Periodontal disease/Periodontitis

Epulis Granuloma


Treatment of Epulis Granuloma

Epulis Granuloma


Removal of Granuloma

 

Dilantin Gingival Overgrowth


In this case, osseous surgery was performed to remove the bone away from the CEJ which lower the gum tissue (gingival contour always followed bone contour). This will help the patient to brush much more effectively. Patient suffered from seizure and thus has to be on Dilantin medication.

Localized Juvenile Periodontitis


9mm probing depth


8mm probing depth


2mm probing depth


3mm probing depth


11mm probing depth


2m mm probing depth
This is our Localized Juvenile Periodontitis (LJP) patient. This is the intraoral photograph at the first appointment. No cleaning has been done. Patient demonstrated very deep probing depth (9-12mm) even though there is very little plaque or calculus. Beside bleeding, the gingiva shows very little sign of inflammation. Note that the deep probing level is only at the central incisors and first molar areas with very little plaque or gingival inflammation, which is a trademark of LJP. Below is the full mouth preop view. Note that very little plaque, calculus, and inflammation. No cleaning has been done, the last professional cleaning was at a year ago). Patient present did not know of her periodontal condition. She presents to our office inquired about her diastemas (gap) in the anterior teeth.

Adult Periodontitis

Initial Photograph

Scaling and Root Planing


Photographs taken immediately after scaling and root planing; even though the plaque and calculus is removed, the inflammation of the gingiva (roll, round, bulbous, bleeding margin) is still needed to be reevaluate at 4-6 weeks. By no mean that scaling and root planing is the end point of periodontal therapy. It is only a first step in periodontal treatment. Remember the disease is a progression of bone and attachment loss and thus must be evaluated over a time frame period with comparison of the attachment measurement over a period of time.

Periodontal Disease
Surgical Treatment


Notes
: Treatment of localized periodontal disease. Bio-Oss is used as bone graft to treat the infrabony defect.

All cases presented here were treated by Dr. Bui, D.D.S., M.S., at Cosmetic Dentist of Katy


Dinh X. Bui, D.D.S., M.S.

What is periodontitis?
Periodontitis referred to many diseases that affecting the periodontal tissues (the alveolar bone, the periodontal ligament, and the cementum). They all have several common characteristic such as they are multifactorial, bacterial etiology, which when occurs will result in destruction of alveolar bone, loss of periodontal ligament and cemental attachment.

Clinically, the sign and symptoms of periodontitis ranges from periodontal pocket formation, suppuration, fibrosis, destruction of alveolar bone and periodontal ligament, tooth exfoliation. Patient may or may not have pain after all, until the tooth is abscess or the disease reaching the nerve.

As a periodontist, I believe that there is an endpoint to the treatment of periodontal disease. If we look at all the factors contributed to the destruction of disease process, removing the cause, regenerate and/or stop the loss periodontal apparatus (bone, cementum, periodontal ligament), and continue to preserve and maintain the dentition with just the periodic prophylactic appointment and good home care program, then we have succeed in eliminating the disease process in that patient. I do not believe in continuous surgery and scaling and root planing through out the life of that individual, nor performing repeated regenerative procedure. It is a very complex dissease, but it usually can be stopped except for those with involvement of other systemic problems that we cannot controlled.

Is gingivitis is the type of periodontitis? Is bleeding gum is a sign of periodontitis?
Gingivitis is not periodontitis. Gingivitis just means the inflammation of the gum. When your gum or gingiva is inflamed, it will bleed. Bleeding is not necessarily means that you have periodontitis. Bleeding gum or gingivitis can be treated by brushing and cleaning the bleeding site so that the inflammation can be subsided. Many people were told to have "deep clean" or scaling and root planing when their gum bleeds. This is a misconception because "deep clean" or scaling and root planing only required when the patient actually lose bone support, and/or cemental attachment. When this occurs, patient is diagnosed to have periodontitis.

Three types of gingivitis that I want to discuss indepth are the pregnancy gingivitis, the medication induced gingival overgrowth, and the acute necrotizing ulcerative gingivitis (ANUG) because of they are very commonly mistaken as periodontitis. The only treatment needed for them is regular cleaning and good oral hygiene. "Deep clean" is NOT required because there is not significant bone destruction. In pregnancy gingivitis, subgingival growth of Bacteroides is enhanced due to the elevation of steroid hormones (estrogen) during hormone. There is an exaggerated inflammatory response to plaque such as spontaneous gingival bleeding, redness, edema (swelling), and enlargement of gingival tissue. In extreme case, pyogenic granuloma may be found. This pregnancy tumor (pyogenic granuloma) should be removed surgically if it causes pain during function or interfere with the occlusion. After birth, the lesion usually resolved. In the adjacent black column is the picture of my patient with pyogenic granuloma during pregnancy. I elected to remove it because it interfered with the occlusion in the posterior teeth.

Medication induced gingival overgrowth happened to those that uses medication such as phenytoin/dilantin (control seizure), cyclosporin (immunosuppressive therapy in transplant patients), nifedipine (high blood pressure medication). These lesion occurs as beadlike enlargement of the gingival margin and papilla. Enlargement continues and the marginal and papillary growths unite. The excessive growth results in pseudopocket and interfere with oral hygiene effort, which leads to inflammation and gum bleeding. In these patients, I recommend strict plaque control (shorten recall appointment), more efficient home care (Sonnicare and plaque disclosing solution), and laser therapy or localized gingivectomy to remove the overgrowth that formed deep pseudopocket and large food impaction areas. These gingival overgrowth sometimes prevent the flow of food (chew) away from the gingiva surrounding the teeth and thus food is packed into the sulcus and causes inflammation and periodontal abscess.

The acute necrotizing ulcerative gingivitis is an acute, recurring, gingival infection of complex etiology (could be oral manifestation of other systemic problems), characterized by necrosis of tips of gingival papillae, spontaneous bleeding, pain, and bad breath. Bacterial invasion of connective tissue by spirochette has been documented in researches. Bacterial etiology involves Bacteroides intermedius and should be treated with antimicrobial therapy (antibiotics) along with cleaning and good home care. This is the only gingivitis that needed the antibiotic therapy.

What are the diseases that can be classified as periodontitis?
Periodontal disease, or periodontitis, can be classified as:

I. Adult Periodontitis: This is the most common periodontitis, occurs because of the multibacterial colonies accumulation in the periodontal tissue, leading to chronic inflammation and infection, and ultimately result in tissue destruction due to host factors (host defense) and bacterial toxins. As discussed later, host factors is very important in the chronic nature of periodontal disease concerning periodontal tissue destruction. Adult periodontitis can be treated with scaling and root planing, antimicrobial and regenerative procedures depending on the extent of destruction.Treatment response is very predictable.

II. Early-Onset Periodontitis: According to Page et al. 1983, it is a genetic based periodontitis of unknown prevalence affecting a prepubertal populous during/after eruption of primary dentition. Two forms or this disease are:

A. Prepubertal Periodontitis: Onset during or immediately after eruption of primary teeth. Treatment result and response varied. In many case, tooth loss is inevitable.

1. Generalized periodontitis (GPP): disease affect all deciduous and mixed dentition, occurs with rapid destruction of bone and aggressive gingival inflammation. Usually the patient's white cell count is elevated with profound functional defects of PMNs (primary polymorphonuclear leukocytes) and monocyte. No PMNs found in the gingiva. Ostitis media and upper respiratory tract infection are frequently found. Patient may become refractory to the treatment, i.e., antibiotic therapy is unpredictable.

2. Localized (LPP): disease affected more localized site; little or no gingival inflammation, however, functional defects PMNs are also found. Less rapid destruction than GPP. Often does not involved with ostitis media and upper respiratory tract infection. In the localized form, the disease is usually can be treated with curettage and antibiotic therapy.

B. Juvenile Periodontitis: characterized by rapid loss of alveolar bone (progress 3-4 times faster than adult periodontitis) in the young individual (14-17 years old) without the presents of significant local factors or irritants (plaque, calculus, oral hygiene, occlusion). The most interesting factor is that the disease is identified with Actinobacillus actinomycetemcomitans(Aa) and Capnocytophaga. Aa is a gram negative, nonmotile coccobacillus which produces leukotoxin, lymphocyte suppressing factor, lipopolysaccharide endotoxin, fibroblast inhibiting factor, collagenase, and epitheliotoxin. It is very destructive and must be eliminated in treating the disease with Tetracyclin/Doxycyclin antibiotics. Capnocytophaga are the gram negative, motile rods (3species) that use CO2 based metabolism. These 3 species produce potent leukotoxin affecting PMNs. Clinically, localized juvenile periodontitis (LJP) patients rarely show calculus or plaque formation and often exhibit little or no gingivitis. However, deep probing, attachment loss, radiographic bone loss are found. Deep interproximal vertical bone loss on first molars and incisors are characteristic of LJP. Juvenile periodontits should be identified and treated early with antimicrobial therapy, scaling and root planing, and also surgery according to extent of destruction.

1. Generalized: affecting most of the dentition.

2. Localized: affecting only first molars and incisors.

C. Rapidly Progressive Periodontitis: Page et al. (1983A) define rapidly progressive periodontitis as the form of disease affecting yound individual from puberty to 35 years, characterized by acute and quiescent phases and inconsistenly pattern of distribution. Active phase demonstrated rapid bone loss and then suddenly may ceased and resolved. Usually these patient have PMNs or monocyte functional defects (83%) and other systemic problems such as obesity, mental depression, malaise, etc. Chen et al. (1991) assoicated the bacterial etiology to Porphyromonas Gingivalis.

III. Periodontitis Associated with Systemic Disease: These associated diseases included Hypophosphatasia, Neutropenia, Papillon Lefevre Syndrome, Leukocyte Adhesion Deficiency, Histiocytosis X, Chediak Higashi Syndrome, Leukemias, Acrodynia (mercury allergy), Juvenile diabetes, and AIDS. These are very hard to treat. Unpredicable response to treatment.

IV. Necrotizing Ulcerative Periodontitis: this is the case of chronic, severe periodontitis that usually occurs in AIDS patient, characterized by fiery red, linear erythema of the gingiva, necrosis of gingival papillae, bleeding, pain, bad breath. Treatment is scaling and root planing, antimibrobial therapy, and regenerative procedures if applicable.

V. Refractory Periodontitis: these are patients who had responded favorably to therapy and then demonstrated the signs of disease reactivation even though his or her home care oral hygiene regime and effort have not changed. The world workshop of Clinical Periodontics described refractory periodontitis as disease in multiple sites in patient which continue to demonstrate attachment loss after apparently appropriate therapy. With all that we know today, this patient population is very rare since so many advances and researches have lead to many treatment option in different area of guided tissue regeneration, guided bone regeneration, growth factor, antimicrobial therapy, and diagnosis. I believe that most of the cases of refractory periodontitis probably could be associated with some systemic factors (neutrophil defect, diabetes, occlusion, oral habits) that were overlooked during diagnosis.

 

What are all the factors in periodontal disease that brought about the bone destruction and tooth loss?
The bone loss and tissue destruction process can be described as followed:

  • Bacterial destruction: Bacterial products and leukotoxin have shown to be very destructive to the periodontal tissue in the disease process. The associate bacteria in juvenile periodontitis, the Actinobacillus actinomycetemcomitan (Aa) produces leukotoxin which is the PMN chemotaxis inhibiting factor. Moreover, Aa also invades the gingival connective tissue leading to tissue destruction. Our treatment of periodontal disease should address this issue. We scale and root plane thoroughly to eliminate plaque and calculus which harbors bactera and baterial products, eliminating inflammation and deep periodontal pockets to allow better oral hygiene and further control the population of pathogenic bacteria. Finally, we use regenerative procedures (guided tissue regeneration) to eliminates infrabony pockets which harbors spirochetes and gram-negative bacteria.
  • Host Destruction: patient reaction to the irritants. Our body tried to defend by increasing chemotasis of antibodies and tissue factors to fight the irritants. According to John Novak et al. 2002, individual inflammatory response account to 90% of the total destruction of the periodontal tissues. The host inflammtory response includes the increased PMNs, white cell, the release inflammatory mediators such as cytokines, prostaglandins, tissue destructive matrix metalloproteinases that includes collagenase, all of which ultimately cause destruction of alveolar bone, gingiva, and periodontal ligament. This is the area that the use of a periodontal medicine called Periostat will prove to be a very advantageous adjunctive treatment especially in the individual where there is a systemic or genetic predisposition to periodontal disease. Treating the host response using host modifying therapy is one of many exciting areas in periodontal research that is dealing with the treatment of nonplaque-induced gingivitis, chronic and severe/aggressive generalized periodontitis, and periodontitis associated with systemic disease or smokers..
  • Local factors: oral hygiene, occlusion, food impaction due to small gaps. My view in this area is very clear. I preferred strict home care regime, verified with the use of plaque disclosing solution and the sonnicare toothbrush. I also use orthodontic therapy to restore the patient occlusion back into the more optimal function, eliminates all the gaps which causes food impaction and gingival tissue irritation/destruction.
  • Systemic factors : secondary destruction from the other systemic disease such as diabetes (high glucose lelel leads to vulnerability to infection and delay wound healing). We always emphasize in our treatment the important of diagnosis and head the patient in proper direction in term of disease control.

In my opinion, we must controll all these four aspects of the destruction process. If we succeed in doing so, periodontal disease can be eliminated completely.

I was prescribed a periodontal rinse (Peridex) for my gum disease. Is there any long term side effect and can my disease be controlled by using this rinse? Do I need antibiotic immediately after scaling and root planing appointment?

Peridex should be used only for post surgical, short term (2 weeks) as plaque control rinse. Long term use will lead to desquamate papillae on the tongue surface, altered taste, and teeth stain, and increased plaque and calulus accumulation. I hardly recommend Peridex after root planing and scaling because of these reasons. We only use it for post surgery plaque control, when tooth brush should not be used in the healing surgical site. I personally think it should not be used after scaling and root planing because we must determine in the follow up appointment whether the scaling and root planing is performed at the efficient level such that it can alone controlled the inflammation in the incipient to moderate probing depth site. For this very reason I do not recommend antibiotic treatment immediately after scaling and root planing either unless as in JP and other associated systemic disease. The end point of periodontal therapy is when the patient can stop the progression of bone and attachment loss without resort to the use of rinse and antibiotics regularly.

What is your view on oral hygiene products in the market today?

There are only two things I recommended for my periodontal patient. The first is the use of Sonnicare toothbrush. The second one is the plaque disclosing solution. They are the only product I have in our office due to the fact that local drug store do not sell the plaque disclosing solution and we supply the sonnicare at a less expensive price than local retail stores. Sonnicare toothbrush is the only brush, I believe, cleaned the interproximal areas very well, break up the complex microbial biofilm (presents as a challenges in disease control process) by using the dynamic fluid movement through the interproximal space. Plaque disclosing solution, the red dye that stains plaque red, is very inexpensive and the best method to teach everyone how to brush properly. Any brand of toothpaste will do as long as they have flouride. I believe that fluoride treatment is very important in geriatric population when areas of gingival recession exposed the root to Lactobaccilus, the primary bacteria associated with root caries.

Is smoker more susceptible to periodontal disease? What about diabetic patient?
Studies have shown that smoking increases the levels of periodontal pathogens in both shallow and deep pockets (Novak et al.). They possess higher level of inflammatory response concerning the release of inflammatory mediators, increase production of collagenase and elastase. Collagenase is an enzyme released by both the host and the pathogenic bacteria that degrades and destroys collagen (bone). In addition, the nicotine in the cigarette adheres to root surface and predispose the surface to plaque and calculus formation. Nicotine also constrict and damage the small capillaries that supplied the gingival tissue. Studies also have shown that when the amount of cigarette consumption (level of nicotine intake) reduced to five cigarettes or less, the healing of the periodontal tissue returns to the normal level as that of the nonsmoker. Other challenging situation of which periodontal disease demostrates more extensive destruction in relation to oral hygiene is the diabetic patient. Again patients with diabetes was observed to have elevated collagenase production. The increased level of glucose in the blood predispose the patients to infection and delay wound healing. However, as the glucose level returns to the control level (70-111), the patient response to wound healing returns to normal level.

Thus in treating the periodontal patients who are smokers and/or systemic problems (such as diabetes), I always use strict plaque control regime, scaling and root planing, and an adjunctive host modulators such as Periostat (doxycycline hyclate) that is taken twice a day for at least 3 months. In diabetic patient, the control of the glucose level in the blood must be emphasized and verified with the patient in order for the treatment to be effective.

These points of discussion reflect Dr. Bui's view point on the topic of periodontal disease. It does not necessarily reflect other operators. Our treatment approach may be different, however, we all should agree that the end point of periodontal therapy is when the patient can maintain and stop the progression of bone and attachment loss without resort to regular use of antibiotic, mouth rinse, or in many case, repeated scaling and root planing.


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