44. Atypical Periodontal Conditions and Pathology

Classical Periodontal Literature Review

a) Mucocutaneous lesions


c) Periodontal Abscesses

d) Atypical periodontal conditions

e) Bisphosphonate therapy (BRONJ)



  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. Nisengard RJ. Periodontal implications: mucocutaneous disorders. Ann Periodontol 1996; 1(1): 401-438.
  1. Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part I. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 100 (1): 40-51.
  1. Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 100 (2): 164-178.
  1. Rogers RS III, Sheridan PJ, Nightingale SH. Desquamative gingivitis: clinical histopathologic, immunopathologic, and therapeutic observations. J Am Acad Dermatol 1982; 7(6):729-735.
  1. Stoopler ET, 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 Periodontol 2004;75:1424-1431.
  1. Layfield LL, Shopper TP, Weir JC. A diagnostic survey of biopsied gingival lesions. J Dent Hyg. 69:175-179, 1995.
  1. Rees TD, 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. Courtois GJ. 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. Horning GM, Cohen ME. Necrotizing ulcerative gingivitis, periodontitis, and stomatitis: Clinical staging and predisposing factors. J Periodontol 66:990-998, 1995.
  1. Shangase L, Feller L, Blignaut E. Necrotising ulcerative gingivitis/periodontitis as indicators of HIV- infection. SADJ. Apr;59(3):105-8, 2004
  1. Novak MJ. 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. Herrera D, Roldan S, Sanz M. The periodontal abscess: a review. J Clin Perio 27:377-386, 2000. (Review)
  1. Dewitt GV, 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. McLeod DE, 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. Page RC, et al. Prepubertal periodontitis I. Definition of a clinical disease entity. J. Periodontol. 54:257-271, 1983.
  1. Sweeney EA, et al : Prevalence and microbiology of localized prepubertal periodontitis. Oral Microbiol. Immunol. 2:65-70, 1987.
  1. Page RC, Altman LC, Ebersole JL, et al. Rapidly progressive periodontitis. A distinct clinical condition. J. Periodontol. 54:197-209, 1983.
  1. Watanabe K. 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. Robertson PB, et al: Periodontal effects associated with the use of smokeless tobacco. J. Periodontol. 61:438-443, 1990.
  1. Yukna RA: 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. LaPorta V 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. Filipowicz FJ, 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. ADA Council 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 Surgeons position 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. Cartsos V, 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





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


Topic: Mucocutaneous Disorders Article

Authors: AAP

Title: Position Paper: Oral Features of Mucocutaneous Disorders.

Source: J Periodontol 2003; 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.

Treatment includes, 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 a linear 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 epithelium resulting 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.


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.


Pharmacologic Agent

Trade Name






Sodium valproate (valproic acid)

Depakene, Depacon, Epilim,Valpro



Phenobarbital, Donnatal







None reported



Neoral, Sandimmune

Adults 25-30%



Calcium channel blockers


Adalat, Nifecard, Procardia,Tenif




None reported


Agon, Felodur, Lexxel, Plendil



Lotrel, Norvasc



Calan, Covera, Isoptin, Tarka,Verelan



Cardizem, Dilacor, Diltiamax,Tiazac


  • 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.
  • Histologically it 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-1β, IL-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.

Topic: Gingival lesions Article

Author: Layfield LL, Shopper TP, Weir JC

Title: A diagnostic survey of biopsied gingival lesions

Source: J Dent Hyg. 69:175-179, 1995.

Type: Survey

Rating: Good

Keywords: Oral health, diagnosis, incidence

Purpose: to determine the most commonly biopsied gingival lesions in a university-based school of dentistry.

Methods: A total of 30.056 biopsies over a 24-year period from 1969-1992 from the LSU medical center were examined. Around 80% of the cases were received from private practice.

Microcomputer technology was used to sort the cases to study gingival lesions. The database also categorized the biopsies into anatomic regions and was used to determine the percentages and frequencies of the most common lesions.


-Of the 30.056, 3859 (12.8%) were taken from the gingiva.

-3827 of these gingival lesions were pathologic.

-The gingival lesions were given 159 different histologic diagnoses.

-The most common diagnoses were:

1st=Periodontal disease (26.4%)

2nd=Fibrous hyperplasia (17.8%) *The majority of these were fibromas

3rd=Pyogenic granuloma (10%)

4th=Peripheral ossifying fibroma (9.6%)

5th=Epithelial hyperplasia/hyperkeratosis 5th (7.7%).

-Malignant lesions composed 1.4% of the pathologic gingival lesion

-Squamous cell carcinoma was diagnosed in 67.9% of the malignant cases, (47.2% female and 52.8% male). The mean age of these patients was 62.3 years (range 29 to 86).

-Squamous cell carcinoma showed a 3:1 ratio of mandibular to maxillary incidence.

Premalignant lesions comprised 2.3%, this yield a combined incidence of 3.7% for premalignant and malignant lesions.

-The ratio of benign to malignant neoplasm was 10:1

-The most common age group was 30-39

-Females predominated with 63.3%

-85.8% of the cases were Caucasian patients.



Topic: Gingival enlargement Article

Authors: Rees TD, Levine RA

Title: Systemic drugs as a risk factor for periodontal disease initiation and progression

Source: Compend Cont Ed Dent 1995; 16:20-36

Type: Review

Rating: Good

Keywords: drug-induced gingival enlargement, anticonvulsants, cyclosporine, calcium channel blockers

Results: Anticonvulsants: 3-6% of the population are epileptic. Phenytoin (Dilantin) blocks Na, K, and Ca ion influx across the cell membrane. It is also used for cardiac arrhythmia and trigeminal neuralgia. Histologically, gingival hyperplasia appears as an increase in CT interstitial substance without marked fibrosis. It interferes with folic acid absorption and can alter the integrity of the oral epithelium and promote inflammation of the underlying gingival CT in the presence of plaque. There is an interrelationship between calcium ion exchange, cellular use of folic acid, inactivation of collagenase and plaque induced inflammation. Prevalence of gingival hyperplasia among patients on phenytoin is 50% and the labial anterior gingiva is most commonly affected. Management should be focused on prevention with excellent oral hygiene and surgical treatment with the use of pressure appliances to avoid relapse. Discontinuance of phenytoin can result in at least partial resolution, but surgical correction is usually necessary to achieve optimal results.

Cyclosporine: Cyclosporine is an immunosuppressant drug that selectively affects the cell-mediated immune response and is used extensively to suppress organ/bone marrow transplant rejection, as well as diabetes, Behcet’s disease, psoriasis, erosive lichen planus and other autoimmune disorders. A less significant side effect of cyclosporine therapy is gingival enlargement. Incidence of gingival overgrowth has been estimated to be present in about 30% of patients taking cyclosporine. Gingival enlargement with cyclosporine resembles phenytoin both clinically and histologically. Cyclosporine use also carries a greater risk of developing malignancies in gingival overgrowth. Cyclosporine often cannot be discontinued. Surgical therapy is usually indicated, along with excellent plaque control and removal of other local etiologic factors. Recurrence, however, is frequent.

Calcium Channel Blockers: CCBs are used to manage cardiovascular conditions, such as angina, arrhythmias, and hypertension. These drugs interfere with calcium influx across cell membranes and reduce the intracellular concentration of calcium in cardiac and vascular smooth muscle cells. Nifedipine is the CCB most associated with gingival enlargement, with an incidence of 15-20% in these patients. Chronic inflammation is always present and gingival enlargement is histologically similar to phenytoin and cyclosporine-induced enlargement. When possible, nifedipine use should be discontinued, which often leads to resolution of the condition.

Sex Hormones: Hyperplastic edematous gingiva has been associated with puberty, pregnancy, oral contraceptives or estrogen and progesterone supplements. High estradiol levels enhance susceptibility to gingivitis due to PMN chemotaxis suppression. This can alter host resistance and microbial flora present in the oral cavity, which can contribute to the development of gingival inflammation.

Cannabis: Extensive use of marijuana has been associated with gingival enlargement, however the mechanism is unknown.

Erythromycin: One case study has reported gingival enlargement triggered by erythromycin administration in a 6 year old boy. Remission occurred when the medication was discontinued.

Conclusion: Management considerations for these patients include baseline examination before patients start taking the drug, frequent recall and excellent oral hygiene. The use of antimicrobial rinses is also recommended. A team approach involving the patient, physician, dentist, and pharmacist should be utilized to manage this condition in patients taking these medications.


  1. What other microorganisms can cause gingival lesions?


Topic: Viral Oral Mucosal lesions Article

Authors: Rivera-Hidalgo, et al:

Title: Oral mucosal lesions caused by infective microorganisms. I. Viruses and bacteria.

Source: Periodontol 2000, 21:106-124, 1999

Type: Review

Rating: Good

Keywords: oral mucosal lesions, injective microorganisms, viruses, bacteria

This article concisely reviews oral lesions that are causes by Virus and bacteria infecting the oral tissue and to state the injury or damage that results from the process by which organisms, capable of causing disease, gain entry to the body and establish colonies. Oral lesions may originate from local infections or may represent the oral manifestations or consequences of a systemic infection. This study reports viral and bacterial stomatitis

Measles: Measles is a highly communicable disease transmitted by inhalation of infective droplets with an incubation period of 10 to 14 days . It is an acute systemic condition with a prodrome in which the patient suffers from cough, conjunctivitis, fever, photophobia, rhinitis and Koplik’s spots (the bluish-gray specks on a red base). Koplik’s spots appear on the mucosa next to the molar teeth.

Mumps: Mumps (epidemic parotiditis) is caused by the mumps virus. Parotid, salivary gland infection may occur unilaterally or bilaterally. Affected salivary glands may be swollen and painful and may be accompanied by erythema and swelling of the parotid (Stensen’s) duct.

Coxsackie virus: These viruses are responsible for hand, foot and mouth disease, herpangina, lymphonodular pharyngitis and ulcerative oropharyngitis, they all producing oral lesions and are transmitted by contaminated aerosol.

Human papillomavirus: The classical oral lesions associated with human papillomavirus are squamous cell papilloma, condyloma acuminatum, verruca vulgaris and focal epithelial hyperplasia. Diagnosis of papillomavirus lesions is made based on the histopathological appearance. Characteristic features include koilocytosis, acanthosis and papillomatosis which, coupled to the clinical appearance, suggest the infection.

Herpes Virus: This virus transmitted from host to host by direct contact with saliva or genital secretions, where they are shed by asymptomatic hosts. The species names and the acronyms of herpes viruses used in the literature are as follows: human herpes virus 1 (HSV- 1), human herpes virus 2 (HSV-2), human herpes virus 3 (varicella zoster virus), human herpes virus 4 (Epstein-Barr virus), human herpes virus 5 (human cytomegalovirus), human herpes virus 6 (HHV-6), human herpes virus 7 (HHV-7) and human herpes virus 8 (HHV-8 or Kaposi’s sarcoma herpes virus).

Infective Stomatitis caused by bacteria mostly includes Spirochetes, Actynomycis, N. gonorrhoeae, M. tuberculosis, M. leprae, M.bovis, Streptococci, T. pallidum and rarely with enteric bacteria such as K. pneumonia, E. coli, H. pylori.

Acute necrotizing ulcerative stomatitis: Acute necrotizing ulcerative gingivitis (or necrotizing gingivostomatitis or necrotizing ulcerative gingivitis) is an acute infection of the gingiva that has been known by different names through the years such as Trench Mouth, Vincent Angina, noma, cancrum oris or gangrenous stomatitis is an extension of acute necrotizing ulcerative gingivitis into the adjacent tissues. Causative organism is Spirochetes. Acute necrotizing ulcerative gingivitis has been reported in recent years in patients with HIV infection or AIDS.

Actinomycosis: Actinomycosis is a chronic disease characterized by the formation of abscesses, fibrosis of tissues and draining sinuses. Has been described, and cases involving most of the oral tissues including the tongue and palate have been reported. As the Actinomyces infection spreads into the tissues, a hard, slow growing, relatively non tender swelling may form. Lesions of the bone and soft tissues may also show multiple abscesses that drain to the surface by sinus tracts. The discharge from the tracts typically contains visible yellowish colonies of organisms called “sulfur granules”.

Bacillary angiomatosis: Bacillary angiomatosis, also called epithelioid angiomatosis, is a rare vasoproliferative disorder that occurs almost exclusively in severely immunocompromised individual, primarily AIDS and cancer patients and organ transplant recipients. The oral lesions have been described as bluish or purple macules, pale bluish patches, and red, edematous lesions occurring on the palate , buccal mucosa and attached gingiva.

Mycobacterial infections: Tuberculosis is a chronic, infectious disease caused by the bacteria M.tuberculosis. It most commonly affects the lungs but may also involve any organ of the body. The most common oral tuberculosis lesion is a chronic, painless, irregular ulcer, with a vegetating surface covered by a gray or yellowish exudate. Other reports describe a nodular, granular or leukoplakic appearance. The disease is an airborne infection spread almost exclusively by droplets from a person with active disease. Leprosy caused by M. leprae and the oral lesions present as nodules that progress to necrosis and ulceration and occur on the palate, dorsum of the tongue, gingiva, uvula and the lips, and when untreated, may cause extensive destruction of the oral tissues.

Syphilis: Syphilis is a venereal disease that has infected humans for centuries. It is caused by the spirochete , Treponema pallidum and occurs clinically in three classical phases: primary (Chancre), secondary (Mucous patch) and tertiary (gumma)

Gonorrhea: Gonorrhea is a sexually transmitted infection with a worldwide distribution. It is caused by Neisseria gonorrhea. Lesions of the oral mucosa may present as a fiery red, edematous and occasionally painful ulceration.

Topic: Oral lesions No Article

Authors: Thomas, S, Rivera-Hidalgo

Tittle: Oral mucosal lesions casused by infective microorganisms. II. Fungi and parasites.

Source: Periodontol 2000, 21:125-144, 1999

Type: Discussion article

Rating: Good

Keywords: Diagnosis, classification, oral lesions, fungi, parasites


Purpose: Review oral mucosal lesions caused by fungi and parasites

Infective stomatitis infections caused by fungi

Candidiasis: Candidiasis or candidosis is an infection caused by a yeastlike fungus of the genus Candida, a normal member of the mouth and gastrointestinal flora. Generally, pts who are immunocompetent do not have oral fungal infections; C. albicans has a low pathogenicity in normal individuals. However, it is opportunistic pathogen and in patients where the host’s response is depressed can produce surface infections of the skin and the mucosa. Candida can also cause systemic infections, which some believe to be deep fungal infections.

  • Erythematous: acute or chronic with inflammatory changes. Common on palate but can be on gingiva. Possibly hypersensitivity reaction. PMN infiltrate with microabscesses.

  • Pseudomembranous: hyphae colonization without an inflammatory infiltrate.

Summary of a new classification for oral candidiasis


Acute: Pseudomembranous and erythematous mucocutaneous

Chronic: Pseudomembranous, erythematous, hyperplastic, nodular and plaque-like

Candida-associated: Denture stomatitis, angular chelitis (often mixed w/ Staph) and median rhomboid glossitis

Keratinized 1o lesion superinfected w/Candida: Leukoplakia, lichen planus and lupus erythematosus


Mucocutaneous presence as a result of systemic disease including immunodeficiency such as HIV—linear gingival erythema

Aspergillosis (Ascomycetes): Lesions are observed mainly in the immunocompromised patient. Oral lesions have been described as yellow or black, necrotic ulcers, typically located on the palate or posterior tongue. Presents as saprophytic but noninvasive, allergic and invasive. Can invade mucous membranes and the walls of small-medium arteries and veins, causing thrombosis and possible infarcts.

Histoplasmosis (Histoplasma capsulutum): Granulomatous fungal dz. Inhalation of spores, common in Mississippi river valley, found in soil near birds and bats. Most commonly diagnosed systemic fungal infection. The oral lesions have been described as beginning as flat, plaque-like, nontender elevations, either papillary or nodular, that later ulcerate and become painful.

Blastomycosis and paracoccidioidomycosis are rare fungal diseases that are becoming more prevalent in HIV-infected individuals. There have been no case reports of oral manifestations in HIV-infected patientsas of this review. However, oral involvement has occasionally been described

  1. Blastomycosis (Blastomyces dermatitidis): The most commonly reported oral lesions are single or multiple ulcerations. Other descriptions have included sessile projections, and granulomatous or verrucous-appearing lesions.

  2. Paracoccidioidomycosis (Puracoccidioides brasiliensi) : South American blastomycosis. Oral paracoccidioidomycosis lesions present as painful, chronic, irregular ulcers, with a granulomatous or vegetating surface, which may be xophytic. They have been described as occurring on the soft and hard palate, tongue, lips and gingiva

Mucormycosis (Mucorales. Zygomycosis): Organism deposits in vascular walls and forms a thrombosis which cause ischemic necrosis to the tissue that is supplied by the vasculature. Oral lesions usually appear as palatal ulcerations or black necrotic masses, which occur as a result of an infection in the nasal cavity or paranasal sinuses. Infection occasionally commences in the palate. Patients may demonstrate facial swelling, nasal discharge, fever and headache. Without treatment, can spread into orbit and brain.

Cryptococcosis (Cryptococcus neoformans): Spores from bird droppings. Inhalation. The oral lesions of cryptococcosis have presented as ulcerations of the tongue and palate and have also occurred in a non-healing extraction wound. Other fungal infections, squamous cell carcinoma or trauma may have a similar appearance.

Fusariosis (Fusarium species): Oral Fusarium infections are rare and usually present as secondary lesions of disseminated disease. The oral lesions, usually representing sites of secondary infection, have been described as black, necrotic ulcers occurring mainly on the palate.

Geotrichosis: Geotrichum candidum. Oral, bronchial, pulmonary or intestinal infection. Sharply defined enanthema with soft palate ulceration.

Trichosporonosis (Trichosporon beigelii, Trichosporon cupitum): One case of oral Trichosporon sp. infection has been reported in a patient with AML. The oral presentation was described as several whitish membranes covering friable erosions in the right mandibular and buccal region of the mouth..

Sporotrichosis (S. schenckii): One report noted oral involvement described as ulcerated or chancre-like lesions that occurred following an initial systemic infection.

Coccidioidomycosis (Coccidioides immitis): The mouth is rarely affected; however, oral lesions described as verrucous as well as necrotic ulcers have been identified

Infective stomatitis infections caused by parasites

Typically obligate anaerobes. Can produce serious infections and sometimes death. This article groups the parasites into arthropods (insects), helminthes (worms) and protozoa.


Myiasis : Myiasis is a general term for infection of any organ of the body by maggots that feed on dead or living tissues. Oral myiasisis (rare), also known as dental myiasis and gingival myiasis, is a larval infection of tissues of the oral cavity. Most patients present with symptoms of pain, gingival swelling and bleeding and an “itchy” feeling in the involved site. Intraoral examination generally reveals

the presence of active larvae, located within swollen, erythematous, bleeding oral tissues.

Cestodes (Plutyhelminthes) (tape worms)

Teniasis and cysticercosis : Cysticercosis in the oral tissues has been reported in more than 40 patients. The most common locations for the cysts are the tongue, lips and buccal mucosa. The lesions present as discrete, firm, non-tender, nodules lying beneath intact mucosa.

Echinococcis: small tapeworms. Form a space occupying lesion known as the hydatid cyst. 6 cases reported in pts. in the oral cavity: well circumscribed, soft or firm, elastic, fluctuant painless swelling.

Nematodes (nonsegmented round worms)

Trichinosis (Trichinella spiralis): Five cases of oral trichinosis have been reported. The cyst is actually a modified, viable cell called the nurse cell. Larvae in the nurse cells can survive for years, but eventually they become calcified, and die. One case report described the radiographic appearance of diffuse indefinite radiolucency on the crest surrounded by sclerotic bone.

Gongylonema. (Gongylonema pulchrum): 3 reported oral cases. Live worms are found encysted in oral tissues.


Leishmaniasis: Mucosalleishmaniasis begins in the nasal mucosa and then may involve the oropharynx and larynx. oral manifestation of either the visceral or mucosal form of the disease. Oral lesions appear as swollen, easily bleeding gingiva, and lesions of the cheeks, uvula and palate described as edematous, red and fissured.

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

Topic: Acute periodontal lesions Article

Authors: Corbet, R.

Title: Diagnosis of acute periodontal lesions.

Source: Periodontol 2000, 2004;34:204-16

Type: Review

Rating: Good

Keywords: NUG, NUP, Acute herpetic gingivostomatitis, gingival abscess, pericoronal abscess, periodontal abscess

Purpose: Review on diagnostic aspects of acute periodontal lesions.

Discussion: failure to treat acute periodontal disease appropriately may result in loss of attachment (making prognosis worse)

Necrotizing ulcerative gingivitis (NUG): painful bacterial infection of interdental & marginal gingival tissues. Rapid onset, pain, ulceration of interdental papilla “punched out; crater like,” sloughing necrotic debris (pseudomembrane: composed of fibrin, necrotic tissue, inflammatory cells, masses of bacteria), bleed readily or spontaneously, fetid breath; possible fever, malaise or submandibular lymphadenopathy. Predisposing factors: stress, malnutrition, smoking, preexisting gingivitis, trauma, immunosuppression & immunodeficiency. Often in pts with HIV. Treatment: debridement & antibiotic therapy.

Necrotizing ulcerative periodontitis (NUP): infection characterized by necrosis of gingival tissues, PDL & alveolar bone (attachment apparatus). Deep interproximal, crater-like defects with denuded interdental bone, possible sequestration of pieces of bone. Consistently occur with systemic conditions such as immunosuppression, severe malnutrition or HIV infections. Treatment: debridement, antibiotic therapy, if unknown HIV status, recommend HIV testing

Acute herpetic gingivostomatitis (AHG): viral ulcerations on the entire oral mucosa with multiple vesicles that coalesce and form shallow, fibrin-covered regular shaped ulcers that persist for more than a week. These are not necessarily tender, no marked tendency to bleed, definite fever, sore mouth

Other conditions to be included in differential of NUG: Viral infection (e.g. recurrent herpes), Mucocutaneous conditions (e.g. desquamative gingivitis, pemphigoid, erythema multiforme, erosive lichen planus), Bacterial infections (e.g. strep gingivitis, gonococcal gingivitis, Treponema pallidum ulcerations), or Traumatic condition (e.g. toothbrushing)

Gingival abscess: confined to marginal gingival tissues, often at previously non-diseased sites. Most commonly from foreign body impaction. Diagnosis generally made by history of 1-2 days of pain, localized gingival swelling, and a red, shiny swelling confined to marginal gingival tissue

Pericoronal abscess: usually associated with partially erupted tooth, absence of any periodontal pocket on the vital tooth or vital tooth adjacent to the partially erupted tooth.

Periodontal abscess: acute or chronic. Distinguishing factor to diagnose between periapical & periodontal abscesses is the high number of spirochetes in the exudate of periodontal abscess. Test vitality. Acute abscess usually present with pain, ask about Hx of periodontal therapy (missed calculus), recent antibiotic therapy (even for unrelated infections) may trigger periodontal abscess formation, possible indication of uncontrolled diabetes. Pt will have swelling, edema and redness, BOP at affected site, usually suppuration on pressure, possibly hypermobility, tenderness to palpation. Probing depths are variable; limited lymphadenopathy, fever or malaise.

Tooth fracture leading to acute abscess: must be excluded in sites with acute periodontal purulent infection. Use a bite test, transillumination or a dye to visualize fracture. Vertical crown-root fracture often presents with narrow, deep periodontal pocket. Diagnosis of vertical root fracture is mainly thru history taking. Might have concurrent periodontal disease: if periodontal treatment is performed and pain on chewing persists, possible vertical fracture.

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

Topic: ANUG Article

Authors: Listgarten M and Lewis D

Title: The Distribution of Spirochetes in the Lesion of Acute Necrotizing Ulcerative Gingivitis: An Electron Microscopic and Statistical Survey

Source: J Periodontol 38:379-386, 1967

Type: Clinical

Rating: Good

Keywords: ANUG,

Background: In a study of gingival lesions of ANUG with electron microscopy it was observed that the typical ulcerated lesion could be divided into 4 zones:

  1. Bacterial zone containing numerous microorganisms, including various morphological types of spirochetes.

  2. A zone rich in neutrophils

  3. A zone of necrosis

  4. A zone where larger spirochetes were observed within the tissues of the host, in large numbers.

Spirochetes were classified into small, intermediate and large.

Small spirochetes were subdivided into “1-2-1” and “2-4-2” types depending on whether 1 axial fibril or 2 fibrils, respectively originated near either end of the protoplasmic cylinder. The intermediate spirochetes were subdivided into “6” and “7” types depending on whether they had 6 or fewer fibrils, or 7 or more fibrils, respectively, originating at either end of the protoplasmic cylinder.

Purpose: To examine the distribution of the different morphological types of oral spirochetes (SP) in ANUG and to gather evidence that the predominant spirochetes in ANUG lesions are, indeed, morphologically different from Borrelia Vincentii (“intermediate” spirochete of the “6” type, that represents the majority of spirochetes in Vincent’s infection).

Method: 15 patients, ages 15-32 years, with 6 or more interdental gingival papillae showing clinical evidence of ulceration. Patients who had received any form of therapy were excluded. Tissue was collected by scraping of the ulcerated interproximal papillae. For 11 patients, samples collected from the various areas in the mouth were pooled as a single representative sample for each of these patients. For 1 patient, separate samples were collected from 6 different sites and kept as separate samples. For 3 patients, 3 sites were sampled in each mouth. At each site a “superficial” and a “deep” sample were obtained. For each sample, 50 or more spirochetes were counted and classified morphologically as “small”, “intermediate” and “large” using electron microscopy.

Results: The median % of “small” spirochetes was 28% (7-39%), of “intermediate spirochetes” was 72% (43.9-90%) and the median % of “large” spirochetes was 3% (0-20%). In 9/11 patients “2-4-2” spirochetes occurred more often than “1-2-1” types“. Within the “intermediate” group the “7” type occurred more frequently than the 6” type in 10/11 patients. In 3 patients, in the ”deep” samples, “intermediate” spirochetes of the “7” type were predominant over spirochetes of the “6” type.

Conclusion: If spirochetes of the 6 type are identical to BV, the results indicates that spirochetes of the type tend to outnumber BV in pooled scraping of ANUG lesions, and they are found in larger % in the deeper portion of the lesions then BV.

The gingival scrapings of an ANUG may not provide true reflection of the distribution of various spirochete types at various levels within the lesion.



Topic: ANUG Article

Authors: Courtois GJ.

Title: Acute necrotizing ulcerative gingivitis. A transmission electron microscopic study.

Source: J. Periodontol. 54:671-679, 1983.

Type: Clinical

Rating: Good

Keywords: ANUG, histology

B: Spirochetes appear to infiltrate the underlying vital tissues, making ANUG the only inflammatory periodontal disease where bacterial invasion of vital tissue occurs during the early lesion stage. Up to this point only Listgarten and Heylings published electron microscopic studies on ANUG and in both studies there is little mention made of the invasive potential of other morphologic types of organisms.

P: To provide evidence that microorganisms other than spirochetes are capable of invading the lamina propria subjacent to the ANUG lesion; to add to the limited number of electron microscopic studies of the ANUG lesion and expand the small body of knowledge in this area of interest.

M+M: 8 patients(17-31, sex not specified, just stated that both sexes represented) with pathognomonic signs of ANUG in 6 or more interdental spaces- interproximal gingival necrosis, ulceration, pain, pseudomembrane formation and presence of or immediate past hx of spontaneous gingival hemorrhage. Patients were heavy smokers, under severe emotional stress and OH was practically nonexistent. Soft tissue biopsies obtained with 15C blade, excising the interdental papilla. The tissue sample processed for LM and TEM.


Spirochetes, fusiforms, cocci, short and curved rods can penetrate viable CT. Spirochetes were present, but comprised minority of the bacteria observed.

  • 4 zones of the ANUG gingival lesion first described by Listgarten, 1965, were observed in the study without diffuclty:

a. bacterial zone — most superficial, consisting of varied bacterial types, including few spirochetes

b. neutrophil rich zone- numerous leukocytes (PMNs) and bacteria, most of which are spirochetes

c. necrotic zone- consisting of degenerated tissue cells, fibrillar material, remnants of collagen fibrils and numerous spirochetes of intermediate and large sizes

d. zone of infiltration — deepest zone infiltrated predominantly by spirochetes of intermediate and large sizes

  • Invasion depth 155-400 microns (measure from apical cell memebrane of nearest basal epithelial cell)
  • Lymphoid cell infiltrate predominated, even though all patients exhibited intensely acute clinical symptoms
  • Local predisposing factors and altered host resistance may be of considerable importance in the initiation of ANUG lesion

BL: Both spirochetes and other morphologic types of bacteria were observed beneath the basal lamina at a depth ranging from 155-400 microns.

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

Topic: Necrotizing gingivostomatitis Article

Authors: Horning GM, Cohen ME

Title: Necrotizing ulcerative gingivitis, periodontitis, and stomatitis: Clinical staging and predisposing factors.

Source: J Periodontol 66:990-998, 1995.

Type: Clinical study

Rating: Good

Keywords: Gingivitis, necrotizing ulcerative; gingivostomatitis, necrotizing; Periodontitis, necrotizing ulcerative; HIV infection, complications; periodontal attachment.

B: Necrotizing ulcerative gingivitis (NUG), necrotizing ulcerative periodontitis (NUP), and necrotizing stomatitis (NS), collectively termed necrotizing gingivostomatitis (NG), represent a dramatic, but rare oral infection associated with diminished systemic resistance, including HIV infection.

P: To examine the clinical features of necrotizing gingivostomatitis (NG), clarify any differences observed between seropositive HIV and HIV seronegative and analyze the relationship of NG to suspected predisposing factors.

M&M: 68 pts from a population of 22,000 military personnel with known HIV status were screened for NG. All pts presented with pain, interdental ulceration and gingival bleeding. Lesions were staged (modified Pindborg), and clinical findings and predictor variables were compared to 68 random control subjects without NG.

R: 10 of the 68 NG pts were HIV-positive. Most cases (52%) were stage 1, with necrosis of the tip of the interdental papilla only; 19% were stage 2, with the entire papilla affected; 22% had necrosis of marginal (stage 3) or attached gingiva (stage 4); and 7% were more advanced, with mucosal necrosis or bone exposure (bone exposure 1%).

  1. Attachment loss was a feature of stage 2 or greater. 88% of the cases presented a white pseudomembrane over the necrotic area, and fetid breath was seen in 87% of the cases.

  2. Beside HIV infection (which was more strongly associated with NG infection than any other predisposing factor), significant predisposing factors included poor oral hygiene, unusual life stress, inadequate sleep, Caucasian race, age 18 to 21 years, and recent illness.

  3. HIV-positive NG cases were clinically indistinguishable from HIV-negative cases regarding course, pattern of healing and clinical appearance.

BL: HIV+ pts had worse staging (NSSD), but the disease is clinically indistinguishable between HIV– and HIV+ pts. AL was consistently observed in ≥ stage 2 supporting the use of NG as a generic term for bacterial-related necrotizing oral infections.


Topic: NUG/NUP in HIV patients No Article

Authors: Shangase L, Feller L, Blignaut E.

Title: Necrotizing ulcerative gingivitis/periodontitis as indicators of HIV-infection.

Source: SADJ. Apr;59(3):105-8, 2004

Type: cross-sectional

Rating: good


Purpose: To evaluate if NUG/NUP in otherwise systemically asymptomatic individuals is indicative of HIV infection (by correlating with CD4+ T cells counts) and whether smoking is associated with HIV status in patients with NUG/NUP.

Methods: Cross sectional study over a 16-month period. Patients included were diagnosed with necrotizing periodontal disease (NPD) and those who were already diagnosed as HIV positive were excluded. 86 patients (46 males and 40 males), age between 5-48 years old. Medical history, habits, other soft tissue pathologies, areas of interdental necrosis, gingival bleeding, pain, AL and other conditions if present were recorded.

Patients were medicated for five days (metronidazole, paracetamol, 0.2% gluconate chlorhexidine for oral rinsing) and mechanical debridement was performed in the end of five days. Blood test for HIV testing and CD4+ T cells counts were carried out in 56 of the patients that consented to HIV testing. Statistical analysis was performed.

Results: Prevalence of NUG/NUP is 0.71% in the general population.

39 out of 56 patients were positive for HIV and CD4+ T cells were below 500 cells/mm3 in 90% of those patients and less than 200/mm3 in 53%. In 83% of the HIV negative patients, CD4+ T cells were more than 500/mm3 and none of them less than 200/mm3. 15 of the HIV patients were diagnosed with other oral lesions too (candidiasis and oral hairy leukoplakia).

No significant association was found between smoking and HIV infection in patients diagnosed with NUG/NUP.

With the predictive value for HIV found in this study there is possibility that 21 of the 30 patients that refused testing might be HIV positive.

Conclusion: NUG/NUP in otherwise systemically health individuals is strongly correlated with HIV infection.


Topic: Necrotizing ulcerative periodontitis No Article

Author: Novak MJ

Title: Necrotizing ulcerative periodontitis

Source: Ann Periodontol 1999; 4:74-78

Type: Review

Rating: Good

Keywords: Gingivitis, necrotizing ulcerative/etiology; gingivitis, necrotizing ulcerative/pathogenesis; periodontitis/necrotizing ulcerative/etiology; periodontology, necrotizing, ulcerative/classification; periodontitis, necrotizing ulcerative/pathogenesis


– The classification was changed from necrotizing ulcerative gingivo-periodontitis to necrotizing ulcerative periodontitis (NUP), without any supporting evidence from the literature other than the clinical observation

– There is no evidence to support the concept that NUP is a natural progression of NUG other than the occurrence of incidental attachment loss.

-There is insufficient information to suggest that NUP is a distinct clinical entity, this reviewer believes the clinical manifestation of NUP and NUG should be grouped into a distinct cluster of diseases termed “necrotizing periodontal disease”


– In an HIV- infected population with NUP, patients were 20.8 times more likely to have CD4+cell counts below 200 cells/mm3 than patients without NUP; however, not all patients with CD4+cell counts below 200 cells/mm3 have NUP, which indicates additional factors are involved.

Since longitudinal studies have demonstrated that attachment loss of >3 mm is likely to occur 6.16 times more frequently in subjects with CD4+cell counts of <200 cells/mm,it is reasonable to suggest a classification based on systemic aggravation of periodontal disease progression.


-It appears that necrotic lesions, including lesions of NUP, may occur in young individuals who may be immunocompromised through malnutrition and/or systemic disease

Refractory Necrotizing Ulcerative Periodontitis

– There are no controlled clinical studies available to suggest that necrotizing periodontal disease is refractory to treatment.

-There is ample evidence to suggest that the disease can be controlled with effective oral hygiene, combined with the use of systemic antibiotics.


– The term NUP would suggest that the pathologic process observed is similar to that observed in periodontitis, but with the addition of tissue necrosis. There are currently no microbiologic or immunologic data to support this.

-Individuals demonstrating necrotic lesions associated with the periodontium may be immunocompromised through systemic disease or malnutrition. The level of immunocompromisation may affect the clinical manifestations of the necrotic lesion.

– Until the etiology and pathogenesis is further understood, NUP should be reclassified as a necrotizing form of periodontal disease and NUG be included as a component of this classification since the necrotic lesions can affect the gingival as well as the PDL and alveolar bone.

-Necrotizing periodontal diseases should be distinct from the classifications of gingivitis and periodontitis since tissue necrosis is the common distinctive clinical feature of NUG and NUP.

  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?

Topic: Periodontal abscess Article

Authors: Herrera D, Roldan S, Sanz M

Title: The periodontal abscess: a review

Source: J Clin Perio 2000; 27:377-386

Type: Review

Rating: Good

Keywords: periodontal abscess, literature review, microbiology, diagnosis, classification, etiolody, prevalence, therapy

Purpose: To describe and characterize the periodontal abscess and report information about prevalence, proposed etiologies, pathogenesis, diagnosis, microbiology, and treatment of this condition.

Results: The periodontal abscess is a lesion with an expressed periodontal breakdown occurring during a limited period of time and has the easily detectable clinical symptom of localized accumulation of pus located within the gingival wall of the periodontal pocket. Periodontal abscesses represent up to 14% of dental emergencies within the US and are the third most common emergency dental infection. In patients with periodontitis, abscesses are more likely to occur in a pre-existing periodontal pocket and lead to a hopeless diagnosis of these teeth. When directly associated with periodontal disease, abscesses may form during exacerbations of existing disease, after therapy, or during reemergence of previously cured disease. When abscesses form in the absence of periodontal disease, it can be due to the impaction of a foreign object, perforation by and endodontic instrument, infection via lateral cysts, or local factors affecting the morphology of a tooth, such as a fractured root.

As bacteria enter the soft pocket wall, inflammatory cells migrate into the site and lead to destruction of connective tissue. Histologically, neutrophils are found surrounding a central area of soft tissue debris and leukocytes. A pyogenic membrane composed of macrophages and neutrophils is organized at a later stage. The rate of destruction of an abscess depends on the growth of bacteria inside the foci, virulence factors of effecting pathogens, as well as the local pH. Abscesses are polymicrobial in nature. Gram-negative anaerobic rods and Gram-positive facultative cocci are often isolated from abscesses, with rods dominating over cocci. The most common species are P. gingivalis, P. intermedia, F. nucleatum, however others have been reported.

Diagnosis is based on symptoms revealed by patients, ranging from slight discomfort to severe pain, tenderness of the gingiva, tooth mobility, tooth elevation, and sensitivity to palpation. Suppuration is a common finding when applying pressure to the abscess. Radiographic appearance may be normal or show some degree of bone loss, ranging from widening of the periodontal ligament to dramatic radiographic bone loss. Periodontal abscesses have been classified according to location (gingival or periodontal), course of lesion (acute or chronic), and number (single or multiple). Treatment typically consists of three therapeutic approaches: drainage and debridement, systemic antibiotics (controversial), and periodontal surgical procedures. Patients should be reexamined 24-48 hours and definitive treatment may begin after one week. Complications can include tooth loss and spread of infection to other body sites.


Topic: Acute periodontal abscess Article

Authors: Dewitt GV, Cobb CM, Killoy WJ:

Title: The acute periodontal abscess: microbial penetration of the soft tissue wall.

Source: Int J Periodont Restor Dent 5(1):39-51, 1985.

Type: Review

Rating: Fair

Keywords: Acute periodontal abscess, microbial, penetration, soft tissue

P: To determine if bacterial infiltration occurs in the soft tissue wall of the acute periodontal abscess.

M&M: Punch biopsies were taken and processed from 12 patients and 3 control sites. Electron and light microscopy were used.

R: Normal epithelium and lamina propria. Approaching the pocket side, there was an acute inflammatory infiltrate consisting of PMNs. Bacterial invasion was shown in 7/9 biopsies. Bacterial morphotypes included gram negative cocci, diplococci, fusiform, and spirochetes. In 100% of the acute lesion biopsies, a fungal component was present and believed to be Candida albicans. The fungus was also found within the vessel walls. There were no bacteria or fungi in control tissues.

BL: Characteristics of periodontal abscesses include mild bacterial invasion and moderate fungal invasion of the soft tissues. The discovery of fungal penetration to the vascular system is important in the overall management in debilitated patients (i.e. diabetes, leukemia, & immunosuppression).



Topic: Periodontal abscess Article

Authors: Herrera, D., Roldan, S

Tittle: The periodontal abscess (I). Clinical and microbiological findings.

Source: J Clin Periodontol 27:387-394, 2000

Type: Clinical Study

Rating: Good

Keywords: Diagnosis, classification, periodontal abscess, bacteria

Purpose: To describe periodontal abscess clinically and microbiologically.

Methods: 29 consecutive pts with presumptive dx of acute perio abscess (Feb 96- Dec 97). Endo abscesses were excluded based on vitality tests & radiographic exams. Included if localized pain, swelling, tenderness, edema, redness in perio area; non-vital teeth were only included if a clear 1o perio lesion was detected. Blood & urine samples were collected, clinical variables recorded (BOP, suppuration, cervical lymphadenopathy, tooth mobility, PD), then microbial samples taken from abscess.

Results: 62% occurred in untreated perio pts.

14% immediately after SCRP,

24% while on maintenance.

93% of lesions in pts with mod-severe p

69% associated w/molars (mostly w/1st molars),

55% in maxilla, 48% appeared on B, ~14% each on L & M, 24% on D.

~90% of abscesses were painful; swelling, edema, redness & BOP were present in 100%. 79% of teeth showed mobility. Mean PD was 7.28mm

Micro: In order of decreasing prevalence, F nucleatum (70.8%), P. micros (70.6%), P. gingivalis (62.5%), P. intermedia (50%) & B fosythus (47%). P. melaninogenic and, C. rectus are seen but in ~20% of lesions.. P. gingivalis & P. melaninogenica, although not found in every abscess, appeared to have the highest percentage of total flora in positive sites.

Lab values: 31.6% had a higher than normal # of leukocytes (w/in normal WBC range, just at high end)

Discussion: Most periodontal abscesses will be diagnosed in an acute phase, so rarely see a sinus tract. Both strict and facultative anaerobes were present in these abscesses. Microflora of the abscess is comprised of perio pathogens. Pain, swelling, deep PD, mobility and inflammation is seen. Regional lympadenopathy is possible but not present in the majority of the cases.

Conclusion: Periodontal abscesses in pts with diagnosed periodontal disease have clear, clinical and microbiological characteristics.



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

Topic: Treatment of acute periodontal abscesses Article

Authors: Herrera D, Roldan S, O’Connor A, Sanz M

Title: The periodontal abscess (II). Short – term clinical and microbiological efficacy of 2 systemic antibiotic regimes.

Source: J Clin Periodontol 27:395-404, 2000

Type: Short-term open parallel longitudinal clinical study

Rating: Good

Keywords: periodontal abscess; periodontitis; azithromycin; amoxicillin/clavulanate; systemic antibiotic; therapy; microbiology

Purpose: The aim of the study was to compare the clinical and microbilogical efficacy of azithromycin and amoxicillin/clavulanate in the treatment of acute periodontal abscesses (APA).

Methods: 29 pt with APA, clinical exam was performed and recorded following variables- pain, edema, redness, swelling, BOP, suppuration, tooth mobility, lymphadenopathy, and PD.

Microbiological samples were taken and pts were randomly assigned to one of the two regimens of antibiotics: 1) azithromycin (Zitromax 500 mg 1 q.d. for 3 days) and 2) amoxicillin/clavulanic acid (Augmentin500, 500+125 mg, 1 t.i.d. for 8 days). Clinical variables recorded and microbiological samples were collected at 3-5 days (2nd visit), 10-12 (3rd visit) and 30 days (4th visit). At 3rd visit, abscess was debrided. Blood and urine samples were taken at baseline and at 3rd visit

Results: The baseline level of pain and edema was significantly reduced in both groups (p< 0.01). After 3-5 days, clinical variables were improved significantly in all subjects as compared to baselines. For both group, PD reduced significantly but a tendency towards a higher reduction in PD was calculated for the Azithromycin group. Microbiologically, short-term reduction was detected with both antibiotics. First re-colonization occurred after the 3rd visit. NSD was found between both regimens. Compliance was better for Azithromycin group since 5 pts (36%) in Augmentin group either missed 1-2 doses (3 pts), stop taking due to improvement of the symptoms (1 pt) or taking extra dose (1 pt).

Conclusion: This present study demonstrated that the APA can be controlled alone with systemic antibiotics without debridement. Both antibiotic regimens were effective in the APA in periodontal pts with better compliance for Azithromycin group.

Topic: Periodontal Abscess Article

Authors: McLeod DE, Lainson PA, Spivey JD

Title: Tooth loss due to periodontal abscess: A retrospective study

Source: J Periodontol 68:963-966, 1997

Type: Clinical

Rating: Good

Keywords: periodontal abscess

Purpose: To evaluate the longevity of teeth that were treated for periodontal abscess and followed on frequent periodontal maintenance.

Method: 114 patients who were treated by a single periodontist over a 5 to 29 year period were included. Inclusion criteria: originally diagnosed with moderate to advanced periodontitis, treated by conventional non-surgical, surgical therapy and maintained on 3 to 6-month recall. Based upon the number of teeth lost by each individual maintenance, each patient was categorized into one of the following treatment response groups : well maintained (0-3 teeth lost), downhill (4-9 teeth lost), extreme downhill (10-23 teeth lost). A diagnosis of periodontal abscess was made after evaluation and interpretation of patient’s chief complaint, medical/dental history, clinical, pulpal examinations and xrays. Patients presenting a diagnostic challenge involving both pulpal and periodontal pathology received endodontic consult and were not included in the study. Teeth that had diagnosis of periodontal abscess were recorded. Only those teeth with periodontal abscess that were lost during maintenance following active treatment were included in the study. The treatment of the abscess included sub-g root instrumentation, limited occlusal adjustment, antibiotics and analgesics.

Results: 42/114 patients had periodontal abscess during maintenance, 30 in the well –maintained, 10 in the downhill, and 2 in the extreme downhill group. Of the 2,899 teeth, 109 (3.76%) had periodontal abscess of which 49 (45%) were lost and 60 (55%) were successfully maintained over an average of 12.5 years. When tooth loss of abscessed teeth was compared between furcated and non-furcated teeth, more furcated teeth were lost. The extreme downhill group showed the greatest tooth mortality per subject followed by the downhill and well-maintained groups.

Conclusion : Teeth with history of periodontal abscess can be treated and maintained for several years.

  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)?

Topic: Prepubertal periodontitis Article

Authors: Page RC, et al.

Title: Prepubertal periodontitis I. Definition of a clinical disease entity.

Source: J. Periodontol. 54:257-271, 1983

Type: Discussion

Rating: Good

Keywords: Prepubertal periodontitis

P: To define prepubertal periodontitis as a clinical entity, establish diagnostic criteria, demonstrate clinical, radiographic, and histological features, documented progression and explore methods of treatment.

M+M: 5 case reports, three patients with localized and two patients with generalized form of disease. Cases were discussed and used to define prepubertal periodontitis as a clinical entity.

DISC: Prepubertal periodontitis:

1. Onset during or immediately after eruption of the primary teeth.

2. Prevalence unknown but probably rare.

3. Possibility of a genetic basis for some types.

4. Generalized Form:

A. Extremely acute inflammation is present with proliferation of gingiva

B. Very rapid destruction of the alveolar bone and gingiva.

C. Profound functional defects of peripheral blood neutrophils and monocytes are seen; neutrophils absent from the gingival tissue.

D. Peripheral blood white cell count is elevated.

E. Otitis media and skin and upper respiratory infections are frequent.

F. Periodontitis may be refractory to antibiotic therapy.

G. All primary teeth are affected; the permanent teeth may or may not be affected

5. Localized Form:

A. Only some teeth are affected; pattern on involvement not yet determined.

B. Gingival tissues may exhibit little or no inflammation.

C. Destruction is not as rapid as in the generalized form.

D. Functional defects are present in either neutrophils or monocytes, but not both.

E. Recurrent otitis media is not a frequent finding and usually no history of frequent infections.

F. The disease is amenable to treatment by curettage and antibiotic therapy.

Topic: Prepubertal Periodontitis Article

Authors: Sweeney EA

Title: Prevalence and microbiology of localized prepubertal periodontitis

Source: Oral Microbiol. Immunol. 2:65-70, 1987

Type: Clinical study

Reviewer: Jyoti Sonkar

Rating: Good

Keywords: prepubertal periodontitis

P: To supplement information available regarding prepubertal periodontitis (PPP).

M&M: Examined dental records (bitewing x-rays) of 2264 children from pedo dept at U of PENN. Bone levels were classified as “normal” or “reduced in height.” 19 children (5-11 yr) identified as having crestal bone loss, parents contacted and 4 presented for exam. During this period of examination, 5 additional pts demonstrating alveolar bone loss around primary teeth were diagnosed in the department. Pts were included in the clinical and microbiological parts of the study, but not in the prevalence estimate because the number of negative cases, which had gone through the clinic in the interim, was unknown. 35 children (8-11 yr) served as control. Evaluated PI, GI, PD, microbial sampling.

R: Prevalence was 0.84%. 10 were Black females, 6 were Black males, 2 were White males, 1 was an Asian male. 11/19 had bone loss at M & D surf of 1st primary molars; 8/19 had it on both primary molars. Only 2 pts had anterior bone loss. None of the pts had systemic disease. High prevalence of black pigmented bacteroides (31/35 samples), mainly Bi [Bacterioddes intermedius (Pi) found in 26/35 samples]. Aa (detected in 5 samples from 3 individuals) & Capnocytophaga spp (24/35 samples) predominant in some samples. Only 2/19pts were correctly diagnosed at the initial exam.

BL: Localized PPP is more common than previously realized and is associated with bacteria regarded as major perio pathogens- types of predominant flora: 1) BPB (Bi); 2) Aa; 3) Capnocytophaga spp.

Cr: No criteria was given for the “reduced in height” bone level (how far away from the CEJ. Must be careful how to interpret demographical data (may not be representative of general population).

Topic: rapidly progressive perio Article

Authors: Page RC, Altman LC, Ebersole JL,

Title: Rapidly progressive periodontitis. A distinct clinical condition

Source: J. Periodontol. 54:197-209, 1983. DOI: 10.1902/jop.1983.54.4.197

Type: case reports

Rating: good

Keywords: rapidly progressive periodontitis; classification; gingivitis;

Purpose: To establish rapidly progressive periodontitis as a clinical entity.

Methods: Seven case reports selected, diagnostic criteria, clinical, radiographic features, relationship between this type of periodontitis and serum antibodies.

Discussion: The suggested classification of periodontitis is: adult, rapidly progressive, juvenile and prepubertal, based on a large number of characteristics.

It is not known whether or not rapidly progressive periodontitis is preceded by gingivitis. Disease progression is highly episodic and cyclic. The amounts of associated microorganisms vary greatly. The destruction may greatly slow or completely arrest for reasons not known. Although bone destruction may be extreme and PD 10mm or more, the gingival tissues may show no clinical signs of inflammation.

Featured of Rapidly Progressive Periodontitis

  1. Age of onset is between puberty and about age 35

  2. Lesions are generalized, affecting most of the teeth, without any consistent pattern of distribution

  3. Some, but not all, patients may have had juvenile periodontitis previously

  4. There is evidence of severe and rapid bone destruction, after which the destructive process may cause spontaneously or greatly slow down.

  5. During the active phase, gingival tissue is inflamed with marginal proliferation. During the arrested phase, the tissues may appear free of inflammation.

  6. The amounts of microbial deposits are highly variable.

  7. Approximately 83% of the pts have functional defects in neutrophils or monocytes.

  8. Some individuals are remarkably responsive to treatment by curettage couples with antibiotic administration.

Available data implicate Gram- anaerobic bacteria especially Bacteroides, Actinobacillus and possibly Capnocytophaga as important pathogens.

Several systemic diseases (Diabetes, Papillon-Levefre syndrome, Down syndrome, Crohn’s disease, Chediak-Higashi syndrome) appear to predispose to periodontitis and the form the disease takes. The feature these diseases and syndromes have in common is defective neutrophil numbers and/or functions.

Based on findings of this study most individuals with rapidly progressive periodontitis who manifest defects in blood cells or serum, but do not have other systemic diseases respond remarkably well to conservative periodontal therapy.


Topic: Prepubertal periodontitis Article

Author: Watanabe K

Title: Prepubertal periodontitis: A review of diagnostic criteria, pathogenesis, and differential diagnosis

Source: J. Periodontal Res. 25:31-48, 1990.

Type: Review

Rating: Good

Keywords: Prepubertal periodontitis, diagnosis, pathogenesis, differential diagnosis

Purpose: To review of the literature on prepubertal periodontitis (PP)


  • Page was the first to characterize the clinical signs of periodontitis in prepubertal children, and he named it prepubertal periodontitis (PP). He classified two types of PP:
    • 1) Localized (L-PP)
    • 2) Generalized (G-PP).
  • G-PP is identified as a manifestation of Leukocyte adhesion deficiency (LAD).
  • L-PP is defined only by clinical criteria, and appears to have a prevalence of ≥ 0.84%
  • According to Page, functional defects are present in either PMN or monocytes in L-PP. In G-PP functional defects are present in both PMN and monocytes.
  • Potential Pathogenic bacteria associated with L-PP: AA, PI, Pg, Capnocytophaga sputigena
  • Contributing factors to L-PP include: Cementum defects, host defense system, especially leukocyte chemotaxis.
  • Diseases associated with prepubertal periodontitis: Papillon-Lefevre syndrome, hypophosphatasia, neutropenia, Chediak-Higashi syndrome, leukemia, histiocytosis X, acrodynia, Leukocyte Adhesion Deficiency, Juvenile diabetes, AIDS
  • There is no unique pattern of bone loss in L-PP
  • L-PP might lead to development of LJP or GJP
  • If AA is involved, SRP+ antibiotics may be the best option.

Diseases known to be assoc. w/ alveolar bone loss (such as those just mentioned) must be definitively excluded in prepubertal children until the pathogenesis of LPP at the cellular and molecular levels is understood, and L-PP can be definitively diagnosed as either as a distinct disease entity or entities.

  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?


Topic: Smokeless tobacco Article

Authors: Robertson PB, et al

Title: Periodontal effects associated with the use of smokeless tobacco

Source: J. Periodontol.1990; 61:438-443

Type: Clinical evaluation

Rating: Good

Keywords: tobacco/smokeless, mouth neoplasms/etiology, mandibular neoplasms/etiology, gingival recession/etiology, periodontal attachment/etiology

Purpose: To characterize the oral effects of smokeless tobacco among professional baseball players

Methods: 1,100 members of 7 major/minor league teams were examined during the 1988 spring training season. Subjects who agreed to be examined also completed a comprehensive questionnaire that evaluated use of tobacco and alcohol, as well as previous dental history. Blood draw confirmed reported tobacco usage. Examiners were blinded to those that used smokeless tobacco and those that did not. Clinical exam included location, size, color, contour, texture, pathology was recorded. PI, GI, recession, AL on mesial and facial surfaces were recorded. Subjects with leukoplakia and erythroplakia were offered a biopsy. Clinical photos were also taken, with intra-examiner agreement at 90%. “Users” were defined as using smokeless tobacco in within the past month. 87% of subjects have never smoked.

Results: Subjects were 1,094 major and minor league players, coaches, and training staff. 70% of the subjects reported receiving regular dental care. 45% had never used smokeless tobacco or had used in the past but not more than once a month (nonusers). 13% had used smokeless tobacco previously at a frequency of greater than once a month but not within one month of the exam. 4% had used smokeless tobacco within the last month but not within the last week. 39% had used it within the last week, with 90% of these users using the day of the exam. Of the current week users, 46% had 214 mucosal lesions that were clinically characteristic of smokeless tobacco-induced leukoplakia, as well as 7 non users, 2 formers, and one current monthly user. 94% of the lesions affected mandibular teeth. There were no significant differences in users, non-users, or former users in PI, GI, recession, and AL in areas where lesions were not present, however where lesions were present, an average of 1 mm of recession exposing the root surface on the buccal was noted in mandibular sites.

Conclusion: No evidence was found correlating poor oral hygiene and gingivitis to development of oral lesions. Even under conditions of youth, minimal levels of inflammation, and regular hygiene care, oral sites where smokeless tobacco is used are at a major risk for mucosal lesions, gingival recession, and attachment loss.



Topic: Cocaine Periodontitis Article

Authors: Yukna RA

Title: Cocaine periodontitis.

Source: Int. J. Periodont. Restor. Dent. 11:72-79, 1991.

Type: clinical study

Rating: Fair

Keywords: Cocaine, Periodontitis


BG: Cocaine users can be from several socio-economic classes, including upper-middle class, with can snort, smoke “free base” form, or IV inject. Snorting cocaine is the most common form of administration; it can erode nasal septum and cause rhinitis or sinusitis. An alternative to snorting is rubbing cocaine on gingival tissues. Chronic cocaine users have increased caries incidence and periodontal disease, particularly ANUG-type lesions, increased bruxism, xerostomia, cervical abrasion, gingival laceration and TMJ disturbances.

P: Case reports (20 cases) of unusual periodontal destruction in documented cocaine users who rubbed the drug on their gingival tissue.

D: Patients present with atypical patterns of periodontal destruction or lack of response to routine initial periodontal therapy. Most cases resembled ANUG clinically but not in usual location or pattern. These patients might not even be interested in treatment, but are primarily there to rule out a serious condition, such as cancer. Cases presented ranged from aspirin-like burns to advanced ANUG destruction.

-Lesions can be physiologically explained with the presence of vasoconstriction, epithelial sloughing, ischemic necrosis, and local anesthesia.

BL: Dentists should be able to recognize the signs of cocaine use intra-orally. One of the cases received FGG twice with poor results probably due to localized ischemia and compromised vascularity.

Topic: Gingivostomatitis Article

Authors: Kerr, D

Tittle: Allergic gingivostomatitis (due to gum chewing).

Source: J. Periodontol 42:709-712, 1971

Type: Clinical Study

Rating: Good

Keywords: Gingivostomatitis, gum

Background: In 1968, Number of cases of unusual types of gingivostomatis appeared throughout the country.

Purpose: To gather information from cases of unusual gingivostomatitis those were potentially allergic reactions due to gum chewing.

Methods: 12 pts ranging in age from 11 to 58 years, 8 were F and 4 M for this study.

Clinical signs and symptoms: Pt presented with intense hyperemia of the free and attached gingiva, edema with stippling. Buccal and vestibular mucosa was hyperemic and very severe cases were eroded. Tongue involvement in all cases with loss of filliform papilla producing with very red clean surface. De-papillation of fusiform papilla, furrowed tongue with lateral indentation. Lips were atrophic, dry, scaly, cheilitis with some intensification of color, fissuring and maceration of the mucosa at the commissure with a perleche-type of lesion. All complaint of sore burning tongue and gingiva. Sudden onset of the dz presented from 3m-2ys with exacerbation and remission.

Lab finding: Hb, CBCT, blood chemistry, bacterial studies done.

Histo: mildly hyperplastic epi, leucocytic infiltration with alteration of basal lamina, heavy plasma cell infiltration of the submucosa

Tx and Results: Prior to referral to Dr Kerr, these pts were treated with multiple regimens: Vit B, C, iron, antibiotics includes mycostatin, kenalog, and Orabase, H2O2mouth washes, Phenergan syrup, benadryl, steroid cream. In reviewing dietary Hx, one thing common to all was habitual gum chewing. After discontinued chewing gum, immediate response became evident. Within 4 weeks, all pt had complete cure of tongue, lip and G changes.

Conclusion: It was apparent that there was some agent in chewing gum, which was the cause for contact Gingivostomatitis. If patient’s are not gum chewers but present with these symptoms, possible that they could suck on hard candy which also may contain the unknown allergen causing this reaction.

Topic: Minocycline-associated inta-oral soft tissue pigmentation Article

Authors: LaPorta N., Nikitakis N., Sindler A, Reynolds M

Title: Minocycline-associated intra – oral soft tissue pigmentation: clinicopathologic correlations and review.

Source: J Clin Periodontol 2005;32:119-122

Type: Case report

Rating: Fair

Keywords: minocycline; oral soft tissues; pigmentation

Background: Intraoral minocycline staining of alveolar bone and teeth has been well described in literature. Minocycline induced discoloration (MID) of oral soft tissues is less common and has been often attributed to staining of the underlying bone.

Purpose: To demonstrate the clinical and histopathologic characteristics of a case of MID intraoral pigmentation with actual soft tissue involvement.

Discussion: 45 y.o Caucasian female presented with pigmentation of the gingiva, lips, and nail beds of recent onset. PMH: initiation of minocycline treatment 6 months earlier for dermatological concerns. Biopsies were obtained from facial gingiva and lip. Histopathological exam revealed increased melanin/melanocytes in the epithelium and melanin/macrophages in the connective tissue. Nine months after pt discontinued treatment, there was a marked reduction of pigmentation.

Conclusion: Minocycline has the potential to induce discoloration of gingival and oral mucosa.

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


Topic: Lateral Periodontal Cyst Article

Authors: Filipowicz FJ, Page DG

Title: The lateral periodontal cyst and isolated periodontal defects

Source: J. Periodontol. 53:145-151, 1982.

Type: Clinical

Rating: Good

Keywords: lateral periodontal cyst

Purpose : Lateral periodontal cyst may be a possible cause of periodontal destruction. This study examined isolated periodontal defects for presence of cystic epithelium.

Method : Over a period of 4 years, 41 periodontal defects were selected for biopsy using the following criteria :

  • Radiographic and clinical probing revealed a lesion that was far more advanced in destruction than any other area of both arches.
  • Pulp vitality was established
  • No obvious local etiologic factors could be identified.
  • Surgical exposure revealed a rounded, sclerotic osseous compartment in the interdental bone adjacent to a root surface. This is in contrast to the narrow, angular defect often associated with periodontal disease.

Surgical removal and histological analysis was performed.

Result: A total of 41 biospies were examined with 20/41 meeting the criteria for Lateral Periodontal Cyst (LPC). In most cases, there was communication with the gingival crevice and probing revealed defects ranging from 6 to 10mm. 24/41 biopsies were obtained from the mandibular anterior region. The nature of the epithelium was reported as surface (9), crevicular (11), definitely cystic (10), probably cystic (10).

There are four possible explanations of the pathogenesis of isolated periodontal defects:

1) An LPC in the marginal periodontal structures could enlarge until it communicates with crevicular epithelium.

2) Crevicular epithelium could migrate apically until it communicates with an existing LPC

3) Apical migration of the crevicular epithelium could communicate with remnants of Herwig’s root sheath and initiate proliferation.

4) Pulpal injury creating damage in accessory canals in the coronal portion of the root.

Conclusion: LPC is a potential etiologic factor in the development of isolated periodontal defects. A conservative approach is recommended to LPC’s with special care to avoid sacrificing marginal alveolar bone. There is more potential for repair in a recently occurring or developmental lesion than in a slowly progressing, longstanding, chronic, destructive lesion. The regeneration of a viable, functional periodontal ligament is a distinct possibility.

  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?

Topic: Oral Bisphosphonates Article

Authors: American Dental Association

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

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

Type: Discussion

Rating: Good

Keywords: oral bisphosphonates, BRONJ, MRONJ

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

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

R: Recommendations:

  • Comp oral eval should be completed on all pts
  • Important to keep surgical procedures conservative, proper sterile technique, use of oral disinfectants
  • Dentist needs to inform pt taking oral bisphosphonates:
    • Very low risk (estimated 0.7 cases per 100,000 person-years’ exposure) of developing BON
    • Ways to minimize risk but not eliminate it
    • Good OH w/ regular dental care best way to lower risk
    • No diagnostic techniques to identify those at increased risk of developing BON
  • Pt needs to be informed of dental tx needed, alternative txs, how any tx relates to risk of BON, other risks associated with various tx options, and the risks of foregoing tx
  • Pt should be encouraged to consult physician about any health risks
  • When tx plan dictates that medullary bone and/or periosteum is going to be involved in multiple sextants, treat one sextant or tooth first. Allow for two month disease free follow-up, treating pt with antimicrobials before other sextants are treated
    • On basis of experience, majority of cases of BON arise w/in 2 months of dental procedure
    • If successful after 2 months with first sextant, tx may be accelerated to a normal pace
    • Sextant by sextant approach does not apply in emergency cases
  • Dentist should document the discussion of risks, benefits, and tx options with the pt and obtain pt’s written acknowledgement of that discussion and consent for tx
  • At this time, limited data regarding effects of implant placement in pts taking bisphosphonates. Before implant placement, the dentist and pt should discuss risks, benefits, and tx alternatives

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

Topic: Biphosphonate Therapy Article

Authors: American Association of Oral and Maxillofacial Surgeons

Title: Position paper on bisphosphonate-related osteonecrosis of the jaws. Advisory Task Force.

Source: J Oral Maxillofac Surg. 2007 Mar; 65(3):369-376

Type: Position paper

Rating: Good

Keywords: bisphosphonate-related osteonecrosis of the jaw, IV bisphosphonates, oral bisphosphonates

AAOMS Position Paper 2007

P: To provide: 1) Perspectives on the risk of developing BRONJ and the risks and benefits of bisphosphonates in order to facilitate medical decision-making of both the treating physician and the pt;

2) Guidance to clinicians regarding the differential diagnosis of BRONJ in pts with a history of tx with iv or oral bisphosphonates;

3) Guidance to clinicians on possible BRONJ prevention measures and management of pts with BRONJ based on the presenting stage of the dz

D: IV bisphosphonates (IVBPH) are used to cancer tx. They do not impact survival, but to improve quality of life (reduction in bone pain and skeletal complications). Oral bisphosphonates (OBPH) are approved to tx osteoporosis and osteopenia.

Definition: pts may have BRONJ if all of the following 3 characteristics are present:

1) current or previous tx with a bisphosphonate;

2) exposed, necrotic bone in the maxillofacial region that has persisted for more than 8 weeks;

3) no history of radiation therapy in the jaws.

Pts taking IVBPH have a cumulative incidence between 0.8-12% of BRONJ (retrospective studies).

Over 190 million OBP prescriptions have been dispensed worldwide. The incidence has been calculated to be 0.7/100,000 persons/years of exposure. Some have reported as high as 0.09-0.34% after extractions for pts treated weekly with alendronate.

Risk factors include drug-related risk factors (potency, duration), local risk factors (dentoalveolar sx, local anatomy, concomitant oral dz), and demographic and systemic factors (Caucasians, age).

Prevention of BRONJ: prior to IVBPH, all invasive dental procedures should be completed and optimal periodontal health achieved. If systemic conditions permit, bisphosphonate therapy should be delayed until the extraction site has mucosalized (14-21 days) or until there is adequate osseous healing. Pts with full or partial dentures should be examined for areas of mucosal trauma, especially along the lingual flange region.

Based on the experience of 2 clinicians with a total of 50 OBPH pts, the risk of developing BRONJ associated with OBPH, although exceedingly small, appears to increase when the duration of therapy exceeds 3 years. In pts that have taken OBPH for 3 years or more and, if systemic conditions permit, it has been proposed that discontinuation of OBPH for 3 months prior and 3 months after elective invasive dental sx may lower the risk of BRONJ. However, these pts need to be informed of the small risk of developing BRONJ. For pts that have not taken OBPH for at least 3 years and have no clinical risk factors, no alteration or delay for the planned sx is necessary.

If dental implants are placed, pts should be informed of possible future implant failure and/or osteonecrosis. It is advisable to contact their provider and suggest monitoring the pt, altering doses of the OBPH, drug holidays, or an alternative to OBPH therapy.

For pts taking an OBPH for less than 3 yrs and have also taken corticosteroids concomitantly, the prescribing provider should be contacted to consider a drug holiday for at least 3 months prior to sx. The OBPH should not be restarted until osseous healing is complete. This strategy is based on the hypothesis that concomitant tx with corticosteroids may increase risk of developing BRONJ and that a drug holiday may mitigate the risk.

When removing necrotic bone, it should be removed without exposing new, uninvolved bone. The extraction of symptomatic teeth within exposed, necrotic bone should be considered because it is unlikely that the extraction will exacerbate the established necrotic process.

Pts with established BRONJ should avoid elective dentoalveolar sx.

The effectiveness of hyperbaric oxygen therapy is undetermined.

Oncology pts benefit greatly from IVBPH therapy. Short-term discontinuation provides no benefit. However, long-term discontinuation may be beneficial (authors do not state what long-term is).

Topic: osteonecrosis of the jaw Article

Authors: Marx, R., Sawatari,

Title: Bisphosphonate-Induced Exposed Bone (Osteonecrosis/Osteopetrosis) of the Jaws: Risk Factors, Recognition, Prevention, and Treatment,

Source: JOMS 2005;63:1567-1575 DOI: 10.1016/j.joms.2005.07.010


Rating: good


Purpose: To review the possible mechanisms of painful exposure of bone in the mandible and maxilla of patients receiving bisphosphonates (pamidronate, zoledronate, alendronate) outline strategies to prevent it, review treatment options and report treatment outcomes.

Methods: Total of 119 patients. 76 consecutive individuals referred to University of Miami OMS Division and 43 patients documented by colleagues were reviewed. Type, dosage and duration of their bisphosphonate therapy, why it was indicated were recorded. 97 of these patients have been followed for 1 year or more.

Results: Type of drug prescribed: 26% pamidronate, 40.3% zoledronate, 30.2% pamidronate initially and later alendronate and 2.5% alendronate. 27.7% had a history of smoking.

Dosage and duration of therapy: Pamidronate: 90mg IV/3 weeks or 1 month. Zoledronate 4mg same intervals. Alendronate: 1 was taking 10 mg by mouth daily for 6 years and the other 2 were taking 10 mg by mouth daily for 3 and 2 years respectively.

Induction time for clinical bone exposure: Mean duration from the first dosage till the first recognition of exposed bone was 14.3 for pamidronate, 12.1 months for pamidronate/zoledronate, 9.4 months for zoledronate and 3 years for alendronate.

Indications for bisphosphonate therapy: 52.1% for multiple myeloma, 45.4% for bone metastasis and 2.5% for osteoporosis.

Findings: 31.1% asymptomatic bone exposure, 68.9% exposed bone and pain, 23.5% one or more mobile teeth 17.6% cutaneous fistula, mucosal fistula or bone exposed through the skin. 73.1% positive radiographic findings (osteolysis, osteosclerosis and widened periodontal membrane).

Location: 68.1% in the mandible, 27.7% in the maxilla and 4.2% simultaneously. Posterior mandible the most common site of exposure.

Medical Comorbidities: Patient’s had underlying malignant diseases, with negative systemic effects on nutrition, immune system and tissue homeostasis. History of chemotherapy and unquantifiable comorbidities alcohol, smoking and advanced age were noted.

Dental Comorbidities: The most common was periodontitis (84%). Dental caries in the area of bone exposure (28.6%) and abscess formation were noticed.

25.2% of cases occurred spontaneously without any apparent disease or trauma. 37.8% were related to tooth extraction, 28.6% to existing periodontal disease, 11.2% to periodontal surgery 3.4% to implant placement and 0.8% to apicoectomy surgery.

Mechanism: There are two theories explaining this complication:

  • The leading theory suggests it is caused by cessation of bone remodeling and turnover by the osteoclast inhibiting effect. This is the more possible theory.

  • The second theory is based only on experimental evidence that pamidronate and zoledronate also inhibit capillary neoangiogenesis. According to this theory, endothelial cell proliferation may be inhibited in the jaws, leading to loss of blood vessels and avascular necrosis.

Prevention: Urgent examination by a dentist and dental and surgical treatments completed before bisphosphonates therapy.

Close and ongoing communication between doctors.

These patients should not be considered candidates for implants (lack of epithelial attachment predisposes to bone exposure.

Antibiotic coverage for any invasive dental procedure (amoxicillin drug of choice, quinolones and metronidazole, erythromycin and metronidazole). Clindamycin alone should be avoided, it does not act against actinomyces. Bisphosphonate therapy should be deferred for 1 month after that.

Once the bisphosphonates therapy starts patients should be under surveillance. Tooth extraction should avoided at all if possible, root canal therapy and amputation od the crown would be preferred. Teeth with or 2+ mobility should be splinted rather than removed. In class III mobility or in presence of periodontal abscess it is possible that osteonecrosis is already present and extraction with antibiotic treatment is the only option.

Treatment of patients with osteonecrosis: Treatment should be directed at eliminating or controlling pain and preventing progression of exposed bone. Patients can live with it as long as it is not infected. Aside from rounding off sharp bony projection debridement surgery is not recommended. If infection occurs, it can be painful and lead to cellulitis and fistula. Long term and sometimes permanent course of antibiotics are prescribed (penicillin 500mg/4 times per day, metronidazole 500mg/3 times per day, or double antibiotic regimen: ciproflaxin or erythromycin ethylsuccinate and metronidazole).

Outcomes of management: 97 patients treated with this antibiotic regimen. 3.3% required a short hospitalization for a cellulitis and pain. 9.9% experienced episodes of pain that required adjustment of or addition to their antibiotic therapy and daily wound irrigations (hydrogen peroxide or chlorexidine 0.12%). 85% no need for chairside irrigations, no pain.

Conclusion: The benefits of IV bisphosphonates far outweigh the risk of developing bisphosphonate-induced exposed bone. The guidelines described help control the osteonecrosis of the bone.



Topic: Oral Bisphosphonate-induced osteonecrosis Article

Author: Marx, R. et al.

Title: Oral bisphosphonate– induced osteonecrosis: risk factors prediction of risk using serum CTX testing, prevention and treatment.

Source: J Oral Maxillofac Surg 65:2397 – 2410, 2007

Type: Review

Rating: Good

Keywords: Oral bisphosphonate-induced osteonecrosis, risk factors, diagnosis, serum, prevention, treatment

Purpose: to assess the risk and time course of oral bisphosphonate-induced osteonecrosis of the jaws


– Thirty cases of exposed bone in the mandible or maxilla that were diagnosed with bisphosphonate-induced osteonecrosis.

-Inclusion criteria included: the presence of nonhealing exposed bone that has persisted for more than 8 weeks in a patient who has received systemic bisphosphonate but has not received local radiation therapy.

-Patients were given a complete oral evaluation, a questionnaire about drug use history.

-Each patient signed consent for a blood draw of 1ml of whole blood, in order for a C-terminal telopeptide (CTX) bone turnover marker assessment to be completed as part of the patients regular osteoporosis follow up.

-Patients received non-surgical management with either 0.12% Chlorohexidine initially or 0.12% Chlorohexidine combined with an antibiotic; penicillin VK 500 mg qid or Levaquin 500 mg once daily if they were allergic to penicillin

-Advanced presentation cases were resolved with surgical debridement or resections guided by CTX values


-All cases occurred in women at a mean age of 64.8 years.

– 29 cases (96.7%) occurred in the posterior mandible while 1 case (3.3%) occurred in the maxilla

– 15 cases (50%) of osteonecrosis occurred spontaneously without a recognized initiating factor, the other 50% occurred as a result from an oral surgery procedure.

– 19 of the 30 patients (63.3%) reported pain associated with their bone exposure

– 90% of cases were caused by Fosamax and 10% by Actonel.

– All patients who developed osteonecrosis took an oral bisphosphonate for more than 3 years.

– 29 of the 30 cases (96.7%) occurring in the mandible. Only 2 cases of the 29 cases occurred in the anterior region (6.4%), 27 cases (93.1%) occurred in the molar region of the mandible

– CTX values improved at an average of 155.3 pg/mL over 6 months or a rate of 25.9 pg/mL each month.


Patients taking oral bisphosphonates for less than 3 years have little risk for osteonecrosis.

– CTX bone turnover interpretation: High risk=<100 pg/mL; Moderate risk=100 pg/mL to 150 pg/mL; Minimal risk= >150 pg/mL as minimal risk.

– A CTX test is highly recommended in any patients who were on oral bisphosphonates for greater than 3 years. If the CTX test is returned with a value of 150 pg/mL or greater, invasive oral surgical procedures can be accomplished with a minimal risk of osteonecrosis.

  • A drug holiday of 4 months to 6 months is recommended before a repeat CTX is accomplished. If the repeat CTX value is less than 150 pg/mL, it is recommended to extend the drug holiday with the agreement of the prescribing physician.


Topic: Bisphosphonate usage Article

Authors: Cartsos V, et al

Title: Bisphosphonate use and the risk of adverse jaw outcomes: a medical claims study of 714,217 people

Source: J Am Dent Assoc 2008; 139(1):23–30

Type: review

Rating: Good

Keywords: Adverse effect, alendronate, bisphosphonates, cancer, drug safety, medical claims, osteonecrosis of the jaw, osteoporosis, pamidronate, surveillance, zoledronic acid


Purpose: To analyze medical claims data from a large national sample to describe the prevalence and to quantify the risk of inflammatory or necrotic adverse bone effects in the mandible or the maxilla in two groups of patients: those with osteoporosis and those with cancer and also to determine if mode of administration and doses used is a significant predictor of adverse outcomes.

Methods: 714,217 subjects were identified through medical claims submitted to an insurance company as having osteoporosis or cancer. Bisphosphonate use was classified into three groups: None- no type of bisphosphonate therapy, Intravenous- pamidronate and/or zoledronic acid infusion, Oral- alendronate, etidronate, ibandronate, risedronate, or tiludronate. ICD-9 codes were used to determine outcome claims for inflammatory conditions of the jaws (ONJ), major jaw surgery due to necrotic or inflammatory indications and jaw surgeries due to malignancies. Statistical analysis was performed on the data collected.

Results: Patients with cancer tend to receive 4-12 times higher doses of bisphosphonates than those treated for osteoporosis. Mean age was 60, with women being much more numerous (as expected). Those with osteoporosis had a significantly reduced risk of developing adverse bone outcomes than those treated for cancer (4x higher in IV group for ONJ, 8x higher for jaw surgery due to necrotic or inflammatory condidtion).

Conclusion: Results of the study suggest that oral bisphosphonates do not carry an additional risk of osteonecrosis, whereas IV bisphosphonate therapy does. IV bisphosphonates are significantly and strongly associated with adverse outcomes in the jaws.

Topic: ONJ Article

Authors: Grbic, J et al

Title: Incidence of osteonecrosis of the jaw in women with postmenopausal osteoporisis in the Health Outcomes and Reduced Incedent With Zoendronic Acid Once Yearly Pivotal Fracture Trial

Source: . J Am Dent Assoc 2008; 139(1); 32-40

Type: clinical study

Rating: Good

Keywords: ONJ, postmenopausal, osteoporosis, Zoendronic acid


P: To determine the incidence of osteonecrosis of the jaws (ONJ) in women with post-menopausal osteoporosis (PMO) who received a once-yearly infusion of 5mg of zoledronic acid/placebo, to reduce the incidence of hip, vertebral and non-vertebral fractures.

M&M: After screening 3,889 patients were enrolled in the test group and 3,876 in the placebo group. A total of 3,409 in the test and 3,517 in the placebo group received at least two infusions and 3,105 in the test and 3,189 in the placebo group received all three infusions. Participants that were taken already bisphosphonates were allowed in the study after a 48-month wash out period. All participants received vitamin D and calcium supplementation. The committee (2 oral surgeons, 2 oral pathologists, and 1 periodontist) defined potential cases of ONJ as exposed bone in the maxillofacial area that had delayed healing for more than 6 weeks despite appropriate care.

R: There was no case of spontaneous ONJ. 101 of the test and 127 of the control group had adverse effects after administration (sinusitis and abscesses). These participants were further monitor after care was given. One subject of the placebo group developed ONJ. After treatment the area healed after 8 months. In the test group one subject (poorly controlled type II diabetes, end stage organ complications, retinopathy, neuropathy, no dental care) had ONJ after multiple extractions (13). The infection spread to the mandibular bone (osteomyelitis) and part of it was necrosed. After treatment with course of antibiotics there was complete resolution. No cases of ONJ in the subgroup of patient that used to take bisphosphonates prior to the study.

BL: In this study the occurrence of ONJ in participants who received zoledronic acid was similar to the placebo group. However, the test group demonstrated significantly reduced incidence of hip, vertebral and non-vertebral fractures, as well as the morbidity associated with them (pain, days of disability)

** Received financial support from Novartis Pharma AG. Some of authors are the employee of Novartis Pharmaceuticals and owns shares. Some are consultants. First author is on the advisory board of the company.

Topic: Oral bisphosphonate Article

Authors: Sedghizadeh, P

Tittle: Oral bisphosphonate use and the prevalence of osteonecrosis of the jaw: An institutional inquiry.

Source: J Am Dent Assoc. 2009 Jan; 140(1):61-66

Type: Clinical Study

Rating: Good

Keywords Oral bisphosphonate, osteonecrosis

Purpose: To investigate the prevalence of osteonecrosis of the jaw following bisphosphonate use.

Methods: Electronic medial record systems were queried to determine the number of patients with a history of alendronate use and all patients receiving alendronate who also were receiving treatment for ONJ.

Results: 208 patients were found to have a previous history of alendronate use for at least 12 months. 9 patients (4%) were found to have active ONJ and were being treated in the schools clinics. All 9 patients were female (age 63 – 80) and were taking 70mg of alendronate orally once a week. ONJ occurred due to denture trauma and tooth extraction.

Conclusion: Even short-term oral use of alendronate can lead to ONJ. This was the first large institutional study to report on ONJ and oral bisphosphonate use and further studies are needed.