Board Preparation and Recertification

Beck JD, Offenbacher S. Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease. J Periodontol 2005;76(11 Suppl):2089-2100.

Mattila KJ, Pussinen PJ, Paju S. Dental infections and cardiovascular diseases: a review. J Periodontol 2005;76(11 Suppl):2085-2088.

Elter JR, Champagne CM, Offenbacher S, Beck JD. Relationship of periodontal disease and tooth loss to prevalence of coronary heart disease. J Periodontol 2004;75(6):782-790.

Kunzel C, Lalla E, Lamster IB. Management of the patient who smokes and the diabetic patient in the dental office. J Periodontol 2006;77(3):331-340.

Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol 2006;77(8):1289-1303.

Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100(1):40-51.

Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100(2):164-178.

American Dental Association Council on Scientific Affairs. Dental management of patients receiving oral bisphosphonate therapy: expert panel recommendations. J Am Dent Assoc 2006;137(8):1144-1150.

Rogers RS III, Sheridan PJ, Nightingale SH. Desquamative gingivitis: clinical, histopathologic, immunopathologic, and therapeutic observations. J Am Acad Dermatol 1982;7(6):729-735.

Discussion: What are the currently accepted treatment modalities for mucocutaneous disorders?

• a. Indications/contraindications for each
• b. Relative strengths and weaknesses for each
• c. Therapeutic endpoints of success for each.

The classification of mucocutaneous diseases is primarily based on the clinical presentation but also includes histologic, immunologic, and laboratory characteristics. Generally, lesions appear erythematous or ulcerative, but in some cases, hyperkeratotic. Diseases considered in this review with intraoral lesions include bullous pemphigoid, cicatricial pemphigoid (benign mucous membrane pemphigoid), chronic ulcerative stomatitis, dermatitis herpetiformis, desquamative gingivitis, epidermolysis bullosa acquisita, erythema multiforme, lichen planus, linear IgA bullous dermatosis, lupus erythematosus, pemphigus, and psoriasis.

Treatment of Bullous Pemphigoid

Treatment of cicatricial pemphigoid (benign mucous membrane pemphigoid)

Chronic Ulcerative Stomatitis

Treatment of dermatitis herpetiformis

Treatment of desquamative gingivitis

Treatment of epidermolysis bullosa acquisita

Treatment of erythema multiforme

Treatment of IGA linear bullous dermatosis

Treatment of Lupus Erythematosis

Treatment of Psoriasis

Beck JD, Offenbacher S. Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease. J Periodontol 2005;76(11 Suppl):2089-2100.

Authors: Mealey BL, Oates TW               

Title: AAP Commissioned Review: Diabetes mellitus and periodontal diseases

Source: J Periodontol. 77:1289-303, 2006

Type: Review

Rating: Good

Keywords: Diabetes mellitus, inflammation, insulin resistance, obesity, periodontal disease

Purpsoe: To discuss the relationship b/w diabetes and periodontal disease.

Discussion:

Mechanism by which diabetes affects the periodontium:

- Some suggest that periodontitis should be listed among the classic complications of diabetes (CVD, neurpathy, nephropathy, retinopathy)

- Fxn of immune cells including neutrophils, monocytes, and macrophages is altered in diabetes. Neutrophil adherence, chemotaxis, and phagocytosis are often impaired.

- The monocyte/macrophage cell line may however be upregulated in response to bacterial antigens. This hyperresponsiveness leads to increased production of pro-inflammatory cytokines and mediators. Peripheral blood monocytes from diabetics produce elevated levels of TNF-α in response P.g.

- Studies have shown that levels of inflammatory cytokines in gingival crevicular fluid are also increased in pts w/ HbA1c levels > 8%

- CT metabolism has been shown to be altered and impaired osseous healing and bone turnover.

- Irreversible glycation of proteins (AGE’s) accumulate in tissue due to their resistance to normal enzymatic degradation. They thicken blood vessels and narrow lumen. AGE-modified vascular collagen as an affinity for LDL which also accumulates in vessel wall contributing to atherosclerotic changes characteristic of macro-vascular complications in diabetes.

- AGE’s also activate a receptor (RAGE) on the surface of smooth m. cells, endothelial cells, neurons, and monocyte/macrophages. Receptor is found in the periodontium and a 50% increase in mRNA for RAGE was found in gingival tissue of pts with type II diabetes.

- AGE-RAGE interaction in periodontal tissues leads to elevated levels of of IL-1β, TNF-α, and prostaglandin E2

- Not very clear the impact of periodontal treatment on glycemic control of diabetes.

Conclusion: Diabetes increases the risk of periodontal diseases. Less clear is the impact of periodontal disease on glycemic control of diabetes and the mechanisms through which this occurs. Inflammatory periodontal disease may increase insulin resistance in a way similar to obeisity, thereby aggravating glycemic control.

Authors: Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K.

Title: Current controversies in oral lichen planus: report of an international consensus meeting. Part I. Viral infections and etiopathogenesis.

Source: Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 100 (1): 40-51.

Type: Review

Rating: Good

Keywords: lichen planus

Background: Lichen Planus is a chronic inflammatory condition that affects oral mucous membranes w/ multiple different presentations: reticular, papula, plaque-like, atrophic and ulcerative.

Purpose: A review to discuss the relationship of oral lichen planus and viral infection w/ emphasis on Hep C and oral lichen planus pathogenesis, especially immune mechanisms leading to lymphocyte infiltration and keratinocyte apoptosis

Discussion: LP affects 0.1%- 4% of the population, more common in middle aged and in women. HSV-1, EBV, CMV, Herpes virus-6 have been implicated. Few patients with HIV have reported lichenoid lesions OR for having Hep C among pts presenting with LP was 4.8 (95% Confidence interval).

Immune dysregulation has also been implicated in the pathogenesis of LP, especially cellular mediated immunity. The inflammatory infiltrate in LP lesions is primarily T cells and macrophages. Plasma cells are rarely seen. The majority of T cells are CD8+ which may induce keratinocyte apoptosis. The apoptosis leads to IFN-gamma upregulation which, when binding to CD4+ cells, increases CD8+ activity leading to more keratinocyte apoptosis and thereby contributes to the disease’s chronicity.

Mast cell density is increased in LP and a large percentage are degranulated. These are thought to cause disruption of the basement membrane.

Possible mechanisms of triggering apoptosis: 1: Tc secretion of TNF-alpha, 2: Tc direct binding, 3: Tc secreted granzyme B (a perforin).

Authors: Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K.

Title: Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation.

Source: Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 100 (2): 164-178.

Type: Discussion

Rating: Good

Keywords: lichen planus

Purpose: To discuss the clinical management and malignant potential of oral lichen planus (LP).

Discussion: Oral lichen planus is a chronic inflammatory disease of unknown cause. Although oral LP is asymptomatic, the atrophic-erosive form can cause symptoms ranging from burning sensation to severe pain interfering with speaking, eating and swallowing. Patients with symptomatic oral LP often require therapy and should be treated if symptoms are significant. As oral LP is a chronic disease, the patient’s medical history, psychological state, and treatment compliance, as well as possible drug interaction, must be considered when evaluating the cost effectiveness of any treatment modalities.

• When oral lichenoid lesions are suspected to be related to the use of a given drug, the medication should be discontinued whenever possible.

• Plaque deposits and calculus are associated with a significantly higher incidence of erythematous and erosive gingival oral LP lesions, good OH is essential and can enhance healing.

• Mechanical trauma of dental procedures, friction from sharp cusps, rough dental restorations, and poorly fitting dental prostheses can be exacerbating factors of symptomatic LP and should receive attention.

Various treatment regimens have been designed to improve management of symptomatic oral LP, but a permanent cure is not yet possible.

• Corticosteroids

Systemic: Are possibly the most effective treatment for patients with diffuse erosive oral LP or multisite disease. Systemic corticosteroids may be indicated in patients whose condition is unresponsive to topical steroids or in patients with mucocutaneous disease.

Topical: Are used in the treatment of LP to reduce pain and inflammation. Topical corticosteroids in adhesive paste, such as betamethasone valerate, clobetasol, fluocinolone acetonide, fluocinonide, and triamcinolone acetonide have been widely used. The more potent fluorinated steroids can be very effective and include fluocinonide 0.05% and fluocinolone acetonide 0.1%. High-potency steroid mouthwashes such as disodium betamethasone phosphate or clobetasol propionate, can be used in widespread oral LP but they may cause significant systemic absorption leading to pituitary –adrenal axis suppression.

• Antifungals: Candida albicans is present in about 37% of oral LP lesions. Symptoms of oral LP may be exacerbated by candida overgrowth. Clinical improvement with relief of symptoms has been reported following use of amphotericin B, nystatin, and azole antifungals. Miconazole gel is found to be effective in the treatment of candidiasis eruptions during topical steroid therapy in every case of oral LP and is useful as adjunctive therapy with topical steroids.

• Cyclosporin: Is a polypeptide that inhibits the transcription of several cytokine genes, thereby suppressing T-cell cytokine production. It may be beneficial for the treatment of oral LP. It should not be considered as a first drug of choice because of the high cost of long-term treatment and the availability of effective alternatives. Disadvantages include bad test and transient burning sensation on initial application. Severe side effects of systemic cyclosporine are HTN and nephrotoxicity.

• Retinoids: systemic and topical forms have been used in the treatment of oral LP. Isotretinoin gel 0.1%, tretinoin ointment and topical fenretinide have been proved to be beneficial in the treatment of oral LP. Systemic etretinate has been used successful for the treatment of severe oral LP. Common side effects of etretinate include, cheilitis, generalized pruritus, hair loss, dryness of mucous membranes, paronychia and increased serum transaminase levels.

• Tacrolimus: Is a potent immunosuppressive agent, inhibiting T-cell activation at 10-100 times lower concentration than cyclosporin. Topical tacrolimus seems to penetrated skin better than topical cyclosporin. Tacrolimus ointment 0.1% is well tolerated and appeared to be effective in erosive oral LP that did not respond to topical steroids. Local irritation is the most common adverse effect.

• Ultraviolet radiation: Photochemotherapy with 8-methoxyprosalen and long-wave ultraviolet light (PUVA) has been used successfully in the treatment of skin lesions and cutaneous LP and was first used in the treatment of recalcitrant oral LP. Side effects include nausea, dizziness, eye symptoms, paresthesia and headache. Photochemotherapy may be useful for severe forms of erosive LP that do not respond to conventional treatment. PUVA therapy has been shown to have oncogenic potential.

• Miscellaneous treatments:

• Antibiotics (aureomycin, doxycycline)

• Antimalarials (hydroxychloroquine sulfate, chloroquine phosphate)

• Azathioprine (immunosuppressive effects)

• Dapsone (adverse effects: hemolysis, headache)

• Glycyrrhizin: successful treatment of oral LP in patients with chronic hepatitis C infection has been reported.

• Interferon

• Levamisole (used as immunomodulator in oral LP)

• Mesalazine

• Phenytoin

• Reflexotherapy

• Surgery (surgical excision has been recommended for isolated plaques or non-healing erosions as it provides tissues specimens for histopathologic confirmation of diagnosis and may cure localized disease. Cryosurgery and CO₂ laser have been used for the treatment of oral LP lesions)

Malignant potential of oral lichen planus: The best evidence currently available on the potentially malignant nature of oral LP is from follow-up studies and retrospective incidence studies. The frequency of oral cancer among oral LP patients reported in 3 of the 4 retrospective studies available from 1985 to present was 1.5% with the follow-up from 4.5 to 7.5 years. The transformation rate of oral LP appears to be around 1% over 5 years, indicating a strong malignant potential of oral LP. However, more research is required. Erosive and plaque-like forms of oral LP have been considered more likely to transform to cancer. Two of the most promising techniques for identification of high risk lesions are DNA content and loss of heterozygosity (LOH).

Authors: American Dental Association

Title: ADA Council on Scientific Affairs. Dental management of patients receiving oral bisphosphonate therapy: expert panel recommendations.

Source: J Am Dent Assoc 2006; 137(8): 1144-1150.

Type: Discussion

Rating: Good

Keywords: oral bisphosphonates, BRONJ, MRONJ

P: Expert panelists selected by ADA Council on Scientific Affairs to develop guidance for dentists treating patients on oral bisphosphonates

M+M: Panelists were selected on the basis of their expertise in the relevant subject matter and on their respective dental or medical specialty. Panelists required to sign disclosure statement that they did not have a significant financial interest that would affect the development of thee recommendations. There is no data from clinical trials evaluating dental management of patients receiving oral bisphosphonates therapy. Panel developed recommendations based on their expert opinion after reviewing literature on bisphosphonate use and osteonecrosis of the jaw.

R: Recommendations:

• Comp oral eval should be completed on all pts

• Important to keep surgical procedures conservative, proper sterile technique, use of oral disinfectants

• Dentist needs to inform pt taking oral bisphosphonates:

  • Very low risk (estimated 0.7 cases per 100,000 person-years’ exposure) of developing BON

  • Ways to minimize risk but not eliminate it

  • Good OH w/ regular dental care best way to lower risk

  • No diagnostic techniques to identify those at increased risk of developing BON

• Pt needs to be informed of dental tx needed, alternative txs, how any tx relates to risk of BON, other risks associated with various tx options, and the risks of foregoing tx

• Pt should be encouraged to consult physician about any health risks

• When tx plan dictates that medullary bone and/or periosteum is going to be involved in multiple sextants, treat one sextant or tooth first. Allow for two month disease free follow-up, treating pt with antimicrobials before other sextants are treated

  • On basis of experience, majority of cases of BON arise w/in 2 months of dental procedure

  • If successful after 2 months with first sextant, tx may be accelerated to a normal pace

  • Sextant by sextant approach does not apply in emergency cases

• Dentist should document the discussion of risks, benefits, and tx options with the pt and obtain pt’s written acknowledgement of that discussion and consent for tx

• At this time, limited data regarding effects of implant placement in pts taking bisphosphonates. Before implant placement, the dentist and pt should discuss risks, benefits, and tx alternatives

BL: These recommendations are a resource for dentists to use in their practice, but must be balanced with the practitioner’s professional judgment and the individual patient’s preference and needs.

Authors: Rogers RS III, Sheridan PJ, Nightingale SH.

Title: Desquamative gingivitis: clinical histopathologic, immunopathologic, and therapeutic observations.

Source: J Am Acad Dermatol 1982; 7(6):729-735.

Type: Discussion

Reviewer: David Long

Rating: Good

Keywords: desquamative gingivitits, mucocutaneous lesions, histology

P: To observe and report on forty-one patients who presented with desquamative lesions limited to the gingiva.

M+M: 41 patients (37F, 4M; 16-86 years old) with lesions limited to the gingiva or masticatory mucosa. All patients had a clinical diagnosis of desquamative gingivitis. Gingiva was erythematous and edematous and involved by a vesiculobullous process that yielded a desquamative, peeling appearance or an erosive or blistering appearance. Biopsy specimens were obtained from tissue peripheral to erosions or bullae and were studied by light microscopy and direct immunofluorescence. Histological specimens stained with hematoxylin and eosin and periodic acid-Schiff.

R:

20/36 patients were treated with dapsone or sulfapyridine. Indications for systemic therapy included subjective complaints, failure to control these with topical corticosteroids, and progression of disease. Response to therapy with dapsone or sulfapyddine: 16 patients had excellent control of inflammation (5 with desquamative gingivitis and 11 with cicatrical pemphigoid), 4 patients had incomplete control or no control (2 with desquamative gingivitis and 2 with cicatricial pemphigoid). Dapsone was drug of choice when topical corticosteroids failed to control signs and symptoms.

BL: Desquamative gingivitis is not a disease, but rather a reaction pattern of the gingiva to stimuli. Cicatricial pemphigoid, lichen planus, and pemphigus vulgaris may present as desquamative gingivitis. Localized oral pemphigoid has been noted to progress slowly and to be responsive to topical corticosteroids or systemic suppressive anti-inflammatory treatment with dapsone or sulfapyridine.

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