44. Atypical Periodontal Conditions and Pathology

HOME PERIO TOPICS 

a) Mucocutaneous lesions

b) NUG/NUP

c) Periodontal Abscesses

d) Atypical periodontal conditions

e) Bisphosphonate therapy (BRONJ)

Mucocutaneous

  1. What are the major types of mucocutaneous disorders? What is the diagnostic classification according to the Armitage paper?

  1. Position Paper: Oral Features of Mucocutaneous Disorders. J Periodontol 2003; 74:1545 – 1556

  1. NisengardRJ. Periodontal implications: mucocutaneous disorders. Ann Periodontol 1996; 1(1): 401-438.

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

  1. LodiG, 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.

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

  1. StooplerET, Sollecito TP, DeRossi SS. Desquamative gingivitis: early presenting symptom of mucocutaneous disease. Quintessence Int. Sep;34(8):582-6, 2003

B. Which medications are associated with gingival enlargement, and how do they affect the periodontal tissues? What other conditions can cause gingival enlargement?

  1. Position Paper: Drug-Associated Gingival Enlargement. J Periodontol2004;75:1424-1431.

  1. LayfieldLL, Shopper TP, Weir JC. A diagnostic survey of biopsied gingival lesions. J Dent Hyg. 69:175-179, 1995.

  1. ReesTD, Levine RA. Systemic drugs as a risk factor for periodontal disease initiation and progression. Compend Cont Ed Dent 1995;16:20-36. (Review)

  1. What other microorganisms can cause gingival lesions?

  1. Rivera-Hidalgo, et al: Oral mucosal lesions caused by infective microorganisms. I. Viruses and bacteria. Periodontol 2000, 21:106-124, 1999

  1. Thomas, S, Rivera-Hidalgo: Oral mucosal lesions casused by infective microorganisms. II. Fungi and parasites. Periodontol 2000, 21:125-144, 1999

  1. What are the different types of acute periodontal lesions?

  1. Corbet, R. Diagnosis of acute periodontal lesions. Periodontol 2000, 2004;34:204-16

  1. What are the important etiologic factors when diagnosing necrotizing ulcerative gingivitis? How does this differ from other periodontal lesions?

  1. Listgarten, M and Lewis, D: The distribution of spirocketes in the lesion of ANUG. J Periodontol 38:379-386, 1967

  1. CourtoisGJ. Acute necrotizing ulcerative gingivitis. A transmission electron microscopic study. J. Periodontol. 54:671-679, 1983.

  1. What medical conditions are specifically associatied with necrotizing periodontal diseases? Should this change the way we approach or treat the conditions?

  1. HorningGM, Cohen ME. Necrotizing ulcerative gingivitis, periodontitis, and stomatitis: Clinical staging and predisposing factors. J Periodontol 66:990-998, 1995.

  1. ShangaseL, Feller L, Blignaut E. Necrotising ulcerative gingivitis/periodontitis as indicators of HIV- infection. SADJ. Apr;59(3):105-8, 2004

  1. NovakMJ. Necrotizing ulcerative periodontitis. Ann Periodontol 1999; 4:74-78.

  1. How do you diagnose and classify a periodontal abscess? Are there specific bacteria associated with this condition? What are some of the causes of the periodontal abscess?

  1. HerreraD, Roldan S, Sanz M. The periodontal abscess: a review. J Clin Perio 27:377-386, 2000. (Review)

  1. DewittGV, Cobb CM, Killoy WJ: The acute periodontal abscess: microbial penetration of the soft tissue wall. Int J Periodont Restor Dent 5(1):39-51, 1985.

  1. Herrera, D., Roldan, S et al: The periodontal abscess (I). Clinical and microbiological findings. J Clin Periodontol 27:387-394, 2000

  1. How do you treat periodontal abscesses? What is the long term prognosis of the teeth associated with these abscesses?

  1. Herrera, D RoldanS et al: The periodontal abscess (II). Short – term clinical and microbiological efficacy of 2 systemic antibiotic regimes. J Clin Periodontol 27:395-404, 2000

  1. McLeodDE, Lainson PA, Spivey JD. Tooth loss due to periodontal abscess: A retrospective study. J Periodontol 68:963-966, 1997.

  1. What atypical forms of periodontal disease affect children prior to puberty? What is the appropriate diagnosis for these conditions (according to the 1999 classification system?

  1. PageRC, et al. Prepubertal periodontitis I. Definition of a clinical disease entity. J. Periodontol. 54:257-271, 1983.

  1. SweeneyEA, et al : Prevalence and microbiology of localized prepubertal periodontitis. Oral Microbiol. Immunol. 2:65-70, 1987.

  1. PageRC, Altman LC, Ebersole JL, et al. Rapidly progressive periodontitis. A distinct clinical condition. J. Periodontol. 54:197-209, 1983.

  1. WatanabeK. Prepubertal periodontitis: A review of diagnostic criteria, pathognesis, and differential diagnosis. J. Periodontal Res. 25:31-48, 1990.

  1. What questions should be asked of any patient presenting with a periodontal issue of unknown etiology? Are there specific medications or products that can cause specific changes in the gingival tissues?

  1. RobertsonPB, et al: Periodontal effects associated with the use of smokeless tobacco. J. Periodontol. 61:438-443, 1990.

  1. YuknaRA: Cocaine periodontitis. Int. J. Periodont. Restor. Dent. 11:72-79, 1991.

  1. Kerr,D et al: Allergic gingivostomatitis (due to gum chewing). J. Periodontol 42:709-712, 1971

  1. LaPortaV et al: Minocycline-associated intra – oral soft tissue pigmentation: clinicopathologic correlations and review. J Clin Periodontol 2005;32:119-122

  1. What is a lateral periodontal cyst? How should it be treated?

  1. FilipowiczFJ, Page DG : The lateral periodontal cyst and isolated periodontal defects. J. Periodontol. 53:145-151, 1982.

  1. What is a bisphosphonate and what is its mechanism of action? For which conditions in this medication prescribed? Should treatment be modified for patients taking this medication?

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

  1. American Association of Oral and Maxillofacial Surgeonsposition paper on bisphosphonate-related osteonecrosis of the jaws. Advisory Task Force. J Oral Maxillofac Surg. 2007 Mar; 65(3):369-376

  1. Marx, R., Sawatari, eta al: Bisphosphonate – Induced Exposed Bone (Osteonecrosis/Osteopetrosis) of the Jaws: Risk Factors, Recognition, Prevention, and Treatemtn, JOMS 2005;63:1567-1575

  1. Marx, R et al: Oral biophosphnate – induced osteonecrosis: risk factors prediction of risk using serum CTX testing, prevention and treatment. J Oral Maxillofac Surg 65:2397 – 2410, 2007

  1. CartsosV, et al: Bisphosphonate use and the risk of adverse jaw outcomes: a medical claims study of 714,217 people. J Am Dent Assoc 2008; 139(1):23 – 30

  1. Grbic, J et al: Incidence of osteonecrosis of the jaw in womrn with postmenopausal osteoporisis in the Health Outcomes and Reduced Incedent With Zoendronic Acid Once Yearly Pivotal Fracture Trial. J Am Dent Assoc 2008; 139(1); 32-40

  1. Sedghizadeh, P et al: Oral bisphosphonate use and the prevalence of osteonecrosis of the jaw: An institutional inquiry. J Am Dent Assoc. 2009 Jan; 140(1):61-66

Mucocutaneous

  1. What are the major types ofmucocutaneous disorders? What is the diagnostic classification according to the Armitage paper?

Topic:Mucocutaneous Disorders                Article

Authors:

Title: Position Paper: Oral Features of Mucocutaneous Disorders.

Source: J Periodontol ;74:1545 – 1556

Type:Position Paper

Rating: Good

Keywords:Mucocutaneous Disorders, Position Paper

Disc: Oral mucosa may be affected by a variety of mucocutaneous diseases.  The erosive gingival lesions associated with vesiculobullous diseases such as lichen planus, mucous membrane pemphigoid, and pemphigus vulgaris have been collectively referred to as desquamative gingivitis.

Desquamative gingivitis is a clinical feature characterized by epithelial desquamation, erythema, ulceration, and/or the presence of vesiculobullous lesions of gingiva and other oral tissues.  Oral lesions may occur first or very early in several mucocutaneous diseases.

Lichen Planus Common, generally develops between 40-70 years old, F>M; etiology unknown, but thought to be a cell-mediated immune response to intraepithelial antigens. Oral manifestations occur in approximately 2% of general population while cutaneous lesions occur in 0.4%. Comes in reticular, plaque-like, and erosive (atrophic, ulcerative, and bullous) with reticular being most common. Patients with erosive may demonstrate positive Nikolsky’s sign (epithelial separation from underlying CT as a result of minor trauma). In addition to the oral cavity, lesions can be seen on the skin, esophagus, genitalia and rarely the eyes. Biopsy specimens essential. 

Histologic features:

  • Epithelial acanthosis and hyperkeratosis

  • Degeneration of epithelial basal cells

  • Saw-tooth rete ridges

  • Dense band-like, sub-basilar infiltrate of T-lymphocytes

  • Direct immunofluorescence may be of value in supporting diagnosis or ruling out other diseases. A linear or shaggy deposit of fibrin or fibrinogen at the basement membrane is often observed.

Treatmentincludes, eliminating potential factors causing lichenoid reaction, local irritants, and effective use of therapeutic agents that suppress excessive lymphocyte function. Patients with erosive lichen planus are often successfully treated with corticosteroids. Topically applied medications such as fluocinonide and clobetasol gel, beclomethasone dipropionate spray (inhaler), or dexamethasone mouthrinses are effective in inducing remission of lesions. Short –term tapering doses of systemic corticosteroids such as prednisone or intralesional injections are useful in severe episodes as well as in recalcitrant cases. Although expensive to use, systemic and topically administered cyclosporine has been shown promising results. Recently, topical tacrolimus has been shown to be an effective form of treatment.

Controversy exists regarding the potential for malignant transformation in patients with lichen planus. Some clinical investigations have demonstrated an increased incidence of oral cancer in lichen planus lesions ranging from 0.4% to 5.6%.

Mucous Membrane Pemphigoid-(benign MMP, cicatricial pemphigoid) is a humoral autoimmune disorder that predominantly affects oral cavity. Other mucosal surfaces may be involved, including the conjunctiva, nares, larynx, esophagus, upper respiratory tract, rectum or genitalia. Mean age of onset is 50 years old, F>M, often have positive Nikolsky’s sign, gingiva most common intraoral site affected. Intraoral manifestations include desquamative gingivitis, vesiculobullous lesions, and ulcerations. Periods of exacerbation and remission are common. Ocular lesions often exhibit progressive scarring leading to fusion of ocular and eyelid conjunctiva (symblepharon formation). Continued scar formation can lead to blindness if untreated.

One or more of several heterogenous antigens (BP180, BP230, laminin 5 and others) found within the basement membrane adhesion complex may be targeted, resulting in immune response.

Histologic features: Direct immunofluorescence reveals alinear deposition of complement (usually C3) and IgG at the basement membrane zone.  Treatment includes eliminating drugs that can cause pemphigoid like lesions, topical corticosteroids alone or in combination with systemic. Dapsone is an antimicrobial agent with immunosuppressive capacity has shown some good results. Periodic blood studies are necessary when administering dapsone due to its potential to induce hemolytic anemia. Patients should be referred to an ophthalmologist for evaluation

Pemphigus Vulgaris– Potentially life threatening autoimmune disease that results in bullae formation involving skin and or mucosa membranes.  40-60 years old and affects individuals of Jewish and Mediterranean descent. Intraoral manifestations included intraepithelial separation resulting in the formation of bullous lesions. Bullae can rupture causing painful erosions, and lead to death due to septicemia or fluid/electrolyte loss. Lip lesions are typical in contrast to pemphigoid where they are rare. Histologic features:

  • acantholysis and suprabasilar bullae formation formation

  • The basal cells lining the floor of the bullae are often arranged in a tombstone pattern and acantholytic keratinocytes (Tzanck cells ) float freely within the blister fluid.

Direct immunofluorescence reveals deposition of complement and IgG, IgM or IgA within the intercellular spaces of the epitheliumresulting in a reticular pattern diagnostic pemphigus vulgaris. The antigenic stimulus is desmoglein III, an intercellular desmosomal adhesion molecule.

Treatment includes moderate to high doses of systemic corticosteroids alone or in combination with topical corticosteroids. Azathioprine may help control recalcitrant cases. Dapson and cyclosporine A have shown some efficacy.

Lupus erythematosus: Autoimmune condition that may involve the oral cavity along with the skin and internal organs. It is classified into the systemic form, a neonatal form, a chronic cutaneous and a subacute cutaneous form. More common in women and blacks. Classic description includes: chronic fever, weight loss, symptoms of arthritis, a malar or butterfly rash, effusion and glomerulonephritis. Oral lesions are present up to 40% of the patients. Oral lesions are characterized by the presence of a central erythematous erosion or ulceration surrounded by a white rim with radiating keratotic striae. Most frequent sites of involvement are hard and soft palate, buccal mucosa and the vermillion border of the lips. Gingiva may present a desquamative appearance and patients may complain of pain and soreness. Other mucosal surfaces can be affected including oropharyngeal mucosa, nares, larynx and epiglottis.

Histologic features:

  • Keratinocyte vacuolization

  • Sub-epithelial PAS-positive deposits

  • Lamina propria edema

  • Severe perivascular lymphatic infiltrate

  • Direct immunofluorescence reveals: IgG, IgM and/or C3 along the basement membrane zone

Oral and skin lesions respond to topical and intralesional corticosteroids with variable results. Systemic antibiotics alone or in combination with other immunosuppressive agents such as cyclophosphamide may be useful in severe cases.

Topic: Mucocutaneous disorders                        Article

Authors:Nisengard RJ

Tittle: Periodontal implications: mucocutaneous disorders.

Source:Ann Periodontol 1996; 1(1): 401-438.

Type: Discussion paper

Rating: Good

Keywords:Diagnosis, classification

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.

Etiology:Unknown

Dx:With the clinical, histological, and immunological criteria, a disease-specific diagnosis is possible in most but not all cases.

Tx: When the disease may involve intraoral sites and extraoral sites, or the therapy may cause potentially significant side

effects; the patient may be referred to an appropriate physician (dermatologist, rheumatologist, ophthalmologist, etc.) for management.

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

Topic:Lichen planus No Article

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).

Topic:Mucocutaneous                             No Article

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).

Topic:Mucocutaneous                         No Article

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.

Topic:Desquamative Gingivitis                         No Article

Authors:Stoopler ET, Sollecito TP, DeRossi SS

Title: Desquamative gingivitis: early presenting symptom of mucocutaneous disease.

Source:Int. Quintessence Sep;34(8):582-6, 2003

Type: Review

Rating: Good

Keywords:desquamative gingivitis, erosive lichen planus, mucous membrane pemphigoid, pemphigus vulgaris. reticular lichen planus

P:To review the etiology, signs, symptoms, and therapies of desquamative gingivitis.

D:Desquamation of the gingiva is a sign that may be encountered in clinical practice. Various diseases can affect the gingival tissue. Mild desquamation that is localized may be associated with irritation or induced by trauma (i.e. aggressive tooth brushing, toothpaste sensitivity especially to tartar-control products). Moderate to severe generalized desquamation associated with ulceration and erythema may be indicative of a more serious systemic condition. Mucocutaneous disease frequently present with gingival desquamation as an early presenting symptom. The most common mucocutaneous diseases are:

Lichen planus:is a skin and oral disease that has several forms (reticular, papular, atrophic, bullous and erosive).

  • Etiology is idiopathic but some lichenoid reactions have similar clinical presentations that are caused by drugs (penicillins, ACE inhibitors, NSAIDs), systemic diseases and contact allergy (i.e. mercury, gold, and cinnamon).

  • Hepatitis C has been associated with LP-like lesions. The diagnosis of LP is by biopsy and characteristics include: dense subepithelial band of lymphocytes, liquefactive degeneration of the basal cell layer, areas of hyperorthokeratosis and hyperkeratosis with a saw tooth appearance to the rete pegs.

  • Lichenoid reactions cannot always be distinguished from LP but may show deep as well as superficial lymphocyte infiltrates, rather than the classic band-like infiltrate of LP. Tx will be by discontinue using the product or the drug and topical (fluocinonide, clobetasol) or sys steroids (tacrolimus) in the erosive types.

  • Poor periodontal health makes management of erosive LP much more difficult, a shorter recall may be necessary (pts may not like to brush because it is painful, resulting in gingival inflammation).  

Pemphigus (P):autoimmune disease characterized by intraepithelial blisters and peeling of skin and mucosa.

  • It has several forms which are P vulgaris (most common, 80% of the cases), P vegetans, P foliaceus, P erythematous, paraneoplastic P, and drug-related pemphigus. P. vulgaris is caused by the loss of cell to cell adhesion due to the desmosomes being bound by autoantibodies, which results in a suprabasilar bulla.

  • Initial signs may include generalized desquamative gingivitis. It is common for oral lesions to present up to 4 months before the skin lesions appear. The biopsy should ideally be taken from an intact vesicle less than 24 hours old.

  • Since these types of lesions are rarely present in the mouth, the biopsy should be taken from the advancing edge of the lesion where the suprabasilar splitting of the epithelial may be observed.

  • A second biopsy should be taken from clinically normal-appearing intact perilesional mucosa and sent for direct immunofluorescence studies. If the DIF is positive for PV, the pattern will reveal a lace-like pattern around epit cells of the tissue specimen. Presents as a thin walled bulla on the gingival and the buccal mucosa. Tx is high doses of corticosteroids (Prednisone), however, lower doses can be given if adjuncts (azathioprine, cyclophosphamide) are given.

Mucous membrane pemphigoid:chronic autoimmune disease causing subepithelial mucosal ulcerations (skin involvement is low).

  • MMP is considered a family of closely related autoimmune disorders in which the various autoantigens are involved in the attachment of basal epithelial cells to the underlying CT.

  • It presents as desquamative gingivitis and erosions or ulcerations of buccal and labial mucosa, palate and tongue. If extraoral signs are observed, the pt should be sent to the appropriate specialist.

  • Routine histo-path will demonstrate sub-basilar cleavage and immunofluorescence will show positive for immunoglobulin and complement in the basement membrane zone in 50-80% of the pts.

  • Treatment is with topical (mild cases) and/or systemic steroids (Dapsone). Approximately 10% of pts with MMP will develop eye lesions which often result in scarring and can lead to blindness.

Topic:gingival enlargement                         No Article

Authors: Academy report

Title:Drug-Associated Gingival Enlargement.

Source:J Periodontol 2004;75:1424-1431. DOI: 10.1902/jop.2004.75.10.1424

Type:Position Paper

Rating: good

Keywords:gingival enlargement; gingival overgrowth, immunosupressants; anticonvulsants; calcium channel blockers.

Purpose:To provide an overview of existing evidence regarding the prevalence, risk factors, pathogenesis, and clinical management of drug – associated gingival enlargement.

Discussion:Gingival enlargement or overgrowth is the preferred term and not the previously used gingival hyperplasia or hypertrophy. Drugs associated are divided into three categories: anticonvulsants (phenytoin), calcium channel blockers (nifedipine, diltiazem, verapamil) and immunosuppressants (cyclosporin A (CsA)).

  • Prevalence:Phenytoin – related 50%, phenobarbitone less than 5%, nifedipine 6-15% and significantly smaller for verapamil, dilitiazem, felodipine or amlodipine, Cyclosporin 25-30% for adults and more than 70% for children.

Category

Pharmacologic Agent

Trade Name

Prevalence

Anticonvulsants

Phenytoin

Dilantin

Sodium valproate (valproic acid)

Depakene, Depacon, Epilim,Valpro

Phenobarbitone

Phenobarbital, Donnatal

<5%

Vigabatrin

Sabril

Carbamazepine

Tegretol

None reported

Immunosuppressants

Cyclosporin

Neoral, Sandimmune

Adults 25-30%

Children

>70%

Calcium channel blockers

Nifedipine

Adalat, Nifecard, Procardia,Tenif

6-15%

Isradipine

DynaCirc

None reported

Felodipine

Agon, Felodur, Lexxel, Plendil

Amlodipine

Lotrel, Norvasc

Verapamil

Calan, Covera, Isoptin, Tarka,Verelan

<5%

Diltiazem

Cardizem, Dilacor, Diltiamax,Tiazac

5-20%

  • Risk factors:Poor plaque control correlates with the severity of gingival enlargement. Patients with evidence of inflammation prior to treatment are more possible to develop severe gingival enlargement.

Other factors may include gender with males being three times more likely to develop overgrowth and an inverse correlation with age. There are no data for correlation with the dosage. Patients receiving CsA with a calcium channel blocker present with a greater severity gingival lesion than those receiving only CsA.

  • Clinical manifestation appears 1-3 months after initiation of treatment. It affects mostly the anterior labial surfaces (with the exception of phenobarbitone which affects more likely the posterior teeth). Gradually the enlargement appears fibrotic, normally confined to the attached gingiva but may also extend coronally, impairing nutrition and oral hygiene.

  • Histologicallyit was shown that the enlargement is primarily due to a connective tissue response rather than epithelial cell layer. Excessive accumulation of extracellular matrix proteins is observed. Varying degrees of inflammatory infiltrate exist and the plasma cells are the predominant type.

  • Mechanisms:the exact mechanism causing the enlargement is not yet completely understood. Fibroblasts with an abnormal susceptibility to the drug or a subpopulation of them is a possible explanation. Synergistic action of cytokines (IL-1IL-6) is also possible, as well as reduced secretion of MMP-1 and MMP-3.

  • Prevention:Elimination of local factors, plaque control, regular periodontal maintenance may ameliorate but not prevent the gingival enlargement. Topically applied 0.12% chlorhexidine can reduce the severity of gingival enlargement.

  • Treatment:The most effective treatment is withdrawal or substitution of the medication, and this can take 1-8 weeks for resolution of the lesions, but still not all patients respond to that treatment especially those with long – standing gingival lesions.

Debridement with SRP has been shown to offer some relief in the patients. In chronically immunosuppressed patients topical antifungal medications can be used.

External bevel gingivectomy is often performed for esthetic reasons in the anterior area, total or partial internal gingivectomy approach has been suggested. Carbon dioxide lasers have shown some utility. Consultation with the patient’s physician should take place especially in the immunocompromised patient.

Recurrence rate of severe gingival enlargement in CsA or nifedipine patients was found to be 40% within 18 months after active treatment.

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22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation

 HOME PERIO TOPICS 

Provide an overview of the pathogenesis of periodontitis. Describe the sequence of events in order of occurrence.

  1. Listgarten M. A. Nature of periodontal disease: Pathogenic mechanisms. J Periodontal Res. 1987; 22: 172-78

  2. Schroeder H: Discussion: Pathogenesis of periodontitis. J. Clin. Periodontol. 13:426-430, 1986. (Review)

  3. PAGE R & K. KORNMAN: The pathogenesis of human periodontitis: an introduction. Periodontology 2004 Vol. 14, 1997, 9-11

  4. KORNMAN K,R. PAGE & M. TONETTI: The host response to the microbial challenge in periodontitis: assembling the players. Periodontology 2000, Vol. 14, 1997, 33-53

  5. Kinane DF: Causation and pathogenesis of periodontal disease. Periodontol 2000. 25:8-20,2001 (Review)

  6. DARVEAAUN R, NET ANNER& ROYC . PAGE: The ,microbial challenge in periodontitis. Periodontology 2000, Vol. 14, 1997, 12-32

  7. PAGE R, S. OFFENBACHER, SCHROEDER, G. SEYMOUR & K. KORNMAN: Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontology 2OW. Vol. 14, 1997, 216-248

Describe Page & Schroeder’s model in detail.

  1. Page RC, Schroeder HE: Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab. Invest. 34:235-249, 1976 (Review)

Discuss Gingivitis

  1. Van Dyke TE, Offenbacher S, et al. What is gingivitis? Current understanding of prevention, treatment, measurement, pathogenesis and relation to periodontics. J Int Acad Perio 1:3-15; 1999. (Review).

  2. Page RC. Gingivitis. J. Clin. Periodontol. 13:345-355, 1986. (Review)

Does all gingivitis become periodontitis? Is gingivitis a prerequisite for periodontitis?

  1. Schroeder HE, Lindhe J : Conversion of stable established gingivitis in the dog into destructive periodontitis. Arch. Oral. Biol. 20:775-782, 1975.

  2. Soames JV, Entwisle DM, Davies RM : The progression of gingivitis to periodontitis in the beagle dog. A histologic and morphometric investigation. J. Periodontol. 47:435-439, 1976.

How do periodontal pockets form? Which tissues are destroyed first?

  1. Ritchey B, Orban B. The periodontal pocket. J. Periodontol. 23:199-213,1952.

  2. Takata T, Donath K : The mechanism of pocket formation – A light microscopic study of undecalcified human material. J. Periodontol. 59:215-221, 1988.

  3. Saglie, Carranza, Newman and Pattison: Scanning electron microscopy of the gingival wall of deep periodontal pockets in humans. J Periodontal Res. 1982; 17: 284-293

List enzymes implicated in periodontal destruction and their origin. Do these enzymes have any therapeutic or diagnostic significance?

  1. REYNOLDS J & MURRAYC . MEIKLE: Mechanisms of connective tissue matrix destruction in periodontitis. Periodontology 2000, Vol. 14, 1997,144-157

  2. Van der Zee E, Everts V, Beertsen W: Cytokines modulate routes of collagen breakdown. J Clin Periodontol. 24:297-305, 1997.

  3. Lee W, et al. Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: Role of active enzyme in human periodontitis. J Periodont Res 1995; 30:23-33

  4. SCHWARTZ, Z., J. GOULTSCHIN D. DEAN & B. BOYAN: Mechanisms of alveolar bone destruction in periodontitis. Periodontology 2000, Vol. 14, 1997, 158.1 72

  5. Mogi M, J. Otogoto, N. Ota and A. Togari: Differential Expression of RANKL and Osteoprotegerin in Gingival Crevicular Fluid of Patients with periodontitis. J DENT RES 2004 83: 166

  6. Nonnenmacher C, K. Helms, M. Bacher, R.M. Nüsing, C. Susin, R. Mutters, L. Flores-de-Jacoby and R. Mengel: Effect of Age on Gingival Crevicular Fluid Concentrations of MIF and PGE2. J DENT RES 2009 88: 639

  7. Johnson RB, Serio FG, Dai X: Vascular endothelial growth factors and progression of periodontal diseases. J Periodontol 70:848-852, 1999

How can the host response be modified as a part of periodontal therapy?

  1. Salvi GE, Lang NP. Host response modulation in the management of periodontal diseases. J Clin Peridontol 2005; 32 (Suppl. 6): 108–129.

  2. Bhatavadekar NB, Williams RC. Commentary: new directions in host modulation for the management of periodontal disease. J Clin Periodontol 2009; 36: 124–126

Provide an overview of the pathogenesis of periodontitis. Describe the sequence of events in order of occurrence.

Topic: Nature of periodontal disease

Authors: Listgarten M.

Title: A. Nature of periodontal disease: Pathogenic mechanisms.

Source: J Periodontal Res. 1987; 22: 172-78

Type: Discussion

Rating: Good                                                               ARTICLE

P: Discussion article on the nature of periodontal disease and pathogenic mechanisms.

D: The oral microbiota, one of the most complex in the body, comprises over 300 species. Of these, about 30 are routinely observed and account for the majority of the cultivable strains. Health of periodontal tissues is maintained in a relatively stable state through the establishment of host-parasite equilibrium compatible with minimal tissue destruction and ready replacement or repair of damaged structures. Alterations in this equilibrium may develop as a result of local or systemic changes that decrease host resistance or from qualitative/quantitative alterations of periodontal microbes which result in increased virulence. These upsets may account for “bursts of disease activity. Bacteria can contribute to periodontal disease by direct injury of the host tissues (toxins, enzymes, toxic metabolic end products) or they can also act indirectly by triggering host mediated responses that may result in self-injury.

Role of bacteria and host-mediated tissue injury is discussed in detail.

Bacteria

  • Non-specific theory of plaque induced periodontal disease (Loesche): Sheer mass of microorganisms (MOs) generate sufficient noxious stimuli to induce inflammatory response in host. Seen in gingivitis.

  • Certain forms of periodontal disease (AgP) caused by particular organisms which cause disease by various mechanisms

Direct toxicity: Variety of substances of bacterial origin which are capable of causing injury. They are usually of large molecular weight and may include some enzymes. Classically toxins have been divided in endotoxins and exotoxins.

  • Exotoxins: proteins released by live microorganisms into their immediate environment where they can cause direct tissue injury. Some exotoxins have a specific affinity for certain cell types. Neurotoxins for nerve tissue, leukotoxins for neutrophils or epitheliotoxins for epithelial cells.

Leukotoxin

  • produced by Aa , associated with outer membrane of A.a cell wall from which it may be shed as membranous vesicles

  • shown to have correlation with periodontal disease.

  • shown to readily lyse human PMNs (Brehni et al)

  • able to kill human monocytes and weaken local host defense (Taichman et al)

Endotoxins: Lipopolysacchirides (LPS) which are structural components of Gram (-) bacteria. Their release occurs primarily after lysis of the cells. Endotoxins can exert a wide diversity of biological events, yet they share a common molecular structure. The linear molecule which is oriented perpendicularly to the bacterial cell surface consists of 3 distinct regions.

  1. Lipid A region which forms part of the outer half of the outer membrane of the cell wall. It is responsible for direct toxicity.

  2. Thecentrally located core polysaccharide

  3. The polysaccharide side chains, where the 0-somatic antigensreside, extend peripherally beyond the outer membrane.

The carbohydrate components provide the lipid A with hydrophilic properties, which enhance its pathogenicity and may increase the resistance of the bacteria to phagocytosis.

Endotoxins:

  • Enhance bone resorbing quality of osteoclasts

  • They can also bind to surface of PMNs or macrophages which internalize the endotoxin. Subsequent internalization of the endotoxin causes the cells to release their lysosomal enzymes extracellularly, with resulting damage to the local tissues and the generation of peptides that are vasoactive and chemotactic for PMNs.

  • Activate complement through the indirect pathway, with the consequent generation of complement-derived mediators of inflammation.

  • Act as modulators of bacterial cell uptake by phagocytic cells, with the endotoxin able to promote or inhibit phagocytosis depending on concentration.

  • Interfere with new attachment to denuded root surfaces.

Enzymes: Bacteria may exert pathogenicity in part through tissue invasion. Assorted enzymes may facilitate bacterial tissue penetration by removing various structural barriers and destroying host proteins that play a key role in host defenses like IgG’s.

  • Proteases, specifically collagenase, hyaluronidase, and chondroitin sulfatase are of particular interest in periodontal disease. They can be found in spirochetes and black pigmented bacteroides.

  • Metabolic products: End products of bacterial metabolism e.g. ammonia, indole, hydrogen sulfide, fatty acids also contribute to initiation and disease progression. Local changes in pH due to metabolism may also affect survival of certain microorganisms.

Indirect toxicity:

Effect on host cells: Bacterial enzymes may play an important role in neutralizing some of the oxygen -dependent antibacterial host defenses. Alterations in tissue oxygen levels may also favor the establishment of anaerobic infections that are associated with periodontitis. Bacterial protease can contribute to indirect injury of the host by destroying the functional activity of humoral antibodies directed against bacterial antigens.

Effect on bacterial cells: Bacterial interactions may play an important role in controlling the ability of microorganisms to colonize the tissues.

Host-mediated tissue injury

  • Caused by inflammation by triggering variety of injurious stimuli including thermal, mechanical, chemical trauma

  • Complement activation (IgG and IgM react with assorted bacterial antigens to form insoluable complexes). The formation of insoluble antigen- antibody complexes can activate the complement cascade with the resulting release of a number of mediators of inflammation into the extracellular environment. These can contribute to the influx of PMNs, the generation of additional vasoactive molecules and the outpouring of hydrolytic enzymes of lysosomal origin into the extracellular environment.

  • The lipoteichoic acid and lipopolysaccharides of the gram-negative cell wall are able to activate the complement cascade through the alternative pathway. While activation of complement has an overall beneficial effect in proecting the host against bacterial attack, some tissue destruction is unavoidable. Tissue injury is due in part to the complement-mediated influx of phagocytic cells and the release of lysosomal enzymes, and the production, by lymphocytes and macrophages, of assorted lymphokines that are able to kill cells and resorb bone.

Topic: Pathogenesis

Authors: Schroeder H

Title:Discussion: Pathogenesis of periodontitis.

Source: J. Clin. Periodontol.13:426-430, 1986.

Type: Review

Rating: Good                                                              ARTICLE

Keywords: Pathogenesis, periodontitis

Purpose: Discussion on the pathogenesis of periodontitis

Discussion:

  • Periodontitis is a local infectious disease caused and chronically maintained by a mixed, predominantly anaerobic bacterial infection of the subgingival portions of the periodontium. There are several difficulties in attempting to classify periodontal disease.

  • Author suggests the use of gingival pocket depth as a diagnostic criterion because it is the precursor of periodontal pocket. A gingival pocket is a shallow pocket (1-2mm) and histopathologically is similar to the periodontal pocket. No doubt that the development of gingival pockets is due to bacterial plaque extending apically along root surface. Once a gingival pocket has formed, gingivitis is no longer reversible with simple reestablishment of OH. Any pocket lined with pocket epithelium presents a pathophysiologic situation of associated with high tissue permeabilityincreased tissue reactivityinfected w/ subgingival bacteriaunattainable to remove w/ OH.

  • Transition from a gingival to a periodontal pocket is also due to the host response. There is no spontaneous shift back from the established lesion to the early.

  • The width and shape of infrabony pocket is also important and should be assessed radiographically.

  • Bone resorption occurs when plaque approaches 0.5 to 2.5 mm to the bone.Large bowel – shaped defects associated with periodontal pockets but extending further than the plaque radius, are probably related to lateral invasion of the soft tissues with plaque.

  • BOP is useful only for the early stages of gingivitis since evaluating it is subjective with regard to severity.

BL:The diagnosis and the pathogenesis of a particular patient with periodontitis are usually unknown. Factors other than bacteria may influence the pathogenesis of periodontitis, like OH, food impaction, iatrogenic factors, all of which interfere with the host-parasite relationship

Topic:Pathogenesis

Authors:Page R, Kornman K

Title:The pathogenesis of human periodontitis: an introduction
Source: Periodontology 2000 Vol. 14, 1997, 9-11

Type:Review

Rating:Good                                                               ARTICLE

Keywords:pathogenesis

Review:The major developments since the 1976 article by Page & Schroeder have been the discovery of the pathways through which bacteria activate host cells and systems in a manner that tissue destruction ensues and elucidation of the pathways through which the extracellular matrix components of the gingival and periodontal ligament are destroyed and alveolar bone is resorbed. Based on the current understanding, evidence is now sufficient for the development and application of new preventive measures, diagnostics and treatments targeted at blocking or altering these pathways.

Conclusion:Periodontitis is not a single homogenous disease but rather consists of a family of closely related diseases each of which may vary somewhat in etiology, natural history and response to therapy. There is a common chain of events of pathogenesis that is influenced by other factors including genetic and other risk factors may differ from one form of disease to another. Antigens and various other virulence factors, and in some cases invading bacteria, comprise the microbial challenge, and the host responds with an immediate inflammatory andimmune response that can influence the challenge. The host response results in production of cytokines, eicosanoids, other inflammatory mediators such as the kinins, complement activation products and matrix metalloproteinases, which perpetuate the response and mediate connective tissue and bone destruction. All of these events are influenced by disease modifiers, both genetic and environmental or acquired. The clinical picture observed is a result of the sum of these events. The severity and rate of progression of disease feedback to influence the nature and magnitude of the microbial challenge by, for example, influencing the pH and availability of oxygen and various nutrients in the periodontal pocket.

Topic:Pathogenesis

Authors: Kornman KS, Page RC, Tonetti MS.

Title:The host response to the microbial challenge in periodontitis: assembling the players.

Source:Periodontol 2000. 1997 Jun;14:33-53.

Type:Review

Rating: Good                                                              ARTICLE

Keywords:pathogenesis, host response

Purpose:To describe the histologic, cellular and molecular changes that occur during the transition from health to disease initiation and progression.

Discussion:Periodontitis is an infectious disease process. Bacteria and their products interact with the junctional epithelium and penetrate into the underlying connective tissue. Inflammation is caused and leukocytes (especially neutrophils) exit the post-capillary venules and end up in the sulcus. Collagen and other components of extracellular matrix are destroyed. Supra-g plaque extends apically and into the gingival sulcus, cells of JE are stimulated to proliferate and a gingival pocket is formed. At an early stage there is an enlarging leukocyte infiltrate and subsequently the lesion becomes dominated by B-cells that produce antibodies. As the disease worsens, periodontal pockets deepen, the components of the extracellular matrix of the gingiva and PDL are destroyed and alveolar bone is resorbed.

Scene 1. Acute bacterial challenge phase: the epithelial and vascular elements respond to the bacterial challenge.

Epithelial membranes, flushing by saliva and GCF protect the tissues from initial bacterial invasion. High turnover rate of epithelium is associated with rapid replacement of damaged cells.

When bacteria start to accumulate the release metabolic products (including fatty acids and the lipopolysaccharides (LPS) of Gram- bacteria) that activate JE cells to release various inflammatory mediators such as IL-8, IL-1αPG-E2, MMPs, TNF. Neural components of the epithelium influence the local vascular response. The bacterial products and epithelial response activate mast cells to release histamine and activate vascular endothelial cells to release IL-8 within the vessels to assist in localizing neutrophils.

Scene 2. Acute inflammatory response phase: the tissues respond to the early signals.

The wide extracellular spaces oh the JE allow neutrophil migration. The vascular leakage and activation of serum proteins such as complement, begin to amplify the local inflammatory response and produce further endothelial cell activation. Leukocytes and monocytes are recruited. Neutrophils exit the inflamed vessels and form a wall between plaque and gingival tissues. They are capable of killing bacteria by phagocytosis and prevent extension apical and lateral extension of plaque. PMNs are the majority of cells in the sulcus and mononuclear cells the majority of tissue infiltrate. IL-8 appears to be critically involved in PMN recruitment.

Macrophages produce mediators of the immune and inflammatory responses including IL-1β, IL-1 receptor antagonist, IL-6, IL-10, IL-12, TNF, IFN, MMPs, PG-E2 and chemotactic substances such as monocyte chemoattractant protein (MCP) and macrophage inflammatory protein (MIP).

Scene 3. Immune response phase: activation of mononuclear cells shapes the local and systemic immune response.

The changes in this phase are associated with periodontal pocket. Soon after inflammation starts the exudate from the vessels becomes predominated by mononuclear cells. T-cells, B-cells and plasma cells become evident in the tissues. T-cells produce IL-2, 3, 4, 5, 6, 10 and 13, TNF-IFN, TGFand chemotactic substances. Plasma cells become prominent in the tissues and produce immunoglobulins such as IgG, IL-6 and TNF-Fibroblasts are also activated and produce MMPs and tissue inhibitor of matrix metalloproteinases (TIMPs). Macrophages become effector cells and depending on the nature of the challenge secrete a restricted set of cytokines and express surface receptors that influence the antigen specific immune response that directly targets the pathogen. Their products alter the local environment in several ways. They produce chemokines that recruit additional monocytes and lymphocytes, they favor collagen degradation (through the production of specific factors such as PGE2 and MMPs) and they activate CD4+ T-lymphocytes and to differentiate to cytokine producing T cells that help B cell differentiation and antibody production.

IL-1 is a major mediator in periodontitis. IL-1β comes mainly from activated macrophages and fibroblasts. IL-1α comes mainly from keratinocytes of the junctional or pocket epithelium. Production is induced by LPS, other bacterial components and by IL-1 which is autostimulatory. IL-1 upregulates complement Fc receptors on neutrophils and monocytic cells, and adhesion molecules on fibroblasts and leukocytes. It enhances production of MMPs and PGs by macrophages, fibroblasts and neutrophils. Finally, it upregulates major histocompatibility complex expression by B and T cells and facilitates their activation, expansion, and Ig production.

Scene 4. Regulation and resolution phase: determinants of protective components in the sulcus and collagen balance in the tissues.

This phase represents the initial loss of attachment. T-cells and macrophages are producing selective subsets of prostanoids and cytokines that favor net loss of collagen and bone and less effective antibody production. The inflammatory mediator load increases and includes contributions by the fibroblasts of interleukins (16, 8), PGE2, TNFa, collagen, MMPs and TIMPs. Plasma cells are prominent.

Topic:Review of Pathogenesis of Periodontal Disease          burst hypothesis             Article

Authors: Kinane D. et al

Title:Causation and pathogenesis of periodontal disease

Source:Periodontology 2000. 25:8-20,2001

Type:Review

Rating: Good                                                              ARTICLE

Keywords:Review, pathogenesis, periodontitis, gingivitis, microbiology

Purpose:To review the causation and pathogenesis of periodontal disease.

Discussion:

  • Gingivitis must precede periodontitis, however, not all gingivitis progresses to periodontitis. Periodontitis has subject and site predilection, is a continuous process that undergoes exacerbation periods (“burst hypothesis”).

  • Prevalence of periodontitis in the USA is 35% in adults (13% moderate to severe, 22% mild).

  • Even in clinically healthy gingiva neutrophils are found in the junctional epithelium, PMN’s are attracted to the area by bacterial products and epithelial cells proteins, but if they become overloaded, “degranulation” and tissue damage occurs from toxic enzymes.

  • Most individuals show signs of gingivitis 10-20 days after plaque accumulation

  • In gingivitis, capillary beds open, there is a transudate and influx of inflammatory cells (macrophages and neutrophils as phagocytic cells; lymphocytes as immune response-related cells).

  • Progression from gingivitis to periodontitis requires time, why some patients develop the periodontitis more readily than other is multifactorial including risk factors of particular bacterial species, age, socioeconomics and race, smoking, systemic disease, and genetics. Destructive processes are initiated by bacteria but propagated by host cells.

  • Microorganisms of normal flora are present in gingivitis while exogenous or usual anaerobic seem to be implicated in periodontitis.

                             The Classification of Kinane and Lindhe

Clinical condition

Histopathological condition

 Pristine gingiva

 Histological perfection (no inflammatory infiltrate)

 Normal healthy gingiva

 Initial lesion of Page and Schroeder (histologically has features of inflammatory infiltrate)

 Early gingivitis

 Early lesion of Page and Schroeder (lymphoid cells immediately below JE, loss of collagen)

 Established gingivitis

 Established lesion with no bone loss or apical epithelial migration

 Plasma cell density between 10-30% of leukocyte infiltrate

 Periodontitis

 Established lesion with bone loss and apical epithelial migration from the CEJ

 Plasma cell density > 50% (plasma cells predominance reflects bone loss)

Topic:Pathogenesis

Authors: DarveauRP et al

Title:The microbial challenge in periodontitis

Source:Periodontology 2000. 1997 Jun;14:12-32.

Type:Review

Rating: Good                                                              ARTICLE

Keywords:dental plaque, biofilm, P. gingivalis, calculus, plaque, innate host response

P: The article reviews the composition of dental plaque, the ability of the bacteria to develop strategies that help them survive in the oral environment and the host defense system that constantly monitors the bacterial colonization status and prevents bacterial invasion into the tissues.

D:

Biofilm: matrix-enclosed bacterial populations adherent to each other and/or to surfaces or interfaces.

Dental plaque formation: Microbial coating of a freshly cleaned tooth surface occurs rapidly. Two initial colonizers are Strep. GordoniiandA. naeslundii. Rapid colonization is favored by the ability of co-aggregation (two genetically distinct bacteria recognize and bind to each other; co-aggregation is based on the specific interaction of a proteinaceous adhesion produced by one bacterium and a respective carbohydrate or protein receptor found on the surface of another bacterium). Some bacteria can bind to each other without co-aggregation. Fusobacteriumspecies co-aggregate with all other oral bacteria, and thus play a major role to biofilm formation.

Dynamics of the dental plaque growth and host inhibition:

·     Dental plaque growth is favored by inter-species cooperation, GCF and biofilm formation (aqueous channels).

·     Host inhibition of supragingival plaque is mainly for the mechanical and anti-microbial properties of saliva. Subgingival plaque is inhibited by limited space and host innate defense system, which components are brought with the GCF.

·     Plaque doubling times are more rapid in early development and slower in more mature films.

·     Saliva:IgA, lactoferrin, lysozyme, peroxidase, antimicrobial proteins (histatins: antifungal and antibacterial activity)

·     GCF:contains nutrients for bacteria. However, also contains lysozyme, vascular permeability enhancers (bradykinin, thrombin, fibrinogen), antibodies, lymphocytes

Role of the dental plaque biofilm in periodontal disease:

·     Non-specific bacterial sheddingprobably represents the major mechanism by which the host is informed of the amount and type of bacterial colonization occurring on the biofilm.

·     Bacteria can have direct or indirect effects (indirect: bacteria activate one cell type which in turn activate another) on host cells.

·     Host cell response is grouped in myeloid (cytokine secretion) and non-myeloid (various inflammatory mediators).

·     The dental plaque biofilm microbial composition can influence innate host inflammatory surveillance. LPS is one of the most probable mechanisms by which the host can sense different biofilm bacteria. Biofilm composition may result in a destructive response.

·     The expression of bacterial virulence requires participation from the dental plaque biofilm. Host cell contact by pathogenic bacteria was shown to activate regions of the bacterial chromosome termed pathogenicity islands.

Potential role of P. gingivalis in periodontitis can be suppression of the innate host inflammatory response to bacteria.

LPS from this bacteria does not activate E-selectin, which would allow for vascular permeability of the endothelial cells for the PMNs to migrate and attack the bacteria.Pg has also shown to impair other bacteria from stimulation E-selectin expression. E-selectin can be activated indirectly by TNF-α and IL-β, however, PgLPS is a poor activator of these cytokines. This is in stark contrast to observations in clinical periodontitis of a large cellular inflammatory infiltrate and increased production of a variety of molecular mediators of inflammation.

·     A gradient of IL-8 expression exists in normal tissue to guide leukocytes to the site of bacterial colonization (in presence of P.g, epithelial cells lose their ability to secrete IL-8, rendering the host unable to locate the source of microbial colonization).

·     P.g is considered an opportunistic pathogen (may be a pathogen provided by the right combination of dental plaque).

·     Aa and Pg invade host cells, providing not only a source of potential re-infection after mechanical debridement, but also a more difficult situation for the host to recognize the bacterial challenge.

Biofilms and therapy:

·     Biofilms are notoriously resistant to surfactants and antibiotics as well as opsonization and complement –mediated phagocytosis and killing.

·     The release of membrane vesicles and cell wall fragments serve to protect bacteria in the biofilm by acting as decoys that bind innate host defense components.

·     The resistance of subgingival biofilms to normal host defenses has important consequences for the patient and for periodontal therapy. Physical removal is essential.

Microbial composition associated with different clinical states of periodontal health:

·     Gingival health: Mostly gram-positive, streptococci and actinomyces, with about 15% gram-negative rod species. Bacterial load is relatively low in gingival health. An individual is more likely to manifest gram-negative bacteria and perio pathogens in healthy sites with increasing age and periodontal disease history.

·     Gingivitis: Increased microbial load and a corresponding increase of gram-negative bacteria.

·     Periodontitis: Increased total microbial load. Elevated proportions of P.g. T.f. and A.a. Elevated counts of the red and orange complex bacteria. Those species will determine the host response.

Clonal analysis has provided new insights into transmission and pathogenesis:

·     Molecular epidemiological tools have identified more intraspecies variation than previously thought (restriction endonucleases analysis, restriction fragment length polymorphism, ribotyping).

·     Transmission of periodontal bacteria occurs more likely through intimate contact, mostly within the family but not within general population communities (school, work environment)

·     Clonal type analysis is being used to determine the presence of different clonal types. Various clonal types of the same bacteria can be found within the same host. Very limited number of clonal types have been identified due to the magnitude of samples necessary to prove clonality.

·     The virulence of numerous clonal types is not clear.

Topic:pathogenesis of perio disease

Authors: Page R, Offenbacher S,

Title:Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions

Source:Periodontol 2000. 1997 Jun;14:216-48

Type:review

Rating: good                                                              ARTICLE

Keywords:periodontal pathogenesis, immune system, periodontitis

Purpose:To present the basic concepts and facts about pathogenesis of human periodontitis based on literature.

Discussion:

  • Periodontitis is a family of diseases that differ in etiology but have a common underlying chain of events. The severity and rate of progression of disease feedback to influence the nature and magnitude of the microbial challenge. Many modifying influences may affect the onset and progression of disease or the response to various kinds of therapy. These influences may last for life, or vary in magnitude of effect at different times.

  • Bacteria are essential but insufficient to cause disease, host factors are equally important. A.a. produces different clinical disease patterns in different people. This appear to be determined by combinations of factors like genetics and smoking.

  • P. gingivalis, A.a. and B. Forsythus cause most cases of periodontitis except for acute necrotizing periodontitis (ANP).

  • Subgingival microbial plaque behaves as biofilm. The behavior of the bacteria (mainly gram -) in it is different. They resist the host defense and also antibiotics. Physical disruption and removal are effective ways of dealing with biofilms.

  • Periodontitis enhances the risk for various systemic diseases, including atherosclerosis, coronary heart disease, stroke and infants with low birth weight.

  • Studies have shown that periodontopathic bacteria can be transmitted among individuals living in close contact.

  • P. gingivalis is special in that its lipopolysaccharide does not activate the expression of E-selectin in vascular endothelial cells (which then triggers binding of leukocytes) therefore blocking the local neutrophil response to itself and other microorganisms in the plaque.

  • The disease process is characterized by destructive periods followed by periods where this process subsides. There is experimented evidence that the responses in periodontal disease behave as if they occurred in a close system and many different balances can occur inside it through the biofilm/host interaction.

  • As the microbial challenge increases clinical signs of inflammation in the gingival margin begin. The junctional epithelium plays a key role, initiating vascular endothelial responses and neutrophils migrate to the sulcus. Macrophages, lymphocytes and plasma cells are the majority of cells in the tissues. If the bacteria are not eliminated inflammation worsens and connective tissue and bone are destroyed. In this procedure host cells, for example fibroblasts or epithelial cells, can be activated to produce prostaglandin E2and matrix metalloproteinases resulting in destruction of the components of the extracellular matrix. These cause apical extension of the epithelium and pocket formation. Rete pegs of junctional epithelium to the connective tissue are also formatted.

  • The stages of periodontitis according to its pathogenesis are initial, early, established and advanced lesions.

  • Several studies agree to the conclusion that bone absorption is observed in a 2.5mm range around bacteria, but Schroeder pointed out lesions much greater than 2.5mm around single teeth.

  • Thesusceptibility to periodontal disease differs between patients as some of them may only develop gingivitis whereas others with the same pathogens and comparable amounts of plaque may proceed to periodontitis, depending on several factors as the host’s response.

  • Cytokines belong to a large protein family that comprises the major regulators of the immunoinflammatory response in periodontitis. Interleukins and chemokines are subfamilies of the cytokines, while interferon – and TGF-also belong to the cytokines.

  • Both Th1 and Th2 clones of T helper cells can be met in periodontal lesions. The first one produces mostly interferon-γ and the second IL-6, IL-7 and IL-8. Whether any of these clones is associated with a specific clinical status is not yet clear.

  • Prostaglandins and leukotrienes are major initiators of inflammation and PGE2is the major mediator of pathological alveolar bone destruction. The progress of the disease is not on dimensional or unidirectional. It is constantly being adjusted as a result of multiple and changing microbial challenges and multiple local and systemic host defenses. Clinically periods of quiescence are followed by bursts of destructive disease activity. The mechanisms that force the transition from one condition to the other are not completely known. Bone absorption is a result of uncoupling the tightly coupled process of bone resorption and bone formation, and more significant after 25-30 years of age.

  • Periodontitis is a multifactorial disease. Bacteria are essential but insufficient to cause it. Several hereditary, host and other risk factors (such as diabetes mellitus, smoking, stress, HIV infection, socioeconomic factors, oral hygiene) coexist and modify the severity and type of the disease. Except for diabetes it is associated with major systemic diseases, such as cardiovascular disease and pre-term low birth weight delivery. Genetics has been shown to influence early onset periodontitis and adult forms. This influence is mediated through polymorphisms in the genes responsible for producing factors important in the pathogenesis of periodontitis (IL-1, IgG2m TNF-).

Describe Page & Schroeder’s model in detail.

Topic:Pathogenesis

Author:Page R., Schroeder H.

Title:Pathogenesis of Inflammatory Periodontal Disease: A Summary of Current Work

Source:Lab. Invest. 34:235-249, 1976

Type:Review

Rating: Good                                                              ARTICLE

Keywords:Gingivitis, Periodontitis, Chronic inflammation, Microbial plaque

Purpose: to discuss and review the current ant historic literature about the pathogenesis of periodontal disease

Discussion:Bacterial substances in plaque comprise the primary etiologic agent in gingivitis and periodontitis; however, many significant features of the disease cannot be accounted by this factor alone. There is a new belief that intrinsic host-related factors play an important role in the destructive process.

Historic Perspective

In the 18th and 19th centuries clinical observation was the predominant method used to understand the pathogenesis of the inflammatory periodontal lesion. In the late 19th century, there was a period of structural and morphologic analysis that began to examine the microscopic structures. During the past decade, the increased power of the electron microscope has provided additional insight into many of the cellular aspects and ultrastructural alterations.

Early concepts of pathogenesis

Gothieb (1946) presented the concept of “cementopathia”. He hypothesized that interference with continuous cementum deposits result in a lack of attachment of the collagen fibers of the gingiva and PDL. Goldman postulated an initial degenerative change in these fiber followed by epithelial cell proliferation and migration. Aisenberg (1948) showed that epithelial cells migrate apically between presumably normal connective tissue bundles. Cohen (1958), expressed the idea that the periodontal lesion may begin as a failure of the oral epithelium to replace the reduced enamel epithelium in the interproximal areas. James and Counsell (1927), and Fish (1935), introduced the zone of injury: Inflammatory cells accumulate in the JE and CT at the base of the sulcus. The zone of injury is located just coronal to the apical termination of the junctional epithelium.

Current view: the Page and Schroeder model.

Initial lesion (2-4 Days):

Lesion is localized to the gingival sulcus. The JE and most coronal portion of the CT are involved.

  1. Classic vasculitis of vessels subjacent to the JE

  2. Exudation of fluid from the gingival sulcus

  3. Increased migration of leukocytes (PMNs mainly) into the JE and gingival sulcus

  4. Presence of serum proteins, especially fibrin, extravascularly

  5. Alteration of the most coronal portion of the JE

  6. Portion of perivascular collagen disappears, and the resultant space is occupied by fluid, serum proteins (especially fibrin) and inflammatory cells.

Early Lesion (4-7 days):

  1. Presence and accentuation of the features described for the initial lesion (no clear cut dividing line).

  2. Accumulation of lymphoid cells immediately subjacent to junctional epithelium at the site of acute inflammation

  3. Cytopathic alterations in resident fibroblasts possibly associated with interactions with lymphoid cells.

  4. Further loss of collagen fiber network supporting the marginal gingiva. (Collagen loss may reach 60-70% within the reaction site)

  5. Beginning proliferation of the basal cells of the junctional epithelium

Established Lesion (2-3 weeks):

  1. Persistence of the manifestations of acute inflammation

  2. Predominance of plasma cells but without appreciable bone loss

  3. Presence of immunoglobulins extravascularly in the CT and JE

  4. Continuing loss of CT substance noted in the early lesion

  5. Proliferation, apical migration, and lateral extension of the junctional epithelium. Early pocket formation may or may not be present.

Advanced Lesion:

  1. Persistence of features described for the established lesion

  2. Extension of the lesion into alveolar bone and PDL with significant bone loss

  3. Continued loss of collagen subjacent to the pocket epithelium with fibrosis at more distant sites

  4. Altered plasma cells in the absence of altered fibroblasts

  5. Read More ›

45. Diagnosis /Indices – Radiographic Interpretation

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Are Radiographs an accurate method of diagnosing periodontal disease?

  1. HardekopfJ, et al. The “furcation arrow” – A reliable radiographic image? J Periodontol. 58:258 – 261, 1986.

  2. DeasDE, Moritz A., Mealey B et al: Clinical reliability of the furcation arrow as a diagnositc marker. J Periodontol 2006;77;1436-1441

  3. OrtmanL, McHenry K, Hausmann E: Relationship between alveolar bone measured by 1251 absorptiometry with abalsysis of standardized radiographs: 2. Bjorn technique: J Periodntol 1982;53:311-314

  4. BuchananSA, et al: Radiographic detection of dental calculus. J Periodontol. 58:747-751, 1987.

What alveolar crest level represents bone loss on a bitewing radiograph??

  1. HausmanE., Allen K., Clerehugh V. What alveolar crest level on a bite wing radiograph represents bone loss? J Periodontol 1991;62;570-572

Are digital radiographs equivalent to conventional radiographs in revealing bone loss?

  1. KhochtA, Janal M, Harasty L, Chang K: Comparison of direct digital and conventioanl intraoral radiographs in detecting alveolar bone loss. J Am Dent Assoc 2003;134;1468-1475

  2. BruderG, Casale J, Goren, A, Friedman S; Alteration of computer dental radiography images J Endod 1999;25;275-276

Are panoramic radiographs ever of value in periodontics?

  1. KasajA, Vasiliu Ch, Willershausen B. Assessment of alveolar bone loss and angular bony defects on panoramic radiographs. Eur J Med Res. 2008 Jan 23;13(1):26-30.

  2. PerssonRE, Tzannetou S, Feloutzis AG, Brägger U, Persson GR, Lang NP. Comparison between panoramic and intra-oral radiographs for the assessment of alveolar bone levels in a periodontal maintenance population. J Clin Periodontol. 2003 Sep;30(9):833-9.

When should cone beam computed tomography (CBCT) be used?

  1. The American Dental Association Council on Scientific Affairs. The use of cone beam computed tomography in dentistry: An advisory statement from the American Dental Association Council on Scientific Affairs. J Am Dent Assoc 2012;143;899-902

  2. MischKA, Yi ES, Sarment DP: Accuracy of cone beam computed tomography for periodontal defect measurements.. J Periodontol. 2006 Jul;77(7):1261-6.

  3. VandenbergheB, Jacobs R, Yang J. Detection of periodontal bone loss using digital intraoral and cone beam computed tomography images: an in vitro assessment of bony and/or infrabony defects. Dentomaxillofac Radiol. 2008 Jul;37(5):252-60.

What if the significance of the lamina dura?

  1. TibbettsJ, Allen K, Hausmann E: Effect of x-ray angulation on radiographic periodontal ligament space width. J Periodontol 63: 114-117, 1992

  2. GreensteinG, Polson A, et al: Associations between crestal lamina dura and periodontal status. J. Periodontol. 52:362-366, 1981.

Can radiographs be used to detect progression of periodontitis?

  1. SelikowitzH-S, et al: Retrospective longitudinal study of the rate of alveolar bone loss in humans using bite-wing radiographs. J. Clin. Periodontol. 8:431-438,1981.

Are radiographs an accurate way to assess healing after periodontal surgery?   Do newer radiographic techniques improve the usefulness of radiographs?

  1. TobackGA, Brunsvold MA, et al. The accuracy of radiographic methods in assessing the outcome of periodontal regenerative therapy. J Periodont 70:1479-1489,1999.

  2. ZybutzM, Rapoport D, Laurell L, Persson GR. Comparisons of clinical and radiographicmeasurements of inter-proximal vertical defects before and 1 year after surgical treatments. J Clin Periodontol 27:179-186, 2000.

  3. GrimardBA, Hoidal MJ, Mills MP, Mellonig JT, Nummikoski PV, Mealey BL. Comparison of clinical, periapical radiograph, and cone-beam volume tomography measurement techniques for assessing bone level changes following regenerative periodontal therapy. J Periodontol. 2009 Jan;80(1):48-55.

  4. GorenAD, Dunn SM, Wolff M, van der Stelt PF, Colosi DC, Golub LM. Pilot study: digital subtraction radiography as a tool to assess alveolar bone changes in periodontitis patients under treatment with subantimicrobial doses of doxycycline. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008; Oct;106(4):e40-5. Epub 2008 Aug 20.

How do Radiographic Measurements Compare to Clinical Examination Measurements?

  1. PapapanouPN, Wennstrom JL: Radiographic and clinical assessments of destructive periodontal disease. J Clin Periodontol.16:609-612, 1989.

  2. MachteiEE, Hausmann E, Grossi SG, Dunford R, Genco RJ. The relationship and clinical changes in the periodontium. J Perio Res 32:661-666, 1997.

  3. EickholzP, Hausmann E. Accuracy of radiographic assessment of interproximal bone loss in intrabony defects using linear measurements. Euro J Oral Sci 108:70-73, 2000.

  4. PilgramTK, Hildebolt CF, et al. Relationships between radiographic alveolar bone height and probing attachment level: data from healthy post-menopausal women. J Clin Perio 27:341-346, 2000.

Comparison of Techniques

  1. ReedBE, Polson AM : Relationships between bitewing and periapical radiographs in assessing crestal alveolar bone levels. J. Periodontol. 55:22-27, 1984.

Reviews

  1. BennDK. A review of the reliability of radiographic measurements in estimating alveolar bone changes. J. Clin. Periodontol. 17:14-21, 1990. (Review)

  2. JeffcoatMK. Radiographic methods for the detection of progressive alveolar bone loss. J Periodontol 63: (Suppl 4) 367-372, 1992. (Review)

  3. TugnaitA, Clerehugh V, Hirschmann PN. The usefulness of radiographs in diagnosis and management of periodontal diseases: a review. J Dent 28:219-226, 2000. (Review)

  4. KimIH, Mupparapu M.Dental radiographic guidelines: a review.Quintessence Int. 2009 May;40(5):389-98. Review

Are Radiographs an accurate method of diagnosing periodontal disease?

Topic:Furcation Arrow

Authors:Hardekopf J, et al.                               ARTICLE

Title:The “furcation arrow” – A reliable radiographic image?

Source:J.Periodontol.58:258-261,1986.
Type: Clinical study

Rating: Good

Keywords:Furcation Arrow, Radiograph

Furcation Arrow:Small triangular shadow across the mesial or distal roots of maxillary molars. Indicates class II or class III involvement.

P: To determine whether there is a consistent relationship between furcation arrows on radiographs and proximal bony furcation involvement in maxillary molars.

M&M: 45 adult human skulls with proximal furcation involvement in maxillary 1st or 2nd molars were used. 66 Degree 1, 53 Degree 2, 43 Degree 3 proximal furcation involvements. An additional 120 proximal furcations without bony involvement served as controls. Furcation classifications were determined independently by two examiners. Each maxillary molar was radiographed radiographed. Film placement was standardized to minimize interproximal overlap and to position the film lingually/palatally on a plane that paralleled the buccal surfaces of the teeth radiographed. Evaluations for the presence of the furcation arrow were made independently by 6 dentists as the radiographs were projected onto a screen. Projected radiographs with identifiable “arrow” images were used.

R: Incidence of furcation arrow image over degree 2 and 3 involvements was significantly greater than that observed over the uninvolved controls. The incidence of the furcation arrow image over the 120 uninvolved proximal furcations was low (18% for mesial and 7% for distal furcations). There was NSD between degree 1 involvement and the controls in the incidence of the furcation arrow image. There was an equal number of furcation arrows observed over mesial and distal furcations. The existence of a buccal furcation involvement of any degree did not influence the appearance of the furcation arrow. The image was no more likely to be observed over Degree 3 involvement than over Degree 2 involvement.

D: As the extent of furcation involvement increased, so did furcation arrow image.  Degree 3 involvement reflected the radiographic image > 50% of the time. The furcation arrow seldom appears over uninvolved furcations, its appearance indicates that there is proximal bony furcation involvement. Absence of arrow does not indicate the absence of a bony furcation involvement.  Root morphology and horizontal angulation of the tube head may be factors in determining whether a given furcation defect will exhibit an arrow.    

BL: The radiographic presence of the furcation arrow appears to be a reliable diagnostic tool for the clinician when evaluating bony furcation involvement.

Topic:Furcations

Authors: Deas DE, Moritz A., Mealey B                               NO ARTICLE

Title:Clinical reliability of the furcation arrow as a diagnositc marker.

Source: J Periodontol 2006;77;1436-1441

Type:Clinical study

Rating: Good

Keywords:Furcation involvement, periapical, bitewings

B:Traditionally, radiographic assessment in conjunction with clinical probing using a curved explorer or furcation probe has been the chief diagnostic methods used for detecting and characterizing furcation involvement.

P:To evaluate the furcation arrow in a clinical setting, with emphasis on testing the assertion that the radiographic presence of a furcation arrow reliably identifies a furcation invasion.

Questions answered: 1. What is the prevalence of furcation arrow images in the radiographs of maxillary molars with periodontitis? 2. What is the interexaminer agreement on what constitutes a furcation arrow? 3. How does the presence or absence of a furcation arrow correlate with the true clinical status of the furcation? 4. What is the sensitivity and specificity of the furcation arrow as a diagnostic indicator?

M&M:89 patients were referred between February 2004-June 2005 for treatment of moderate to advanced periodontitis that required surgical access to at least one maxillary posterior sextant. Before surgery, one of five calibrated examiners viewed PA and BW radiographs of the surgical site and recorded the presence or absence of a furcation arrow at each proximal furcation. Before administering anesthesia, the same examiner recorded a Hamp index value of each proximal furcation. After flap reflection and debridement, the examiner recorded a second Hamp index at each proximal furcation. After surgery, each of the four remaining examiners independently reviewed the radiographs for furcation arrows. Descriptive statistical analysis was performed to correlate the appearance of the furcation arrow image to the actual degree of furcation invasion as determined by the intrasurgical Hamp index.

R:

  • 164 maxillary molars were examined, providing 328 interproximal furcations

  • 111/328 (33.8%) furcations were determined at surgical debridement to have a furcation invasion of Hamp degree of 1 or greater.

  • When comparing the appearance of the radiographic image to the extent of furcation invasion, 20/64 (31.3%) Hamp 1 furcation invasions and23/47 (48.9%) Hamp 2 and 3 furcation invasions were predicted by furcation arrows observed by at least three of five examiners.

  • The multirater k statistic for interexaminer agreement on the presence or absence of the image was 0.489 (low)

  • The sensitivity of the furcation arrow image as a diagnostic marker was 38.7%, and the specificity was 92.2%  Most actual furcation invasions were not associated with a furcation arrow: a high number of false negatives. The absence of a furcation arrow had a much higher likelihood of not having an accompanying furcation invasion present: a low number of false positives.

  • The positive predictive value of the image was 71.7%, and the negative predictive value was 74.6%.

  • Of the 324 furcations used to compare clinical indices, the agreement of pre-anesthesia and post-debridement Hamp indices was 0% for degree 3, 83.7% for degree 2, and 98.4% for degree 1 furcation lesions.

C:Clinical probing, post-anesthetic sounding and surgical access provide more diagnostic data about furcations than the radiographs to the clinicians. The image is difficult to interpret and highly subjective and can correctly predict furcation invasions only 70% of the time when present on the radiograph. In addition, when furcation invasions are truly present, the furcation arrow is seen in <40% of sites.

Topic:standardized radiographs

Authors: Ortman L, McHenry K, Hausmann E                              NO ARTICLE

Title:Relationship between alveolar bone measured by 1251 absorptiometry with analysis of standardized radiographs: 2. Bjorn technique

Source:J Periodntol 1982;53:311-314

Type:Skull study

Rating:Fair

Keywords:standardized radiographs, Bjorn technique

B:Bjorn developed a bone scoring technique using the projected 5x magnification of periapical radiographs on a scale which divides the tooth into 5% portions.

P:To compare the Bjorn and Henrikson (125I absorptiometry) techniques in their ability to detect small bone changes.

Omnell demonstrated that established principles of radiation absorptiometry permitted measurement of alveolar bone mineral mass. Henrikson applied these principles to development of an 125I absorptiometry technique capable of detecting alveolar bone mass changes on the order of 5%. The technique utilizes an essentially monoenergetic radiation beam, a collimating device and a scintillation counter for directly determining the amount of absorbed radiation.

M&M: 4 periodontal defects were created in dried human skulls between 1stand 2nd PM and 1st M of differing sizes, with incremental reduction of approximately 10%. The defects were made either by reducing the buccal wall or creating crater like defects and were measured using both of the techniques utilizing stents for standardization.

R:In initial bone loss, the Bjorn technique consistently underestimated the amount. 53% of the bone as measured by 125I absorptiometry needed to be reduced before the Bjorn technique could detect any loss. In advanced bone loss, the Bjorn technique was shown to overestimate the amount of loss in 2 of the sites and underestimate in the two other sites.

Conclusion:When bone loss is under 30%, the Bjorn technique tends to underestimate how much true loss has occurred and when over 60%, it is inconsistent.

Topic:Radiography

Authors: Buchanan SA, et al                               ARTICLE

Title:Radiographic detection of dental calculus.

Source:J Periodontol. 58:747-751, 1987

Type:Clinical

Rating: Good

Keywords:calculus, radiographs, sensitivity, specificity.

P:To quantify the sensitivity, specificity and observer error associated with radiographic detection of dental calculus on proximal surfaces of teeth in patients with severe periodontitis.

M&M:18 patients that required extraction of at least 3 teeth because of severe periodontitis participated in the study. Excessively rotated or malpositioned teeth were not included in the study. Radiographic presence of calculus was determined by two examiners. After tooth extractions teeth were prepared and examined microscopically for calculus.

R:275 proximal tooth surfaces and the corresponding radiographs were available for evaluation. Mean AL was 5.8mm.

Of the 153 surfaces with calculus noted visually, radiographically calculus was detected 43.8% (false negative 56.2%), (low sensitivity).

Of the 73 surfaces with calculus present radiographically, 91.8% were determined calculus present clinically.

Of the 160 surfaces assessed radiographically as calculus absent, 46.3% were verified by visual examination to have no calculus.

Radiographic evaluation of calculus was not an effective diagnostic method in most surfaces with thin or moderate deposits.

C:Conventional radiographs are a poor diagnostic method for detection of calculus. Radiographic analysis predicted calculus on less than half of the proximal surfaces where deposits were present visually.

Whatalveolar crest level represents bone loss on a bitewing radiograph??

Topic:Radiographic measurement of bone

Author: Hausman E., Allen K., Clerehugh V.                                ARTICLE

Title: What alveolar crest level on a bite wing radiograph represents bone loss?

Source: J Periodontol 1991;62;570-572

Type:RCT

Rating:Good

Keywords:bone level, radiographic interpretation

P: Compute the distance from the CEJ to the alveolar crest on radiographs at sites where there was no clinical loss of attachment.

M&M:

  • Bitewing radiographs were taken on 68 pts (13-14 years old). A second set of radiographs were taken 18 months later.

  • The radiographs were taken using a routine unstandardized clinical technique and were processed under standardized conditions using a Refrema processing machine.

  • At each radiographic examination probing attachment level measurements were made at the mesio-buccal surfaces of the first molar teeth. Only the sites with zero attachment loss (attachment at the level of the CEJ) at both baseline and at 18 months were included in this study. A total of 134 sites included in the study.

  • A computer program was developed to measure the CEJ-crest distance (mm) in a line parallel to the long axis of the tooth.

R: The mean radiographic CEJ- alveolar crest distance (mm) for the 134 sites with zero loss of clinical attachment was 1.11 ±0.37 mm. at the initial examination and 1.19 ±0.34 mm at the same sites examined 18 months later . The 95% confidence limits were 0.4 mm to 1.9 mm.

BL: No crestal bone loss is consistent with a range of CEJ- alveolar bone crest distance between 0.4 and 1.9 mm as evidenced on bitewing radiographs.

Are digital radiographs equivalent to conventional radiographs in revealing bone loss?

Topic:Radiographic Interpretation

Authors: Khocht A, Janal M, Harasty L, Chang K:                               ARTICLE

Title: Comparison of direct digital and conventioanl intraoral radiographs in detecting alveolar bone loss.

Source: J Am Dent Assoc 2003;134;1468-1475

Type:Clinical Study

Rating: Good

Keywords:conventional radiographs, digital radiographs

P: To compare direct digital (D) and conventional (C) radiographic estimates of alveolar bone under normal clinical use.

M&M:25 subjects with perio with age range b/w 18-65 years and had full set of PAs and BW for diagnostic purpose and tx planning. All subject had min of 15 teeth without any intraoral pathology or systemic dz. A long cone parallel technique was used to take PAs and a paper sleeve with biting tab was used for BW. Within 4 weeks, a second set PAs and BW was taken with digital system (Shick). The distance from the CEJ (surfaces with non-identifiable CEJs due to restorations or overlapping were excluded) to the interproximal alveolar crest (where the PDL space ends on the root surface) was measured. 3rd molars were excluded. One examiner measured with a plastic ruler on the C x-rays while another examiner measured the D x-rays. Overall % agreement of first and second readings in C x-rays was 99 and it was 92 for the D images. The examiners performed their measurements independently from each other. Each examiner measured the conventional or digital radiographs twice and took two sets of measurements for each subject. The examiners took the second set of measurements without having access to the initial set.

R: Examiner measured 857 PAs and 315 BW image sites match on both radiographic systems.

  • Measurements in the D images for BW averaged about 0.3mm greater bone loss than did C x-rays.

  • For BW, the difference between C x-rays and D was not found in all mouth sextants.

  • Rather,more bone loss was indicated by D x-rays only in the posterior mand region (BW); measures in the posterior maxillary region were similar between the two methods.

  • Measurements from C PA images showed more bone loss in all max sextants.

  • Categorical bone levels (normal<3 mm, early-to-moderate loss 4-6mm and advanced loss>7mm) were assigned to evaluate how each rx method revealed bone level and loss. Agreement between D and C x-rays in revealing bone levels as normal or having early-to-moderate loss was low (D x-rays revealed more early-to-moderate sites).

It seems that digital radiographs impart a constant addition of millimeters to measures taken in the posterior mandibular.

C:  Under normal clinical use and without standardized film positioning, the average bone level measurements varied SS between C and D radiographs in certain regions of the mouth and that the disagreement between these two systems is influenced by the type of image PA or BW as well.

Cr: It is very difficult to take x-rays at the exact same angle with the sensor/film in the exact same place to compare measurements. Also, there may be error in calculating exactly where the CEJ is on the x-ray. The digital sensor is a different size, not flexible, and can be more difficult to position than conventional films. Having the USB cord attached to the digital sensor may interfere with subjects biting down on the BW tabs.

Topic:radiographic alterations

Authors: BruderG, Casale J, Goren, A, Friedman S                               NO ARTICLE

Title:Alteration of computer dental radiography images

Source:J Endod ;25;275-276 DOI: 10.1016/S0099-2399(99)80159-9

Rating: good

Keywords:radiography, distortion, digital images, alterations

P:to determine if digital images could be exported, altered, and then restored without visible signs of alteration

M&M:Images were exported from the computer radiography program, files were altered, then files were restored to the Schick format and printed

D:Digital images are relatively easy to export and alter with the use of a photo editing program. The need to implement technologies to safeguard digital radiography must be addressed to prevent potential abuses.

Are panoramic radiographs ever of value in periodontics?

Topic:Radiographs

Author: Kasaj A., Vasiliu Ch, et al.                               ARTICLE

Title:Assessment of alveolar bone loss and angular bony defects on panoramic radiographs

Source:Eur J Med Res. 2008 Jan 23;13(1):26-30

Type:Prospective study

Rating: Good

Keywords:Panoramic radiographs, angular bony defects, periodontal disease, bone loss

P: To investigate the prevalence and severity of alveolar bone loss and angular bony defects in randomly selected panoramic radiographs.

M&M: 500 panoramic radiographs of adult patients were studied. The mean age of the subjects was 51 years (range 20-80). Panoramic radiographs were placed on an x-ray viewer and evaluated by the same examiner. A calibrated periodontal probe was used to assess horizontal and vertical defects. If the interproximal projection of the CEJ was not identifiable, the apical termination of the restoration or crown margin was used for the measurements. A site was considered as having an angular bony defect if the bottom of the oblique radiolucency was located at least 2mm apical to the most coronal level of the interproximal alveolar bone.

R:

-In majority of subjects (86.7%) had some form of bone loss (horizontal and vertical).

–Angular bony defects were found in 49.8 % of the patients.

-Angular defects were more present in the mandible than in the maxilla, most frequently in the mandibular posterior, and least frequently in the mandibular anterior.

-The mean depth of the angular bony defects was 6.0 mm with the greatest mean depth in the maxillary anterior area (6.8 mm).

-The mean M-D width of the intrabony defects was 2.44 mm, and was most pronounced in maxillary molars (3.1 mm).

-Female subjects exhibited a gradual increase of vertical defect with age whereas in male subjects vertical bone loss was most prevalent in the age group 40-60 years and decreased in the older age group (60% vs. 40%).

-Interradicular molar radiolucencies demonstrated 38.3 % of the subjects and were more frequent in the md (first molar) than mx.

C: This study demonstrated a high prevalence of angular bony defects found on panoramic radiographs suitable for regenerative periodontal treatment.

Topic:Radiography

Authors: Persson RE, Tzannetou S, Feloutzis AG, Brägger U, Persson GR, Lang NP                               NO ARTICLE

Title:Comparison between panoramic and intra-oral radiographs for the assessment of alveolar bone levels in a periodontal maintenance population

Source:J Clin Periodontol. 2003. 30(9):833-9

Type:Clinical study

Rating: Good

Keywords:orthopantomogram; radiographs; alveolar bone level; diagnosis; periodontitis; maintenance population; agreement

P:To assess the level of agreement between intraoral and panoramic radiograph for direct measurements of the distance between the CEJ and the alveolar bone level (BL) as well as the proportional relationship (CEJ-BL/root length) and to explore the symmetry between left and right sided measurements.

M&M: Intraoral (IO) and panoramic (OPG) images were obtained from 292 patients on maintenance therapy. Two examiners performed measurements on digitally processed images. The distance between the CEJ and marginal BL was measured at the mesial and distal aspects of each tooth. The distance between the CEJ and apex of the tooth was also measured. The proportional distance between CEJ and BL relative to the length of the root was calculated.

R:All measurements between the two examiners showed no statistically significant differences. The largest mean proportional difference between CEJ and BL was seen in the maxillary right posterior segment, suggesting advanced periodontal disease in these sites. The largest difference between IO and OPG reading was observed between measurements for the maxillary anterior sextant, while the smallest difference was seen in the mandibular anterior sextant.

C: The study suggests that BL measurements between IO and OPG radiographs are highly comparable. The mean differences observed for the distance CEJ-BL in proportion to root length were neither statistically nor clinically different. A significant degree of symmetry of alveolar bone loss between the left and right side of the dentition was also found.

When should cone beam computed tomography (CBCT) be used?

Topic:CBCT in dentistry

Authors: The American Dental Association Council on Scientific Affairs.                               NO ARTICLE

Title:The use of cone beam computed tomography in dentistry: An advisory statement from the American Dental Association Council on

Scientific Affairs.

Source:J Am Dent Assoc 2012;143;899-902
Type:Discussion

Rating: Good

Keywords:CBCT, ALARA

ADA Council on scientific affairs 2012: The use of CBCT in dentistry

CBCT imaging provides three-dimensional volumetric data construction of dental and associated maxillofacial structures with isotropic resolution and high dimensional accuracy.

A CBCT scanner uses a collimated x-ray source that produces a cone- or pyramid-shaped beam of x- radiation, which makes a single full or partial circular revolution around the patient, producing a sequence of discrete planar projection images using a digital detector. These two-dimensional images are reconstructed into a three-dimensional volume that can be viewed in a variety of ways, including cross-sectional images and volume renderings of the oral anatomy.

Although CBCT units produce a higher radiation dose than one would receive from a single traditional dental radiograph, the radiation dose delivered typically is less than that produced during a medical multichannel computed tomographic scan. CBCT radiation doses also vary widely according to the device used, x-ray energy and filtration, tolerance for image noise and motion artifacts and the size of the imaging area that is used to acquire volumetric data.

Principles for the safe use of dental and maxillofacial CBCT

– Should be used only after review of pt’s health, and imaging history and thorough clinical examination

– Should be used only after professional justification that the potential clinical benefits will outweigh the risks associated with exposure to ionizing radiation

-The clinician should prescribe traditional dental radiographs and CBCT scans only when he or she expects that the diagnostic yield will benefit patient care, enhance patient safety, sig- nificantly improve clinical outcomes or all of these.

-Should be considered as an adjunct to standard oral imaging modalities

– ALARA(As-low-as-reasonably-achievable) principle

– Should take every precaution to reduce radiation dose and ensure the patient’s safety. The use of thyroid collars and lead aprons is recommended when they do not interfere with the examination.

– Regardless of the primary purpose for the selection of CBCT, the complete image data set must be interpreted by a qualified health care provider. The prescribing clinician should receive a thorough radiological report

– Dental practitioners who use CBCT devices must receive appropriate training and education in the safe use of CBCT imaging systems

– Facilities using CBCT systems should consult a health physicist to perform equipment performance and compliance evaluations initially at installation and then follow a schedule in compliance with local, state and federal requirements

– Staffs of facilities using CBCT should establish a quality control program. This program can be based on the manufacturer’s recommendations

Topic:Radiograph

Authors: Misch KA, Yi ES, Sarment DP:.                                ARTICLE

Title: Accuracy of cone beam computed tomography for periodontal defect measurements.

Source: J Periodontol. 2006 Jul;77(7):1261-6.

Type: Clinical study

Rating: Good

Keywords:Periodontal defect, CBCT

P:To compare linear measurements of periodontal defects using CBCT to traditional methods.

M&M: 2 human dry cadaver skulls with existing horizontal bone loss up to 20% were examined. Infrabony buccal, lingual, and interproximal defects with varying width and height were created with a bur in mandibular molar and premolar regions. Grooves were also placed vertically into the roots from the CEJ to the depth of defect. Gutta percha cones were superglued into the grooves. CBCT (i-cat) and PA radiographs were taken.

Measurements were taken from A) CEJ-depth of pocket, B) CEJ to alveolar crest, C) width of the defect. Impressions of the defects were taken, and all measurements were compared to electronic caliper measurements. The accuracy of impression and caliper measurements were verified using another set of defects with known height and width prepared in cast acrylic blocks. Statistical analysis was done.

R:

All infrabony defects were detected using CBCT and the probe.

Average correlation was 0.4 for direct, 0.53 for PA, 0.62 for CBCT and 0.95 for impressions.

Correlation varied b/w 0.09 and 0.99 within examiners.

NSSD between all the methods for CEJ-depth of pocket, detection of isolated IP defects, and for buccal and lingual defects.

C: CBCT measurements compared well to traditional methods, with the advantage of allowing observation of defects in all directions. Further investigation is needed.

Topic:CBCT vs intraoral radiographs

Authors:Vandenberghe B, Jacobs R, Yang J.                               ARTICLE

Title:Detection of periodontal bone loss using digital intraoral and cone beam computed tomography images: an in vitro assessment of bony and/or infrabony defects.

Source:Dentomaxillofac Radiol. 2008 Jul;37(5):252-60.

Type:Skull study

Rating:Good

Keywords:periodontium, crater, furcation involvement, intraoral radiography, cone beam computed tomography

P: To determine the diagnostic values of digital intraoral radiographs and cone beam CT (CBCT) in the determining bone loss, infrabony defects, and furcation involvement.
M&M: A cadaver head with upper and lower jaws fixed with 10% formalin and a dry skull covered with a soft tissue substitute were used to measure 71 selected periodontal defects. To assess bone levels, the CEJ was used as a reference point for the fixed jaws, and gutta-percha fixated onto the buccal and lingual of teeth for the dry skulls. Intraoral radiographs were obtained with standardized bite blocks. CBCT was obtained with I-CAT. For the CBCT the observation were made on a 5.2 mm panoramic reconstruction view and on .4mm thick cross-sectional slices. First part of the study: 43 randomly selected sites with linear or vertical defects were chosen for radiographic and CBCT assessment of the bone loss and compared to the actual measurements. Second part of the study, 11 teeth containing vertical defects or furcation involvement was compared to actual measurements. The defects were categorized by 1, 2, 3 and 4 walls and the furcations by class 1, 2,3. Readings were performed by 3 examiners a medical imaging master and PhD student, and two radiology faculty members.

R: No intra- or interobserver effect was found. No significant differences were found when comparing the radiographs with those on the panoramic reconstruction image of the CBCT. The mean error for bone level measurements was 0.56 mm for radiographs, 0.47 mm for the CBCT panoramic view and 0.29 mm for the .4mm thick cross-sectional slices.SSD between the cross sectional slices and the radiographs. The detection of crater and furcation failed 29% and 44% with radiographs, and 0% with CBCT.

C: CBCT allowed more accurate assessment of periodontal bone loss.

What if the significance of the lamina dura?

Topic:Lamina Dura

Authors: Tibbetts J, Allen K, Hausmann E                               ARTICLE

Title:Effect of x-ray angulation on radiographic periodontal ligament space width

Source:J Periodontol 63: 114-117, 1992

Type:Clinical

Rating: Good

Keywords:Periodontal ligament/anatomy and histology; periodontal ligament/radiography.

P:To determine the influence of known changes in x-ray beam angulation anticipated under clinical conditions on the change in radiographic ligament space width. Radiographs of molars and incisors were studied to determine the influence of anatomical factors on changes associated with alteration in x-ray beam angulation

M&M:Pairs of radiographs were taken of incisor and molar locations in whole dried human skulls with known differences in x-ray beam angulation. To be acceptable, radiographs had to meet the following requirements: 1) no overlaps of contact areas of adjacent teeth, 2) visible interdental alveolar bone, 3) no cone-cut in the radiograph, 4) sufficient contrast to read any anatomic structures present. Baseline for vertical angulation was set perpendicular of the long axis of the tooth. For each tooth site, radiographs were taken at 2 vertical angulations: 1) perpendicular to tooth’s buccal surface 0° and 2) 10° off the perpendicular. 5 different horizontal angulations at each of the 2 indicated vertical angulations 1) baseline 0°, 2) -3° and -6° from the perpendicular, 3) +3° and +6° from the perpendicular. Replicate radiographs were taken at 0° and at each of the 2 vertical angulations. The radiographs were converted to digitized images and PDL width measurements were made utilizing a computer program. Data were analyzed separately for the incisor and molar sites.

R:The variation between the mean difference of baseline measurements was compared with that of discrepant-angle combinations, 10/20 pairs of radiographs which differed in horizontal angle only were significantly different from results of baseline replicates. 2/5 groups of pairs of radiographs which differed in vertical angle only were significantly different from results of baseline replicates. 11/20 groups of pairs of radiographs which differed in both vertical and horizontal angulation were significantly different from results of baseline replicates. Mean PDL width differences for incisor locations were SS from the mean baseline PDL width difference, posterior PDL width difference showed no statistical variation from the mean baseline width difference

C:Changes in x-ray angulation resulted in a SS change in radiographic PDL width at incisor locations, no such significant effect was found at molar locations. At molar area, thick bone overlying PDL will tend to reduce the difference in density seen on the radiograph of the ligament space and adjacent interproximal bone. It is suggested the radiographs should be taken with controlled projection geometry when clinical interpretation of change in PDL width is desired.

Topic:Lamina dura

Author:Greenstein G, Polson A, et al                              ARTICLE

Title:Associations between crestal lamina dura and periodontal status.

Source: J. Periodontol. 52:362-366, 1981.

Type:RCT

Rating:Good

Keywords:lamina dura, radiographic diagnosis, bitewing radiographs

P:To investigate the association between the radiographic presence of crestal lamina dura and the clinical periodontal status of the corresponding interdental area.

M&M:

  • 90 pts (53F, 37M; 21-45 years old) had 4 interproximal locations evaluated.

  • Sites were scored for visual inflammation, BOP, presence of PD> 3mm, and loss of attachment.

  • Bitewings and full mouthseries radiographs taken.

  • The radiographs were examined and scored for the presence or absence on an intact crestal lamina dura.

R:  NSSD correlations were obtained between PA radiographs, presence of lamina dura and inflammation, PD, or attachment loss. On bitewings, there was a SSD between presence of crestal lamina dura and inflammation (81.9%) versus absence of crestal lamina dura and inflammation (72.5%).No SSD with the other parameters and bitewings. However, there were significant discrepancies on whether the crestal lamina dura was present (agreed 24% of the time) and agreed 89% of the time when absent.

BL: Radiographically, the crestal lamina dura did not appear to be related to the presence or absence of clinical inflammation, BOP, presence of pockets, or loss of attachment.

Can radiographs be used to detect

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