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Periodentitis Vs pre-implantitis,
the same disease?
Same treatment ?
pre-implantitis disease
Periodontology
Prepared By:杰拉德，
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Periodentitis Vs pre-implantitis, the same disease?
Same treatment ?
Introduction:
Periodontium refers to the specialized tissues that both surround and support the teeth,
maintaining them in the maxillary and mandibular bones. The word comes from the Greek terms
peri-, meaning "around" and -odons, meaning "tooth." ". Periodontics is the dental specialty that
relates specifically to the care and maintenance of these tissues. The following four tissues make
up the periodontium:
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Alveolar bone
Cementum
Gingiva or gums
Periodontal ligament
Anatomy of the teeth compared to implants:
Nature Tooth
Implants
1-Presence of cement and PDL
1-no cementum or PDL
2-Collagen fibers attached in horizontal
orientation
2-collagen fibers in vertical orientation not
attached to implant
3-same epithelial attachment (JE)
3-more collagen fibers, fewer fibroblasts and
fewer blood vessels the peri-implant
connective tissue
4-same biological space (3mm)
4-same epithelial attachment (JE)
5- same biological space (3mm)
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Periodontitis
Is an infectious disease that leads to the destruction of hard and soft tissues surrounding the teeth.
Bacterial adhesion to and colonization of the teeth surface, biofilm accumulation, and tissue
invasion results in clinical symptoms of inflammation, leading to gingivitis. Gingivitis
inflammation is confined to the gingiva and is reversible after treatment. If the situation is left
without treatment, it may lead to periodontitis where the inflammation extends into deeper tissues,
leading to gingival swelling and bleeding. In the late phase of the disease, the supporting collagen
of the periodontium degenerates, alveolar bone begins to resorb, and the gingival epithelium
migrates along the tooth surface, forming a periodontal lesion.
Periodontitis is characterized by the following:
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Gum inflammation, with redness and bleeding
Deep pockets (greater than 3 mm in depth) that form between the gum and the tooth
Loose teeth, caused by loss of connective tissue structures and bone
Categories of periodontal disease, including:
Chronic Periodontitis. Chronic periodontitis (also referred to as adult periodontitis) may begin in
adolescence as a slowly progressing disease that becomes clinically significant in the mid-30s and
continues throughout life. Some dentists question whether it is a chronic, unrelenting condition
and instead suggest that it waxes and wanes depending on the response of the immune system.
Aggressive Periodontitis. Aggressive periodontitis (also referred to as early onset periodontitis)
often occurs in young people. It is subdivided according to whether it begins before or after
puberty. Immune deficiencies and a genetic link have been shown to be possible factors for all
types of aggressive periodontitis. If the condition is localized and treated, the outlook is positive.
People with severe and widespread aggressive periodontitis are at high risk for tooth loss.
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Periodontitis that occurs before puberty is very rare. It begins with the eruption of
primary teeth in the first year and causes severe inflammation and bone and tooth loss.
Juvenile periodontitis begins at puberty and is defined by severe bone loss around the first
molars and incisors. It is more common in girls than in boys. The clinical signs -- such as
inflammation, bleeding, and heavy plaque accumulation -- are not present in this relatively rare
disease. The treatment is the same as in chronic periodontitis.
Rapidly progressive periodontitis occurs in the early 20s to mid-30s. Severe inflammation
and rapid bone and connective tissue loss occur, and tooth loss is possible within a year of onset.
Disease-Related Periodontitis. Periodontitis can also be associated with a number of systemic
diseases, including type 1 diabetes, Down syndrome, AIDS, and several rare disorders of white
blood cells.
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Acute Necrotizing Periodontal Disease. Acute necrotizing periodontal disease is an acute
infection in the gums
Peri-implantitis:
Peri-implantitis is regarded as an “infection-induced inflammatory process affecting the tissues
around an osseointegrated implant in function, resulting in loss of supporting bone”. Although
dental implant therapy has been considered to have an excellent prognosis, recent reports on the
long-term success of implant therapy have presented surprisingly high prevalence rates of
perimucositis and peri-implantitis. A number of risk factors have been identified, including 1- poor
oral hygiene, 2-a history of periodontitis, 3- diabetes, and 4- smoking .
The aetiopathogenesis of peri-implantitis remains somewhat unclear, but has a similar infectious
and inflammatory background to the pathogenesis of periodontitis . The soft and hard tissues
surrounding an osseointegrated (bone-to-implant contact) implant show some similarities with the
periodontium in the natural dentition. A big difference lies in collagen fibers being non-attached
and parallel to the implant surface instead of being perpendicular and in a functional arrangement
from bone to cementum. A periodontitis-like process, peri-implantitis, can affect dental implants,
and, since untreated periodontitis may ultimately lead to the loss of natural teeth, peri-implantitis
can result in the loss of dental implants.
MICROBIOLOGY
* Microbiological Findings Periodontitis,
Especially chronic periodontitis, is initiated by an overgrowth of specific, Gram-negative bacterial
species . In human chronic periodontitis, five bacterial species have been found in active lesions:
Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Porphyromonas gingivalis,
Tannerella forsythensis, Fusobacterium nucleatum and Campylobacter rectus.
actinomycetemcomitans is also associated with different forms of aggressive periodontitis. These
organisms have the ability to penetrate the gingival epithelium and to release endotoxins and
cytotoxic enzymes and molecules. Pathogens are necessary, but insufficient for disease activity to
occur. Factors influencing such activity include the susceptibility of the individual host and the
presence of interacting bacterial species . A. actinomycetemcomitans produces specific leucotoxin,
and the immunologic response of the host to this antigen may be one explanation for the unique
pattern of tooth involvement in aggressive periodontitis. P. gingivalis in particular produce
trypsin-like enzymes which can act as a virulence factor in periodontal inflammation.
** Microbiological Findings in PeriAmplantitis
It has been shown that the pathogens associated with periodontal disease are a Gram-negative,
black-pigmented anaerobic flora. Published studies have shown that the bacterial flora at failing
implant sites consists of Gram-negative rods, including Bacteroides and Fusobacterium ssp..
Failing implants were clinically characterized by increased mobility and peri-implant radiolucency,
and probing depths greater than 6 mm were associated with periodontal pathogens, including A.
actinomycetemcomitans, P. intermedia, and P. gingivalis in more than one-third of the sites
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examined by DNA analysis . It has been demonstrated that the bacteria found in the implant
crevice in the success- ful implant case are basically the same flora as found in the natural tooth
crevice/sulcus in a state of health. Mombelli and Mericske-Stern (1990) studied the microflora
from 18 edentulous patients with "successful" implants and found 52.8% facultative anaerobic
cocci and 17.4% facultative anaerobic rods, but only 7.3% Gram-negative rods and no
P. gingivalis or spirochetes. Haanaes (1990) verified that the microflora around the stable vs. the
failing implant parallels the patterns. Another study (Rams et al, 1990) reported on periimplantitis
lesions that exhibited a higher proportion of staphylococci (15.1%) than were present in gingivitis
(0.06%) or periodontitis (1.2%) lesions, suggesting that the staphylococci may be of greater
etiological significance than was previously assumed
TREATMENT THERAPY
* PERIODONTAL THERAPY
Periodontitis is initiated and sustained by microbes which are present in supra and subgingival
plaque in the form of uncalcified and calcified (calculus) biofilms. Initial periodontal therapy or
basic treatment of periodontitis involves the removal of both sub and supragingival plaque.
The clinical outcome is largely dependent on the skill of the operator in removing subgingival
plaque and the skill and motivation of the patient in practising adequate home care.
periodontitis can be successfully treated with noninvasive therapies. If you have pockets that are
5 mm or less in depth.
Scaling removes tartar and bacteria from your tooth surfaces and beneath your gums. It may be
performed using instruments or an ultrasonic device.
Root planing smoothes the root surfaces, discouraging further accumulation of tartar.
prescribe antibiotics or other medications to help control bacterial infection. Recent advances in
topical antibiotic treatment may reduce the need for systemic medications that, in addition to the
potential for side effects, increase the likelihood of antibiotic-resistant bacteria.
antibiotic mouth rinses. insert threads and gels containing antibiotics into the space between
teeth and gums or into pockets after deep cleaning. Although more research is needed, these
products appear to lower bacteria levels and may help prevent future problems.
advanced periodontitis — the depth of the pockets is more than 5 mm — and tissue may not
respond to nonsurgical treatments. In that case：
Flap surgery (pocket reduction surgery). In this procedure, make tiny incisions in gum so that a
section of gum tissue can be lifted back, exposing the roots for more effective scaling and planing.
Because periodontitis often causes bone loss, the underlying bone may be recontoured before the
gum tissue is sutured back in place.
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Soft tissue grafts. When lose gum tissue to periodontal disease, gumline recedes, making
teeth appear longer than normal. Replacing the damaged tissue — which is usually accomplished
by removing a small amount of tissue from palate and attaching it to the affected site — serves
several purposes: It helps reduce further gum recession; it covers exposed roots, protecting them
from decay and making them less sensitive to heat and cold; and it gives teeth a more
cosmetically pleasing appearance.
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Bone grafting. This procedure is performed when disease has destroyed the bone
surrounding tooth root. The graft may be composed of small fragments of your own bone or the
bone may be synthetic or donated. Not only does the graft help prevent tooth loss by holding
tooth in place, it serves as a platform for the regrowth of natural bone. In that case, it's usually
performed in conjunction with a technique called guided tissue regeneration.
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Guided tissue regeneration. This allows bone destroyed by bacteria to regrow. In one
approach, your dentist places a special piece of biocompatible fabric between existing bone and
your tooth. The material prevents unwanted tissue from entering the healing area, allowing bone
to grow back instead. Another cutting-edge technique involves the application to a diseased tooth
root of a gel that contains the same proteins found in tooth enamel.
** PER- IMPLANTITIS THERAPY:
1) Mechanical cleaning should be carried out on implants with evident plaque or calculus deposits.
Since conventional steel curettes or ultrasonic instruments with steel tips damage and roughen the
implant surface, cleaning should be done with carbon fiber curettes, rubber cups and polishing
paste. Roughening the implant surface should be avoided since initial plaque colonization begins
at surface irregularities, and rough surfaces accumulate and retain more plaque. Rough implant
surfaces have also been found to harbor up to 25 times more bacteria subgingivally than smooth
surfaces
2) Antiseptic treatment should be performed if the peri-implant pocket depth has increased to 4-5
mm, there is bleeding on probing and possible suppuration. Treatment involves daily rinsing with
a chlorhexidine digluconate solution (0.12–0.2%) for three to four weeks, and is usually done in
conjunction with mechanical cleaning. Application of chlorhexidine gel on the surface of a
cleaned implant for five minutes provides topical disinfection.
3) Antibiotic therapy should be administered after mechanical cleaning and antiseptic treatment if
pocket depths reach 6 mm or more. Some studies advocate bacterial culture of a sample to
prescribe the correct antibiotic. In suppurative cases, a combination of amoxycillin and
metronidazole is useful. Although systemic antibiotics are typically used, local administration via
a controlled delivery device has been successful for some cases where infection is localized.
Systemic agents are preferable when there is suppuration.
4) Once infection is controlled, treatment to restore or reshape the implant support can be
attempted. This may be accomplished either with resective procedures (bone resection and
apically repositioned flaps) or regenerative procedures (guided bone regeneration or bone grafts).
Resective procedures are preferable when there is minimal bone loss, while cases with major bone
loss require regenerative procedures.
Summary
In disease, the bacterial flora associated with the natural tooth and the implant are quite similar-,
predominantly Gram-negative pathogens, especially P. gingivalis, P. intermedia, and A.
actinomycetemcomitans. The implant surface must be detoxified before regeneration of the
supporting tissues is attempted. This is best accomplished by the application of citric acid, 40%,
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pH 1, for approximately 30 sec. Guided tissue regeneration (GTR) as it applies to the natural tooth
and guided bone regeneration (GBR) as it applies to the dental implant can be accomplished with
the same barrier membrane and, depending on the topography of the defect and the need for
space-making, can be used in conjunction with grafting materials. The need for the membrane to
remain non-exposed and free of bacterial colonization for optimum osseous regeneration and bone
fill has been documented.
A clinical view describing features of experimental peri-implantitis in the beagle dog. (b) A clinical
view describing features of experimental periodontitis in the beagle dog
REFERENCES:
1- Clinical Periodontology and Implant Dentistry 4th edition Jan Lindhe
2- Article: PERIODONTITIS VS. PERMMPLANTITIS ：R.M. Meffert Department of Periodontics, University of Texas Health
Science Center, San Antonio,
3-Article: PERIODONTITIS AND PERI-IMPLANTITIS BIOMARKERS IN HUMAN ORAL FLUIDS AND THE
NULL-ALLELE MOUSE MODEL。
4- Article :Position Paper Dental Implants in Periodontal Therapy
5- Article :Alphabio professional, Correlation Between Dental Implants, Natural Teeth and Periodontal Disease Jan2009
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