Periodentitis Vs pre-implantitis, the same disease? Same treatment ?



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Periodentitis Vs pre-implantitis,

the same disease?



Same treatment ?



pre-implantitis disease

Periodontology

Prepared By:杰拉德,


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:


  • 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)


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:


  • 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.

  • 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.

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 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.

  • 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.

  • 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.

  • 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%, 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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