Removal of Granuloma
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.
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.
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.
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.
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
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
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
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
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
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
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
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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