ the healthy tissue beneath the nonhealing granulation layer is not affected by the low energy. As noted earlier, biofilm can penetrate soft tissues. Removal of “bioburden” from the wound has a significant impact on wound bed preparation and wound healing.³¹ Steed et al.³² showed that more frequent debridement resulted in better healing than debriding less frequently. Moritz et al.¹⁹ reported that the bleeding index improved in 96.9% of the patients treated with laser-assisted periodontal therapy after conventional therapy, compared with 66.7% of patients treated conventionally without laser. The authors concluded that “the diode laser assisted periodontal therapy provided a bactericidal effect, reduced inflammation, and supported healing of periodontal pockets through elimination of bacteria.”¹⁹ Administering laser energy to the affected tissues at specific, repeated intervals is key in targeting biofilm during periodontal therapy.

Lasers also have the ability to seal capillaries and lymphatics, reducing swelling at the treated site and minimizing postoperative discomfort.³³

Another benefit of laser-assisted procedures is the healing stimulated at the cellular level.³⁴ Medrado et al.³⁵ found that low-level laser treatment depresses the exudative phase while enhancing the proliferative processes during acute and chronic inflammation. Laser photobiomodulation can activate the local blood circulation and stimulate proliferation of endothelial cells.^36,37 Wound healing is supported with reduced edema, polymorphonuclear (leukocyte) neutrophil (PMN) infiltrate, increased fibroblasts, more and better organized collagen bundles.³⁸ Karu³⁹ suggests these effects are caused by an increase in mitochondrial synthesis. The slight scattering that occurs with more deeply absorbed energy of certain lasers may have photobiomodulation effects beyond the direct application. The aiming beams of the lasers may also have a photobiomodulation effect (see Chapter 15). More research needs to be conducted in this area.

Laser Types

Laser wavelengths used to treat active phase I periodontal infection include the diode, Nd:YAG, CO₂, and erbium lasers. Chapter 2 provides further information on each wavelength.

Diode Laser

The semiconductor diode lasers are available in four different wavelengths, as follows:

810 to 830 nm

940 nm

980 nm

1064 nm

Both the 810- to 830-nm and the 980-nm wavelengths may be used for nonsurgical periodontal therapy and are supported by the literature. As yet, no published studies have examined the use or advantages of the 940-mn wavelength.

As with the argon lasers, diodes also use fiberoptics for energy delivery in contact or noncontact mode, depending on the procedure. Diodes in this wavelength range are absorbed in hemoglobin and pigment (e.g., melanin). These chromophores, or organic compounds that absorb light at a specific frequency, are present in high concentrations within the diseased periodontal pocket, making these wavelengths applicable for sulcular debridement.

The 980-nm wavelength has more absorption in water than the other three diode wavelengths, which may be an added benefit to the laser interaction within the pocket. However, no definitive studies yet show that the superior absorption in water leads to superior clinical results compared with other diode wavelengths. Diode lasers are bactericidal^19,41,42 and aid in coagulation.

Diode lasers may be operated in continuous-wave mode (energy emitted as constant beam), with low settings and short application time, or in gated-pulse mode (energy constant but interrupted or pulsed at specific intervals), with higher settings and longer application time. The newest lasers in the 980-nm wavelength offer specific on/off time controls, allowing higher power to be applied to the tissue for shorter pulse durations and much longer off times, which allow the tissues to cool adequately before receiving another pulse of energy. This decreases accumulated heat, which decreases thermal collateral damage. Less collateral damage means less postoperative discomfort for the patient. Some 980-nm diode lasers incorporate coaxial water irrigation for tissue cooling and lavage as an option during use.

Fundamentals of Laser Physics

Understanding basic laser physics is important to make needed adjustments while administering laser treatment. In laser-assisted procedures, laser energy is absorbed by the chromophore and transformed into photothermal energy. Observing laser-tissue interaction is critical. Tissues containing different concentrations of the wavelength-specific chromophore will require different parameters.

The patient’s comfort is also important. Often a treatment area is fully anesthetized during the initial debridement and lasing appointment, but may require only topical or no anesthetic for lasing at repeat visits. Making adjustments will improve the patient’s comfort while accomplishing the treatment goal.

The treatment goal for nonsurgical periodontal therapy is decontamination and coagulation rather than incising. Procedures are accomplished through control of tissue temperature. The factors that affect tissue temperature are the mJ and Hz settings, speed at which the laser beam moves over the target tissue (hand speed), and cooling factors such as pulse “off time,” high-volume evacuation, and water application.

Some lasers allow more control of these parameters than others. For a free-running pulsed laser such as the Nd:YAG, high mJ with low Hz means more energy per pulse but more thermal relaxation time between pulses. Typically this will improve hemostasis. If lower mJ is selected with more Hz, there is less energy in each repetition, but also less thermal relaxation time because more pulses are emitted into the tissue every second. This may cause more even thermal absorption. Diodes are operated in either continuous or gated mode; continuous wave does not allow any thermal relaxation. Lower power settings should be chosen to prevent temperature increase beyond the treatment goal of decontamination/coagulation. If gated (pulsed) mode is selected, a higher energy may be required to raise the tissue temperature with each pulse. The gated mode allows the tissue to cool before the succeeding pulse.

All tissues have an absorption threshold; tissue can absorb only so much energy before it is overloaded by the energy and becomes painful and is damaged. Think of sitting on a beach and getting a nice suntan. Your tissue (skin) absorbed a certain amount of energy (sunlight). Think again of sitting on a beach and absorbing much more energy. Your tissue (skin) was overloaded with too much energy (sunlight), and the result is pain and charring of the tissue (sunburn). Pain occurs when more energy is irradiated onto the target tissue than it can absorb.

When the patient feels discomfort, the following adjustments can be made without adjusting the mJ or Hz settings:

Move the laser fiber more quickly (adjust hand speed), decreasing total energy exposure.

Move the suction closer to the operative site so that the circulating air decreases the accumulating temperature.

Add a light spray of water to dissipate heat.

These adjustments work well with all wavelengths. However, because the CO₂ wavelength is highly absorbed in water, too much water will inhibit tissue interaction, whereas not enough will increase discomfort.

Conversely, if the tissue is not responding, alterations are needed. First, check the settings, then inspect the aiming beam, ensuring patency of the optics. If parameters are correct, test-fire the laser on an appropriate chromophore, moving the laser more slowly. If results are still negative, increase the settings incrementally until interaction occurs. If a large increase is necessary, the laser likely has a technical problem and should be serviced by a certified technician. The clinician must understand the wavelength employed to provide optimal, beneficial laser treatment.

Treatment Objectives with Soft Tissue Lasers

The objective of active phase I periodontal infection therapy is to remove biofilm and deposits found above the gumline and within the periodontal pocket, whether on the tooth structure, on the tissue wall, or in the crevicular fluids. Such therapy assists the body’s healing response. This is accomplished through conventional scaling and root debridement as well as laser-assisted sulcular debridement. Sulcular debridement addresses the pocket wall for profound decontamination and seals the capillaries and lymphatics through coagulation.

Sulcular Debridement with Fiberoptic Laser Delivery

Preprocedural Decontamination

Preprocedural decontamination is a laser application done before any instrumentation, even probing. The objectives are to affect the bacteria within the sulcus, reducing the risk of bacteremia caused from instrumentation, and to lower the microcount in aerosols created during ultrasonic instrumentation.⁴⁴ The technique uses very low energy. The fiber is placed within the sulcus and is swept vertically and horizontally against the tissue wall, away from the tooth, with a smooth, flowing motion, for 7 to 8 seconds on the lingual aspect, then on the buccal of each tooth’s tissue wall. The benefits of preprocedural decontamination are seen in the reduced microbial translocation through the circulatory system.

Decontamination

Just as conventional root debridement removes biofilm and accretions from the hard tooth surface, laser decontamination removes biofilm within the necrotic tissue of the pocket wall. The laser energy interacts strongly with inflamed tissue components (from preferential absorption by chromophores, which are more abundant in diseased tissues) and less strongly with healthy tissue. This nonsurgical therapy uses very low settings and decontaminates rather than cuts the tissue.²⁸

The administration of laser decontamination requires an understanding of current periodontal pocket topography, proficiency in technique, and recognition of laser-tissue interaction to determine the end point of therapy. An updated periodontal chart is needed for reference throughout therapy. With conventional root debridement provided just before laser decontamination, the pocket depths may need to be reprobed for accuracy of laser treatment. Laser therapy should address sites presenting with inflammation and/or pocketing of 4 mm or greater. It is helpful to visualize the surface area being treated. For example, the diseased pocket lining requiring treatment in a case with 50% generalized bone loss has an estimated tissue surface area of 40 cm² (6.2 in²), and in a case with 4 to 5 mm of generalized pocketing, 20 cm² (3.1 in²).⁴⁵ Knowing the depth and shape of pockets and area to be addressed enables the clinician to be thorough with technique.

With fiberoptic technique, the fiber tip engages every millimeter of the diseased tissue wall that corresponds to the indicated sites marked on the periodontal chart. To begin, calibrate the fiber exposed to measure 1 mm less than the pocket depth (Figure 3-1). Begin lasing with the fiber placed just inside the gingival margin, progressing apically, or place the fiber 1 mm short of the depth of the pocket, working coronally (Figure 3-2). The edge of the canula indicates the treatment depth of the pocket being reached. Use a rapid, gliding, multidirectional motion with the tip of the fiber in constant contact with the pocket wall. The strokes should address small sections and should be systematically overlapping. It is helpful to divide the pocket into affected sections, such as interproximal to the line angle, the direct buccal or lingual surface, and the line angle to the interproximal area. Continually inspect the fiber tip and remove any accumulated debris (Figure 3-3) with water-moistened gauze.

FIGURE 3-1 • Calibrating fiber length using periodontal probe.

FIGURE 3-2 • Laser fiber in periodontal pocket.

FIGURE 3-3 • Small amount of granulomatous tissue debris on fiber tip.

When exiting the pocket, take care to inactivate the laser, preventing overexposure of the gingival margin’s thin tissue. If the fiber tip becomes irreversibly coated (Figure 3-4), cleave the fiber, calibrate the length of the pocket, and continue the procedure.

FIGURE 3-4 • Excessive amount of debris on fiber. At this stage of treatment, the fiber should be cleaved and recalibrated.

Completion of laser decontamination is determined by laser parameters used, delivery time, and clinical signs. Decontamination is accomplished with less mJ and more Hz than for coagulation. A more inflamed pocket may require less average power because of increased concentration of the laser’s preferred chromophores. If working with an initiated fiber and lower settings in continuous wave, interaction is concentrated and will require less treatment time than a noninitiated fiber with higher settings in pulsed mode. A deeper pocket will require longer treatment time because of increased surface area. As lasing progresses in an area, less and less debris should collect on the fiber. Fresh bleeding will occur, however, when the pocket wall is fully decontaminated and debrided (Figure 3-5). Keep in mind the laser parameters and application time. Observing tissue interaction is essential in determining how long a diseased site should be treated.

FIGURE 3-5 • Gingiva immediately after fiber-based laser treatment, showing fresh bleeding from the pocket.

EXERCISE

To illustrate laser technique, try this simulation exercise. On paper, draw an area measuring 20 cm² (3 × 1–inch rectangle). Use a mechanical pencil with fine lead (0.5 mm) to color the area using flowing, methodical, overlapping, multidirectional strokes, leaving no areas uncolored. The laser fiber is actually only 0.4 or 0.3 mm, but this activity reflects the time and thoroughness needed for treatment within the pocket.

Coagulation

When biofilm has been removed, the second objective in active phase I periodontal infection therapy is coagulation, sealing the capillaries and lymphatics of the healthy tissue. As previously noted, biofilm tends to continue its invasion of the host tissue through the vessels. Coagulation may inhibit the biofilm’s progression. It also counteracts the swelling that occurs with the inflammatory process. Coagulation is accomplished with increased mJ and decreased Hz compared with decontamination. Coagulation also requires less time within the pocket and does not address every millimeter of tissue.

A newly cleaved fiber is moved back and forth through the pocket, administering laser energy beyond the end of the fiber into the tissue. The application raises the temperature within the pocket slightly, to promote protein denaturation and sealing of the vessels. If continued hemorrhaging occurs when exiting the pocket, the fiber may be used in noncontact mode to coagulate at the gingival margin, keeping the laser energy directed away from the tooth surface.

After coagulation, firm digital pressure applied to areas with deep pockets will support the re-adaptation of the tissue to the tooth and further enhance reattachment. Coagulation assists the first stages of healing after debridement.

Sulcular Debridement with CO₂ Laser

Whereas the argon, diode, and Nd:YAG lasers employ a contact technique for sulcular debridement, the micropulsed 10,600-nm CO₂ laser uses a defocused, noncontact technique. Marginal dehydration and pocket decontamination are two steps applied in CO₂ laser therapy. Because the CO₂ laser’s wavelength will be absorbed by the crevicular fluids and water content in the diseased tissue wall, it is important to direct the energy parallel to the tooth surface and toward the tissue.

Begin by directing laser energy to the coronal edge of the marginal gingiva. Hold the tip perpendicular to the tissue crest at a distance of approximately 1 mm. Tissue interaction is observed with a slight “frosting” of the surface (Figure 3-6). Marginal dehydration will improve entry of the tip by drawing the tissue slightly away from the tooth structure. The epithelium will be inhibited by this application. This is the first step before pocket decontamination.

FIGURE 3-6 • Laser marginal dehydration of gingival tissue immediately before pocket debridement and decontamination with carbon dioxide (CO₂) laser.

The technique for decontamination involves placement of the laser’s defocusing tip 1 to 2 mm into the pocket (only 1 mm for pockets up to 6 mm in depth; only 2 mm for pockets >6 mm). Treatment should include the complete circumference of each tooth presenting with disease. Activate the laser as the tip is drawn through the crevicular space in an even, slow motion, working from the distal aspect to the mesial aspect on the buccal and again on the lingual side of the tooth. The laser tip is kept parallel to the long axis of the tooth (Figure 3-7).

FIGURE 3-7 • Tip of CO₂ laser in periodontal pocket. Note parallelism of tip to root surface.

Treatment time is a maximum of 16 seconds per buccal or lingual surface. The length of application time depends on the extent of disease and the surface area; larger teeth such as molars are treated longer than smaller teeth such as lower anteriors.⁴⁶ The tip must be kept open and free of coagulum for efficient energy flow. Keeping the tissue slightly moist and working in a single direction will enhance the laser’s efficiency. Vertical up-and-down movements or pushing the tip toward the tissue can cause the tip to clog. If the tip becomes occluded, the tip and detritus inside will continue absorbing the energy, heating the tip excessively. Coagulation occurs simultaneously with decontamination. No additional steps are necessary in lasing with the CO₂ laser. Figure 3-8 shows the gingiva after-lasing.

FIGURE 3-8 • Gingiva immediately after CO₂ laser treatment.

Healing and Tissue Rehabilitation

Healing typically occurs without complications as the body responds to therapy. Through the first 24 to 72 hours, the patient may feel tenderness and experience light bleeding when eating or cleaning; after tooth debridement and tissue decontamination, epithelium begins to regenerate after 24 hours, then progresses 1 mm per day, protecting the tissue wall. Within 1 week, the wound surface is covered. Connective tissue begins proliferation by day 5. Because laser decontamination procedures are repeated at 10-day intervals, the epithelium is impaired during laser biofilm reduction. This allows the fibroblasts to continue organizing into a connective tissue attachment apparatus. The attachment will continue to mature for 12 months.⁸ Because this attachment is easily disrupted, only light-pressure probing is recommended after several months and normal probing after 6 months of postoperative therapy.⁵¹

Classic signs of tissue rehabilitation include improved color, consistency, texture and stippling, and contour. These signs, as well as a decrease or elimination of hemorrhaging during gentle tissue manipulation and a reduction of pocket depth, are all desired indications of healing tissues. Figure 3-9 shows initial periodontal probing before treatment and periodontal probing 6 months after treatment. Figure 3-10 shows three sets of probings: initial probing, 8 weeks after treatment, and 5 months after treatment. Analysis of the probing results shows a resolution of 86% of the bleeding sites, a decrease in 86% of the pocketing sites, and a 58% decrease in the number of teeth exhibiting periodontal disease.

FIGURE 3-9 • A, Periodontal pocket probing before CO₂ laser treatment. B, Periodontal pocket probing 6 months after CO₂ laser treatment. C, Periodontal pocket probing before fiber-based laser treatment. D, Periodontal pocket probing 6 months after fiber-based lase/>

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