What was Aggressive periodontitis previously known as? What is the current classification of AgP and what are the typical clinical findings?
Orban B, Weinmann JP : Diffuse atrophy of the alveolar bone (periodontosis). J Periodontol. 13:31-45, 1942.
Burmeister JA, Best AM, Palcanis KG, et al : Localized juvenile periodontitis and generalized severe periodontitis: Clinical findings. J. Clin. Periodontol. 11: 181-192, 1984.
Albandar JM, Brown J, Loe H. Clinical features of early-onset periodontitis. JADA 128:1393-1399, 1997. (Review)
Page RC, Altman LC, Ebersole Vandesteen GE, Dahlberg WH, Williams BL, Osterberg SK. Rapidly progressive periodontitis. A distinct clinical condition. J Periodontol. 1983 Apr;54(4):197-209.
Page RC, Bowen T, Altman L, Vandesteen E, Ochs H, Mackenzie P, Osterberg S, Engel LD, Williams BL. Prepubertal periodontitis. I. Definition of a clinical disease entity.J Periodontol. 1983 May;54(5):257-71.
Parameter on aggressive periodontitis. American Academy of Periodontology. J Periodontol. 2000 May;71(5 Suppl):867-9.
Califano JV Position paper: periodontal diseases of children and adolescents. Research, Science and Therapy Committee American Academy of Periodontology. J Periodontol. 2003 Nov;74(11):1696-704.
What is the prevalence and sex ratio of AgP in the US? Does it differ by race?
Califano H Title: Early onset periodontitis in the United States of America: Early onset periodontitis in the United States of America. J Periodontol. 62:608-616,1991
Brown LJ, Albandar JM, Brunelle JA, Löe H. Early-onset periodontitis: progression of attachment loss during 6 years. J Periodontol. 1996 Oct;67(10):968-75.
Discuss the bacterial etiology of AgP. Why do we prescribe antibiotics in the treatment of AgP?
Zambon JJ. Actinobacillus actinomycetemcomitans in human periodontal disease. J. Clin. Periodontol. 12:1-20, 1985. (Review)
Christersson LA, Slots J, Zambon JJ, Genco RJ : Transmission and colonization of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients. J. Periodontol. 56:127, 1985.
Shenker B, Tsai C, Taichman N: Suppression of lymphocyte responses by Actinobacillus actinomycetemcomitans (Aa). J. Periodontal Res. 17:462- , 1982.
Tinoco EMB, Sivakumar M, Preus HR. The distribution and transmission of Actinobacillus actinomycetemcomitans in families with localized juvenile periodontitis. J Clin Periodontol 25:99-105, 1998.
Christersson LA, et al : Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. I. Light, immunofluorescence and electron microscopic studies. J. Periodontol. 58:529-539, 1987.
Waerhaug J : Subgingival plaque and loss of attachment in periodontosis as evaluated on extracted teeth. J. Periodontol. 48:125-130, 1977.
Mullaly BH, Dace B, Shelburne CE, Wolff LF, Coulter WA. Prevalence of periodontal pathogens in localized and generalized forms of early-onset periodontitis. J Periodontal Res 35:232-241, 2000.
Fine DH, Markowitz K, Furgang D, Fairlie K, Ferrandiz J, Nasri C, McKiernan M, Gunsolley J. Aggregatibacter actinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis: longitudinal cohort study of initially healthy adolescents.J Clin Microbiol. 2007 Dec;45(12):3859-69. Epub 2007 Oct 17.
What antibiotic regimens are used in the treatment of AgP and what regimens are used?
Slots J, Rosling BG : Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline. J. Clin. Periodontol 10:465-486, 1983.
Van Winkelhoff AJ, et al : Metronidazole plus amoxycillin in the treatment of Actinobacillus actinomycetemcomitans associated periodontitis. J Clin Periodontol 16:128-131, 1989
Mandell RL, Socransky SS : Microbiological and clinical effects of surgery plus doxycycline on juvenile periodontitis. J. Periodontol. 59:373-379, 1988.
Discuss the success of non-surgical, surgical and regenerative periodontal therapy in AgP patients.
Lindhe J, Liljenberg B : Treatment of localized juvenile periodontitis: results after 5 years. J. Clin. Periodontol. 11:399-410, 1984.
Kornman KS, Robertson PB : Clinical and microbiological evaluation of therapy for juvenile periodontitis. J. Periodontol. 56:443-446, 1985.
Wennstrom A, et al : Healing following surgical and non-surgical treatment of juvenile periodontitis (JP). A 5-year longitudinal study. J. Clin. Periodontol. 13:869-882, 1986.
Christersson LA, Slots J, Rosling BG, Genco RJ. Microbiological and clinical aspects of surgical treatment of localized juvenile periodontitis. J. Clin. Periodontol. 12:465-476, 1985.
Evans GH, Yukna RA, Sepe WW, et al: Effect of various graft materials with tetracycline in localized juvenile periodontitis. J Periodontol 60:491-497,1989.
What are the inheritance patterns of AgP? Discuss the role of genetics in AgP?
Saxen L. Heredity of juvenile periodontitis. J. Clin. Periodontol. 7:276-,1980.
Marazita ML, Burmeister JA, Gunsolley JC, Koertge TE, Lake K, Schenkein HA. Evidence for autosomal dominant inheritance and race-specific heterogeneity in early-onset periodontitis.J Periodontol. 1994 Jun;65(6):623-30.
Melvin WL, Sandifer JB, Gray JL. The prevalence and sex ratio of juvenile periodontitis in a young racially mixed population. J Periodontol. 1991 May;62(5):330-4.
AgP associated with any defects in any immune cells or immunoglobulins?
Van Dyke TE, Horoszewiez HU, Genco RJ : The polymorphonuclear leukocyte (PMNL) locomotor defect in juvenile periodontitis. Study of random migration, chemokinesis, and chemotaxis. J. Periodontol. 53:682 - , 1982.
Mason JD, Thompson JJ, Yukna RA. Local immunoglobulin synthesis in juvenile periodontitis: Initial findings. J Dent Res 63:1211-1213, 1984.
Spindler SJ. Juvenile periodontitis. I. Demonstration of local immunoglobulin synthesis. J Periodontol. 1986 May;57(5):300-4
Van Dyke T, et al : Neutrophil function in localized juvenile periodontitis-Phagocytosis, superoxide production and specific granule release. J. Periodontol. 57:703, 1986.
Gronert K, Kantarci A, Levy BD, Clish CB, Odparlik S, Hasturk H, Badwey JA, Colgan SP, Van Dyke TE, Serhan CN. A molecular defect in intracellular lipid signaling in human neutrophils in localized aggressive periodontal tissue damage. J Immunol. 2004 Feb 1;172(3):1856-61.
Is AgP associated with altered caries levels and altered root surfaces?
Fine DH, Goldberg D, Karoi R. Caries levels in patients with juvenile periodontitis. J. Periodontol. 55:242-246, 1984.
Waldrop TC, Hallmon WW, Mealey BL. Observations of root surfaces from patients with early-onset periodontitis and leukocyte adhesion deficiency. J Clin Periodontol 22:168-178, 1995.
What was Aggressive periodontitis previously known as? What is the current classification of AgP and what are the typical clinical findings?
Topic: Alveolar bone atrophy
Authors: Orban B, Weinmann JP ARTICLE
Title: Diffuse atrophy of the alveolar bone (periodontosis)
Source: J Periodontol. 13:31-45, 1942.
Type: discussion
Rating: Good
Keywords: alveolar bone, atrophy, periodontosis
P: To discuss diffuse atrophy of alveolar bone in periodontosis
R: Discussion based on findings from a human jaw, where diffuse atrophy was diagnosed before histological sectioning.
According to clinical observations, the earliest finding of diffuse atrophy of alveolar bone is migration of teeth. This occurs without inflammation in the periodontal tissues. Subsequently, the teeth loosen, pocket formation and inflammation area secondary factors.
Histopathological findings can recognize 3 different stages that follow a sequence:
Degeneration of principal fibers and widening of PDL.
The 1st consequence of this process is probably the cessation of cementum formation. Simultaneously, resorption of the alveolar bone sets in, due to lack of functional stimuli from the tooth, as well as an increase in tissue pressure, resulting from the accumulation of edema and the proliferation of capillaries. The increase of tissue pressure also results in tooth migration. Intrinsic factors should be considered primarily as a cause for the initiation of pathologic events. Such factors are dysfunction of the endocrine glands, toxins, metabolic disturbances, dietary deficiencies, etc. The preference of the disease for a certain localization may be due to functional insufficiency of the suspensory apparatus. No inflammation is seen in this stage and no proliferation of the epithelial attachment. Dissolution of CT- “dermolysis” seldomly noticed clinically. Causes: trauma, toxic origin, or both. Repair is possible at any time.
Migration of epithelial attachment (EA) along affected cementum and onset of inflammatory reaction.
Migration possible after fibers have lost their attachment to the cementum. Probably, cementoblasts are affected before any other changes can occur. Slight cell infiltrate (plasma cells) into the CT accompanied by numerous branching, thin capillaries. Traumatic changes at apex and distal surfaces-resembling traumatic occlusion. Epithelial rests in the PDL appear enlarged. Where epithelial attachment shows extensive migration, the chronic inflammatory reaction may be due to toxic influences, originating in the sulcus.
Epithelial attachment separates from root and deep gingival crevices develop. Inflammation increases, causing more bone resorption, large portions of the supporting tissue destroyed and even normal occlusal forces, cause secondary trauma results. Most frequently observed clinically. The most characteristic feature is the development of the deep pocket(s), with the symptoms of inflammation.
BL: Periodontosis is caused by atrophy of PDL, epithelial attachment migration, then pocket formation. Trauma must be eliminated as a cause but must be included as a predisposing factor.
Topic: Aggressive periodontitis
Authors Burmeister JA, Best AM, Palcanis KG ARTICLE
Title: Localized juvenile periodontitis and generalized severe periodontitis: Clinical findings.
Source: J. Clin. Periodontol. 11: 181-192, 1984
Type: Clinical study
Rating: Good
Keywords: Aggressive periodontitis, juvenile periodontitis
Purpose: To determine sex, race and age relationships to advanced periodontitis in an available sample of adolescents and young adults and to determine the relationship of plaque and gingival inflammation to the extent and severity of the disease
Method: 103 healthy patients (10-32 years old) with localized Juvenile periodontitis (LJP) or generalized severe periodontitis (GSP) were analyzed for interrelationships of sex, race, age, and clinical findings (PI, GI, PD, recession, BOP, Al).
LJP (46 pts): Localized pattern of severe periodontal destruction limited to first molar and/or incisor teeth up to 2 additional teeth.
GSP (57 pts): Generalized pattern of severe destruction with attachment loss of at least 5 mm at 8 or more teeth, at least 3 of which were not first molars or incisors.
Each subject was examined at 4 sites per each tooth: mesial, facial, distal and lingual surfaces.
Results:
LJP group had marked destruction limited to first molars and incisors.
Mean AL values were greater for GSP in the first molar and incisors.
Age range was the same for LJP and GSP but the mean age for GSP was SS greater.
Both GSP and LJP had 2:1 female: male ratio.
LJP had 3.1 more black than whites and GSP had equal number.
For both GSP and LJP affected sites had SS higher PI and GI than non-affected sites and this showed a positive relationship with AL.
There was no relationship btw age and extent or severity in LJP.
Age was SS related in GSP to extent and possibly to severity.
Conclusion: LJP and GSP are significantly associated with plaque and gingival inflammation levels. In the GSP there is also a positive correlation between severity and age when plaque level was a covariate.
Topic: Early onset periodontitis
Authors: Albandar JM, Brown J, Loe H. ARTICLE
Title: Clinical features of early-onset periodontitis.
Source: JADA 128:1393-1399, 1997.
Type: National survey
Rating: Good
Keywords: early onset periodontitis, aggressive periodontitis
Purpose: To assess prevalence of Early Onset Periodontitis in U.S adolescents and describe some clinical features that can help identify patients at higher risk developing the disease.
Methods: Screened 14,013 students 13-17 years old for oral health, assessing CAL loss, BOP, and subgingival calculus at the mesio-buccal and mid-buccal surfaces of all permanent teeth except 3rd molars. EOP was defined as CAL loss of 3mm or more on 1 or more teeth. EOP pts divided into 3 groups: localized (one first molar or central incisor), generalized (several teeth + more than 2 canines, PM or molars) and incidental (the subjects who did not meet the criteria of the previous two groups, mostly 1-3 teeth with <3 teeth missing).
Results: White adolescents had lowest level of EOP, 0.05%, 0.01% and 1.2% for generalized, localized, and incidental. Black (1.6%, 1% and 7.5%) and Hispanic (0.3%, 0.2% and 4.4%) adolescents had higher prevalence. Slightly more males than females (3.7 vs. 3.0%) had EOP. The prevalence was higher in the 16-17 year old group (4%) than the 13-15 year old group (2.7%). So EOP is age-dependent and may begin on or after ages 12-13 years. Patients with EOP had significantly higher sites with subgingival calculus (especially generalized group) than subjects with no periodontitis and noticeably more caries (7.7 surfaces untreated vs 5.8 surfaces), as well as BOP and missing teeth.
Conclusion: EOP affects 10% of Black, 5% of Hispanic and 1.3% of white U.S. adolescents between ages of 13-17 years old when using a threshold of CALoss >3 mm. If left untreated, EOP may progress rapidly, causing pronounced tooth loss. Clinical exam with a perio probe and radiographic eval should be done for these patients.
Cr: Prevalence may be higher since they only measured two sites per tooth. True prevalence may be 13.3% black, 6.65% hispanic and 1.73% white, if adjusted by a factor of 0.33% (not sure where they got the 0.33% from)
Topic: Aggressive Periodontitis
Authors: Page RC ARTICLE
Title: Rapidly progressive periodontitis. A distinct clinical condition
Source: J Periodontol. 1983 Apr;54(4):197-209.
Type: Discussion
Rating: Good
Keywords: rapidly progressive periodontitis
Purpose: To establish rapidly progressive periodontitis as a clinical entity.
Discussion: 7 case reports were used to provide diagnostic criteria, describe clinical, radiographic and histologic features, demonstrate a relationship among this form of periodontitis and serum antibodies and defects in host’s mechanisms and methods of treatment.
The first case was a 36-year old Caucasian female. She reported problems with the gums since she was in high school but never had periodontal treatment in the past. She was referred to the hospital because of general malaise, depression, loss of appetite, loss of weight and advanced periodontitis with unusual features. Clinically and radiographically she has significant amount of bone loss and recession mainly in the posterior teeth with no overt acute inflammation. Blood was drawn, monocyte chemotaxis was normal but neutrophil chemotaxis was significantly depressed. After SRP and systemic administration of TTC 250mg qid for 2 weeks, systemic manifestations improved rapidly and the patient was discharged from the hospital on the 5th day.
The rest of the cases also described a similar treatment was followed (in some cases included occlusal adjustment if indicated) with similar results. Other findings included significant serum antibodies against B. gingivalis, increased or reduced antibodies against A. a., enhanced neutrophil chemotaxis, unremarkable medical history.
Rapidly progressive periodontitis appears to be a distinct entity on the basis of the features listed in the table below.
Several systemic diseases and syndromes predispose to periodontitis (diabetes mellitus, Down’s syndrome, Papillon-Lefevre, Crohn’s disease, neutropenia). The feature all of these diseases have in common is defective neutrophil numbers and/or function.
Based on authors’ observations, individuals with rapidly progressive periodontitis who manifest defects in blood cells or serum but no other systemic diseases, appear to respond very well in treatment with SRP combined with antibiotics.
Topic: juvenile periodontitis
Author: Page RC, Bowen T, Altman L, Vandesteen E, Ochs H, Mackenzie P, Osterberg S, Engel LD, Williams BL NO ARTICLE
Title: Pre-pubertal periodontitis. I. Definition of a clinical disease entity.
Source: J Periodontol. 1983 May;54(5):257-71.
Type: Case series/discussion article
Rating: Good
Keywords: juvenile periodontitis, histology, aggressive periodontitis
Purpose: To define pre-pubertal periodontitis as a clinical entity, establish diagnostic criteria, demonstrate clinical, radiographic, and histological features, documented progression and explore methods of treatment.
Materials and methods:
· 5 case reports, three patients with localized and two patients with generalized form of disease. Cases were discussed and used to define pre-pubertal periodontitis as a clinical entity.
Discussion: Pre-pubertal 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: Aggressive Periodontitis
Authors: American Academy of Periodontology NO ARTICLE
Title: Parameter on Aggressive Periodontitis
Source: J. Periodontol. 2000 May; 71 (5 Suppl): 867-9
Type: Clinical study
Rating: Good
Keywords: Aggressive periodontitis, Aa, neutrophil
P: Discussion paper on Aggressive Periodontitis
D:Definition: Encompasses distinct types of periodontitis that affect people who, in most cases, otherwise appear healthy. It tends to have a familial aggregation and there is a rapid rate of dz progression. It may by localized (usually circumpubertal onset with perio damage to 1M and incisors) or generalized (usually affects people under 30, generalized interproximal ALoss affecting at least 3 permanent teeth other than 1M and incisors).
-Secondary features: microbial deposits inconsistent with severity of destruction; progression of attachment and bone loss may be self-arresting
-Generalized aggressive:
-Associated with Aa and Pg as well as neutrophil function abnormalities.
-General medical evaluation may determine if there is any systemic involvement.
-Initial therapy alone is often ineffective. However, in the early stages of dz, lesions may be treated with SRP and antimicrobial therapy.
-If primary teeth are affected, eruption of permanent teeth should be monitored to detect possible ALoss.
-Evaluation and counseling of family members may be necessary.
Considerations:
Consultation with the patient’s physician may be indicated to coordinate medical care in conjunction with periodontal therapy. Modification of environmental risk factors should be considered.
Early stages of disease, lesions may be treated with adjunctive antimicrobial therapy combined with scaling and root planing with or without surgical therapy.
The long-term outcome may depend upon patient compliance and delivery of periodontal maintenance at appropriate intervals, as determined by the clinician.
If primary teeth are affected eruption of permanent teeth should be monitored to detect possible attachment loss.
The desired outcomes of periodontal therapy in patients with aggressive periodontitis should include:
1. Significant reduction of clinical signs of gingival inflammation;
2. Reduction of probing depths;
3. Stabilization or gain of clinical attachment;
4. Radiographic evidence of resolution of osseous lesions;
5. Progress toward occlusal stability;
6. Progress toward the reduction of clinically detectable plaque to a level compatible with periodontal health.
Areas where the periodontal condition does not resolve may occur and be characterized by the presence of:
1. Persistent gingival inflammation
2. Persistent or increasing probing depths;
3. Progressive loss of clinical attachment;
4. Persistent clinically detectable plaque levels not compatible with periodontal health;
5. Increasing tooth mobility.
Topic: aggressive perio
Authors: Califano JV; NO ARTICLE
Title: periodontal diseases of children and adolescents.
Source: J Periodontol. 2003 Nov;74(11):1696-704. DOI: 10.1902/jop.2003.74.11.1696 Research, Science and Therapy Committee American Academy of Periodontology.
Type: Position paper
Rating: good
Keywords: periodontal disease, aggressive periodontitis, periodontal disease in children and adolescents.
Purpose: A summary of the current state of knowledge about periodontal diseases in children and adolescents.
Discussion: Clinically distinct periodontal infections that can affect young individuals include:
1) Dental plaque-induced gingival diseases:
It is characterized by the presence of inflammation without detectable bone loss. Microbiology is not completely characterized.
It can be modified by systemic factors associated with the endocrine system (gonadotropic hormone during the onset of puberty, insulin levels in diabetic patients), however gingival condition usually responds to treatment.
2) Periodontitis: Chronic periodontitis, aggressive periodontitis, periodontitis as a manifestation of systemic diseases:
Children and adolescents can have any type of periodontitis. Aggressive periodontitis is more common in this group than in adults.
Primary features: History of rapid attachment and bone loss with family aggregation.
Secondary features: Phagocytic abnormalities and hyperresponsive macrophage phenotype. It can be localized or generalized.
In LAP patients have interproximal AL on at least two permanent first molars and incisors and AL on no more than two teeth other than these. GAP patients exhibit generalized interproximal attachment loss including at least three teeth that are not first molars and incisors. Some retrospective studies suggest that bone loss around primary teeth can be early finding of LAP.
Prevalence of LAP is generally low (0.2%) but greater in African American populations (2.5%). Many reports state that very little supragingival plaque and calculus is found in patients with LAP, other that the amounts are comparable to those found to patients with other periodontal diseases. Highly virulent strains of Aa in combination with Bacteroides-like species are important in the etiology of LAP.
Functional defects of the neutrophils are possible to play a role in the susceptibility of individuals with LAP.
GAP can start at any age and affects the whole dentition. Patients with GAP have heavy accumulation of plaque and calculus. Prevalence in adolescents is 0.13% High percentages of non-motile, facultatively anaerobic, Gram-rods including P. gingivalis are found in affected subgingival sites. Neutrophils often exhibit suppressed chemotaxis, which suggests a relationship between the two variants of aggressive periodontitis.
Alterations in immunologic factors such as Ig are known to be present in aggressive periodontitis. IgG produced as a response seem to have a protective action. This response is modified by patients’ genetic background and environmental factors (smoking, bacterial infection).
Combination of surgical and non-surgical treatment on conjunction with antibiotic therapy is recommended for LAP treatment. Most successful antibiotics reported are the tetracyclines, sometimes prescribed sequentially with metronidazole. Amoxicillin in combination with metronidazole is also used.
GAP does not always respond well to conventional mechanical therapy or to commonly used antibiotics. Alternative antibiotics may be required after lab tests of plaque samples, when patients don’t respond to standard periodontal therapy.
Chronic periodontitis in children and adolescents can be localized (less than 30% of dentition affected) or generalized. It is characterized by slow to moderate progression, and the severity can be mild (1-2mm AL), moderate (3-5mm AL) or severe (more than 5mm AL).
Papillon-Lefevre syndrome, cyclic neutropenia, agranulocytosis, Down’s syndrome, hypophosphatasia and leukocyte adherence deficiency are associated with chronic periodontitis. Diabetes is a significant modifier of all forms of periodontitis.
Periodontitis as a manifestation of a systemic disease is rare and often begins at the time of eruption of the primary teeth up to the age of 4 or 5. Affected sites harbor elevated percentages of putative periodontal pathogens such as Aa, P. intermedia, E. corrodens and Capnocytophaga. Treatment in children has been reported to include surgical and non- surgical mechanical debridement and antimicrobial therapy.
3) Necrotizing periodontal diseases:
Varying frequency, low in North American and European children and greater in certain populations of developing countries.
Most significant findings are the presence of interproximal necrosis and ulceration and the rapid onset of gingival pain.
High levels of P. intermedia and spirochetes. Factors that predispose children to NPD include viral infections, malnutrition, emotional stress, lack of sleep and a variety of systemic diseases.
Treatment involves mechanical debridement, antibiotics if the patient is febrile, oral hygiene instructions, and careful follow-up.
What is the prevalence and sex ratio of AgP in the US? Does it differ by race?
Topic: Early onset periodontitis
Title: Early onset periodontitis in the United States of America
Source: J Periodontol. 62:608-616,1991
Type: Survey
Rating: Good
Keywords: Periodontitis, juvenile/epidemiology; oral health surveys; adolescents.
Purpose: to report the first estimates of prevalence of juvenile periodontitis based on a national probability sample of school children in the USA.
Materials and Methods
-A national survey of US children from kindergarten through grade 12 conducted by the National Institute of Dental Research (NIDR) from 1986-1987
-The sample consisted in all public and private schools in the US except Alaska and a multi-stage probability sample was selected representing 45 million children.
- A total of 40,694 students were examined.
-Staff consisted of 13 coordinated teams. Staff was trained and calibrated by NIDR.
-The NIDR probe was used to measure the following: 1-loss of periodontal attachment (LA)
2-Recession; 3-Distance from FGM and bottom of sulcus
-Gingival assessment at each buccal and mesial site was measured for absence or presence of BOP.
-A single calculus score was recorded for each tooth indicating presence or absence of calculus.
-Radiographs were not taken.
- A total of 11,007 individuals ages 14-17 years received a periodontal assessment and were used in this analysis.
Age, gender, race, school grade, urban/rural, and region of the country were identified for each individual. These were included in the distributions of the demographic characteristics table.
-Three groups of adolescents were classified:
1) Localized Juvenile Periodontitis: at least one 1st molar and 2 incisor or 2nd molar
and 2 or fewer cuspid or premolars had >3mm LA
2) Generalized juvenile Periodontitis: if 4 or more teeth had >3mm LA and at least 2
affected teeth were 2nd molars, cupids or premolars
3) Incidental loss of periodontal attachment: Didn’t meat other inclusion criteria and
had 1 or more teeth with >3mm LA
Results
-Prevalence: of the 11,007 students studied, 50 had localized juvenile periodontitis, 14 general juvenile periodontitis, and 175 had incidental LA.
-Nationwide, 0.53% of 13 million were estimated to have LJP, 0.13% to have GLP and 1.61% Incidental LA, In total 2.27% of all adolescents exhibited advanced loss of attachment.
-Males were clearly more likely (4.3 to 1) to have generalized juvenile periodontists than females. Gender associations were more complicated for localized juvenile periodontitis b/c gender interacted with race.
-Black males were 2.9 times as likely to have LJP as black females.
-White females were more likely than white males to have the disease by about the same odds.
-Hispanic children were 2.4 times more likely to have LJP than non-Hispanics.
Discussion
-The prevalence of periodontitis did not increase greatly with age among these adolescents.
-Juvenile periodontitis was more prevalent among blacks.
-Blacks were 15 times more likely than whites to have LJP, and even greater odds with GJP
-Black males were at much greater risk to have all forms of juvenile periodontitis than white males and that black females in region IV are also at higher risk
Topic: Aggressive periodontitis
Authors: Brown LJ, Albandar JM, Brunelle JA, Löe H ARTICLE
Title: Early-onset periodontitis: progression of attachment loss during 6 years
Source: J Periodontol. 1996 Oct;67(10):968-75
Type: longitudinal study
Rating: Good…
Keywords: adolescents, follow-up studies, periodontitis, early-onset, periodontal attachment
Purpose: To study the clinical characteristics and pattern of progression on early-onset periodontitis and the changes in the extent and severity of the condition over a 6-year period.
Methods: 91 patients (51 males, 40 females, 72 African americans, 6 Hispanics, and 13 Whites) with early onset attachment loss were re-examined 6 years after an initial exam and reclassified as having localized juvenile periodontitis (LJP), generalized juvenile periodontitis (GJP), incidental attachment loss (IAL), or no attachment loss.
LJP- at least one first molar and one incisor or second molar, and two or fewer cuspids or premolars had ≥ 3 mm loss of attachment.
GJP- if LJP criteria were not met and if 4 or more teeth had ≥ 3mm loss of attachment and at least 2 affected teeth were second molars, cuspids, or premolars.
IAL- did not meet the criteria for LJP and GJP but had ≥ 3mm loss of attachment in one or more teeth.
Results: Most patients showed an increase in number of sites with attachment loss. In all subjects, incisors had the worst increase of attachment loss followed by molars and then premolars. Of the 34 subjects who were classified as LJP at baseline, only three received treatment but with no details available. 62% continued to have LJP, 35% had GJP, and only one patient had complete resolution. Of the 11 patients with GJP, only one was reclassified as LJP and one reclassified as having incidental attachment loss (only had 1 lower incisor and 1 upper canine with attachment loss). Of the 46 subjects with incidental attachment loss, 28% developed either LJP or GJP, 41% remained as incidental attachment loss group, and 31% had complete resolution. The highest mean annual attachment loss was found in GJP (0.2 mm/ year) followed by LJP (0.08 mm/ year) and Incidental attachment loss (0.02 mm/ year).
Conclusion: It seems that patients with attachment loss at an early age (13-17 years) tend to worsen with time. The difference between LJP and GJP is the number and type of teeth involved and two classifications progress similarly with some cases of LJP developing into GJP.
Discuss the bacterial etiology of AgP. Why do we prescribe antibiotics in the treatment of AgP?
Topic: Actinobacillus actinomycetemcomitans
Authors: Zambon JJ. ARTICLE
Title: Actinobacillus actinomycetemcomitans in human periodontal disease
Source: J. Clin. Periodontol. 12:1-20, 1985. (Review)
Type: Review
Rating: Good
Keywords: A. actinomycetemcomitans, morphological, biochemical, serological, periodontitis.
This paper reviews the morphological, biochemical and serological characteristics of A.a, evidence about its virulence and pathogenesis, and the fact that it is the primary periodontopathogen of LJP.
Background: Actinomycetemcomitans was isolated from cervicofacial actinomycosis. “Actinobacillus” refers to the internal star shape morphology of its bacterial colonies on solid media.
Morphological biochemical and Serological characteristics:
A. Actinomycetemcomitans (A.a.) grows poorly in air but grows well in 5% CO2 in air or under anaerobic conditions. A.a bacterial cells are non-motile cocci which can occur singly, in pairs or in small clumps. Ultrastructural studies reveal features typical of gram negative organisms including an outer cytoplasmic membrane, a periplasmic space and an inner cytoplasmic membrane.
Biochemical characteristics: fermenative, non hemolytic, indole negative micro-organism that produces catalase.
The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose, and into 3 serotypes on the basis of heat stable, cell surface antigens.
Serotypes a and b are the most common serotypes found in oral cavity, while serotype c comprises only 10% of A.a human oral isolates. A.a serotypes a and b approximately equal prevalence, serotype b is increased in localized juvenile periodontitis.
A.a. in Human Periodontal disease:
Recent research strongly implicates A. actinomycetemcomitans in the etiology of localized juvenile periodontitis.
A.a is primary ecologic niche is the oral cavity. It can be found in dental plaque, in periodontal pockets, and in buccal mucosa in up to 36% of the normal population. This organism can seed from these sites to other parts of the body and cause serious infections (including brain abscesses or endocarditis). The most important site of extraoral A.a infection is the heart and it is associated with bacterial endocarditis.
There is significant evidence that implicates A.a as the primary organism in the etiology of LJP:
Increased prevalence of the organism in almost all LJP patients and their families
LJP patients exhibit elevated antibody levels to A.a in serum, saliva and GCF. Mainly, increased IgG response that inhibits the spread of A.a to uninfected sites.
Positive correlation between elimination of A.a from sub-g plaque and resolution of juvenile periodontitis lesions.
Histopathologic evidence shows that A.a invades the CT in LJP patients. A.a can not be completely eradicated from periodontal pocket by mechanical debridement alone. A combination of systemic antibiotics and conventional periodontal therapy appears to be the optimal treatment.
The pathogenic products of A.a
Facilitate its adherence to mucosal surfaces,
Inhibit host defense mechanisms
Leukotoxin: heat labile protease sensitive product which lyses human PMNs, human monocytes and the neutrophil -like promyelocytic HL -60 cell line by causing pertubations in the cell membrane. Leukotoxin may impair local host defense mechanisms by destroying significant numbers of PMNs while releasing hydrolytic enzymes which can exacerbate local tissue destruction.
Cause tissue destruction
LPS- Lipopolysaccharide: macrophage activation, platelet aggregation, it is a potent mitogen that can cause bone resorption.
Collagenase produced by A.a in combinations with collagenase from leukotoxin lysed neutrophils may account for a significant portion of tissue destruction
Epitheliotoxin: capable of causing tissue destruction, assists A.a penetrating sulcular epithelium and gaining access to underlying connective tissue.
Topic: Aggressive periodontitis
Authors Christersson LA, Slots J, Zambon JJ, Genco RJ ARTICLE
Title: Transmission and colonization of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients.
Source: J. Periodontol. 56:127, 1985.
Type: Clinical study
Rating: Good
Keywords: Aggressive periodontitis, juvenile periodontitis
Purpose: To study the transmission of Aa through a periodontal probe.
Method: 3 pts with LAgP (12, 18, and 20 years old) had microbiologic sampling of subgingival plaque for detection of Aa using paper points in deep pockets(PD>6mm) and healthy sites (PD<3mm). Periodontal probe (Michigan probe) inserted into the diseased sites, probe was sampled to check for Aa, other probes inserted into deep pockets and then transferred to the healthy sites which were also probed with either gentle or excessive force, healthy sites sampled before and after, healthy sites were irrigated with saline after sampling, resampling weekly from 3 - 12 weeks. This procedure was performed 30 times, using 19 different healthy sites. 16 transmission attempts were made using very gentle probing forces, while 9 attempts were made with probing forces sufficient to induce bleeding. Controls included 6 healthy gingival sites, which were gently probed with instruments contaminated with microorganisms from healthy gingival sulci in the same individual known to be free of A. actinomycetemcomitans.
Results:
All deep pockets showed A.a.
Virtually all probes inserted into deep pockets became contaminated
28/30 healthy sites showed A.a. after probing with contaminated probes (directly sampled after probing).
Only two sites were still infected by the 2nd week and none were infected at 3 or 12 weeks
Conclusion: The periodontal probe can transfer Aa from diseased to healthy sites, this appears to be transient possibly due to mechanisms within the host that limit the spread of Aa in LAgP patients. Aa is eliminated from the recipient sites in 3 weeks.
Topic: A. actinomycetemcomitans
Authors: Shenker B, Tsai C, Taichman N NO ARTICLE
Title: Suppression of lymphocyte responses by Actinobacillus actinomycetemcomitans (Aa
Source: J. Periodontal Res. 17:462- , 1982.
Type: Clinical
Rating: Good
Keywords: A. actinomycetemcomitans, A.a., lymphocytes
Purpose: To assess the immunosuppressive effects of A.a. and show that exposure to human lymphocytes to A.a. extracts suppress the T-cell response.
Methods: Lymphocytes were isolated from heparinized blood of healthy donors. The cells were exposed to soluble extracts of A.a. Lymphocyte cell cultures were established and mitogenic and antigenic responses were assessed following a 3 day and 5 day incubation respectively. After 6 days the generation of anti-red blood cell -termed plaque forming cells (PFC)- from human B-cells in response to pokeweed mitogen (PKM) was determined by hemolysis in gel.
Results: A.a. can alter the lymphocyte responses to PKM and the streptococcal antigen SKSD, as well as inhibit the responses of PHA (a mitogen that acts on T cells) and SKSD in a dose dependent manner. The A.a. leukotoxin was derived from all strains of A.a. and is able to suppress leukocyte responsiveness to the same extent. There was no effect in cell viability. Y4 strain has effect on B-cells in a dose dependent inhibition of anti-RBC plaque forming cell response to PWM.
Conclusion: Sonic extracts prepared from A.a. are capable of suppressing both B and T cell functions which may be mediated by common mechanism, contributing to the pathogenesis of the disease. The A.a. lymphocyte suppressive factor may play an important role in the etiology of A.a. infection and the resulting disease, by causing a state of depressed immune function in the patient, which may enhance the pathogenicity of A.a. itself or that of other opportunistic pathogens.
Topic: Aggressive Periodontitis
Authors: Tinoco EMB, Sivakumar M, Preus HR ARTICLE
Title: The distribution and transmission of Actinobacillus actinomycetemcomitans in families with localized juvenile periodontitis.
Source: J Clin Periodontol 25:99-105, 1998.
Type: Clinical
Rating: Good
Keywords: A.a., juvenile periodontitis
Purpose: To describe the acquisition or transmission of A.a. within native Brazilian families where knowledge and practice of general and oral hygiene were low.
Materials and methods: 25 LJP subjects and family members (78 total) were sampled for the presence of A.a. 10 families met all the requirements to enter the study. They had at least one Aa positive proband and one additional positive family member living in the household. OH habits were not established and none of the participants had access to dental services. PI and GI were assessed. Sub-g bacterial plaque was obtained from all subjects by placing on paper point for 10sec into the pockets. Isolates of Aa were cultured. DNA from sub-g Aa from each proband and family members were amplified by PCR.
Results: Of 10 selected families (78 subjects), 22 of examined family members carried Aa. 6/10 families had at least 1 parent positive for A.a and 15/26 siblings (57%) were colonized by Aa. 18/43 family members had periodontitis, including 4 with LJP. Low OH was shown among the probands and family members. Arbitrary PCR in this population showed only 3/36 children who were positive for Aa were colonized by the amplitype as one of the parents, and only 4 families had a sibling carrying the same strand of Aa as the proband. None of the spouses were found to have the same amplitype if both were Aa positive.
Conclusion: 35% of the parents and 57.7% of the siblings in the LJP population harbored Aa. In families with low socioeconomic and educational levels and poor OH, transmission of Aa is a more common incident than in American population with established OH habits. Comparison of the PCR generated amplitypes showed that there was a wide distribution of amplitypes among the probands and immediate relatives. No clear transmission paths were observed in the specific population, and it may be speculated that at least some forms of LJP in this particular population may be the result of an exogenous infections outside the family.
Topic: juvenile periodontitis
Author: Christersson LA, et al ARTICLE
Title: Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. I. Light, immunofluorescence and electron microscopic studies.
Source: J. Periodontol. 58:529-539, 1987
Type: Histological study
Rating: Good
Keywords: juvenile periodontitis, histology, aggressive periodontitis, A. a
Purpose: To determine prevalence and gingival localization of A.a. in periodontal lesions of juvenile periodontitis (JP) patients.
Materials and methods:
12 patients with JP (10-36 years old) in good health.
Gingival biopsies obtained from one to seven periodontal lesions in each patient, with a total of 35 gingival biopsies at the time of periodontal surgical treatment (phase I already completed).
Control biopsies taken from 2 healthy patients, 1 severe adult periodontitis patient, and 1 monkey.
Prior to biopsies, plaque samples taken with paper points to isolate and culture A.a.
Biopsies processed and examined using light microscope (LM) and transmission electron microscope (TEM). Immunofluorescence (IF) microscopy used to localize A.a. in the gingival sections.
Results:
Bacteria culture: Subgingival A.a. specific antigen in 11/12 JP patients, at 91% of the periodontal lesions (2 of 3 sites negative for A.a. had been treated with systemic tetracycline at phase I). 2 of 3 control sample negative for A.a. cultivation; one healthy control had small numbers of bacteria.
LM: Prominent PMN infiltrate, sometimes forming microabscesses. Plasma cells present in CT where collagen fiber bundles were deteriorating. Severity of inflammatory infiltrate usually increased apically. Bacterial infiltration into tissue was variable.
IF: 80% of lesions were positive for A.a. antigens in subepithelial tissues, both extra and intracellular. 69% of specimens had extracellular A.a. in CT. 12% of specimens showed subgingival bacterial aggregates attached to epithelium. 23% of the lesions stained positive for A.a. within epithelial cells.
TEM: Gram (-) rods in CT and single bacterial cells, often adjacent to collagen fibers.
BL: A.a. appears to be a key pathogen in JP lesions. A.a. is able to penetrate into epithelium and CT. As the levels of A.a. in subgingival plaque increases, the tissue infiltration increases. A.a. persists after traditional SRP in patients with JP, possibly because of its ability to invade tissue, so additional treatment with systemic antibiotics or surgery is often necessary.
Topic: Aggressive Periodontitis
Authors: Waerhaug J NO ARTICLE
Title: Subgingival plaque and loss of attachment in periodontosis as evaluated on extracted teeth.
Source: J. Periodontol. 48:125-130, 1977.
Type: Clinical study
Rating: Good
Keywords: Attachment loss, subgingival plaque, attachment apparatus
P: To assess to what extent subgingival plaque was correlated with CALoss on teeth extracted because of periodontosis (a condition in which the supporting tissues are rapidly broken down in young individuals).
M&M: 27 teeth extracted from 16 “periodontosis” patients that were 12-22 years old with advanced bone loss. A notch was made on the tooth to distinguish sub-g and supra-g plaque prior to extraction. Roots were stained with toluidine blue to disclose subgingival and supragingival plaque. Loss of attachment measured as distance between the CEJ and the remnants of PDL fibers on the central part of 4 surfaces.
R: Subgingival plaque was very thin (exact thickness impossible to estimate, but it was about 0.25mm). Where the sub-g surfaces were plaque-free, the supra-g surfaces were also plaque-free. The distance between the subgingival plaque front and the nearest periodontal fibers (where attachment had been lost) was an average of 0.94 mm (range 0.2-1.5 mm) in the area of the CEJ and 0.43mm (range 0.2-1.0mm) at the area closest to the apex. Less CAL loss was observed on surfaces that had no supragingival plaque (more efficient tooth brushing). Even in areas with CALoss, symptoms of inflammation appear to be minimal and confined to the gingival margin.
C: Plaque is indicated as etiology of destruction of attachment apparatus. Areas that have efficient supragingival plaque removal do not appear to have subgingival plaque or resultant CALoss.
BL: The speed of ALoss is directly correlated with the speed of advancement of the sub-g plaque. Loss of attachment never occurred unless sub-g plaque was found 1.5mm or less from the nearest attachment fibers (as close as 0.2mm in some areas). The destructiveness is due to a host-parasite imbalance, rather than a degenerative condition.
Topic: aggressive perio
Authors: Mullally BH, Dace B, Shelburne CE, Wolff LF, Coulter WA NO ARTICLE
Title: Prevalence of periodontal pathogens in localized and generalized forms of early-onset periodontitis.
Source: J Periodontal Res. 2000 Aug;35(4):232-41.
Type: clinical
Rating: good
Keywords: periodontal disease, early-onset periodontitis,
Purpose: To investigate the prevalence of a panel of 8 putative periodontal pathogens in the subgingival plaque of subjects with EOP and evaluate the microbial differences between localized and generalized forms of this condition.
Methods: 42 Caucasians subjects with early-onset periodontitis (EOP). Less than 35 yrs, one or more teeth with radiographic bone loss greater or equal to 30% and a minimum of 4 sites each with a PD of at least 5mm and CAL of at least 2mm. Subjects were classified into localized or generalized EOP (depending on the pattern of bone destruction and more or less of 14 teeth were affected). Two diseased sites were selected per patient, and one healthy. In 14 subjects, there was no site meeting the criteria to be categorized as healthy. BOP, AL and PD were measured and subgingival plaque samples were collected (total of 112 subgingival plaque samples).
Eight species were examined (B. forsythus,T. denticola, A.a., P gingivalis, P. intermedia, P. nigrescens, E. corrodens, C. rectus).
Results: Bacterial prevalence: In 13 healthy sites, bacterial DNA was detected. Three were positive for periopathogens (1 for P. gingivalis and 2 for E. corrodens). The bacterial DNA specific for C. rectus was detected in 80 out of 84 diseased sites.
No significant associations between tooth type and pathogen recovery were found. Molars tended to have deeper PD and higher PI scores than incisors.
For most species, there was no difference between males and females. P. gingivalis was recovered from 22.6% of females but not from any male. C. rectus was found in all female subjects and 72.7% of males.
In general PD were deeper for sites harboring bacterial species than the ones negative for the panel of eight pathogens. Presence of A.a. was associated with the deeper sites. P. gingivalis and A.a. had slightly higher prevalence on BOP sites. Also A.a. was found more frequently in non-smokes compared to smokers, while C. rectus was recovered more often from smokers than non-smokers. No significant differences were found between smokers and non-smokers for the rest of the bacteria.
LEOP: 7 out of 8 subjects positive for A.a.
Associated (84%) with cluster group comprised of A.a., E corrodens, P. gingivalis and P. intermedia.
GEOP: 1 out 8 subjects positive for A.a. Significantly higher proportion of sites with P. nigrescens and P. intermedia than LEOP.
Associated (82.4%) with the cluster group consisting of B. forsythus, C. rectus, P. nigrescens and T. denticola.
Similar distribution between the two forms of EOP for B. forsythusm T denticola, P. gingivalis, E. corrodens and C. rectus.
Conclusion: EOP is heterogenous disease. It was possible in 83% to discriminate between LEOP and GEOP using the microbiological data. These data support the proposition of Socransky that groups of periodontal pathogens associate in clusters and that these appear to relate to the clinically observed disease entities.
Topic: Localized aggressive periodontitis
Author: Fine DH, Markowitz K, et al. NO ARTICLE
Title: Aggregatibacter actinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis: longitudinal cohort study of initially healthy adolescents
Source: J Clin Microbiol. 2007 Dec;45(12):3859-69. Epub 2007 Oct 17
Type: Longitudinal cohort study
Rating: Good
Keywords: Aggregatibacter actinomycetemcomitans, localized aggressive periodontitis, longitudinal cohort study, adolescents
Purpose: This is a longitudinal cohort study relating A. actinomycetemcomitans to initiation of LAP.
Methods: A periodontal assessment was performed on 1,075; primarily African-American and Hispanic school children, ages 11 to 17 years.
-Salivary samples were taken from each child to assess for A. actinomycetemcomitans.
-A cohort of 96 students was established that included a test group of 38 A. actinomycetemcomitans-positive students (36 periodontally healthy and 2 with periodontal pockets) and 58 healthy A. actinomycetemcomitans-negative controls.
-All clinical and microbiological procedures were repeated at 6-month intervals.
-Bitewing radiographs were taken annually for definitive diagnosis of LAP.
Results:
-Initial examination: clinical probing attachment measurements indicated that 1.2% of students had LAP, while 13.7% carried A. a., including 16.7% of African-American and 11% of Hispanic students.
- In African-Americans: A. a serotypes a, b, and c were equally distributed.
-In Hispanic students: Serotype c predominated.
-Longitudinal phase: Survival analysis was performed to determine whether A.a- positive as compared to A.a- negative students remained healthy or progressed to disease with attachment loss of >2 mm or bone loss.
Students without A.a at baseline had a significantly greater chance to remain healthy compared to the A.a-positive test group.
8 of 38 A.a-positive and none of 58 A.a-negative students showed bone loss.
A.a serotype did not appear to influence survival.
A.a is associated with bone loss
Not all subjects who carry A.a will develop LAP
Conclusion: These findings suggest that detection of A.actinomycetemcomitans in periodontally healthy children can serve as a risk marker for the initiation of LAP.
What antibiotic regimens are used in the treatment of AgP and what regimens are used?
Topic: Aggressive periodontitis
Authors: Slots J, Rosling BG ARTICLE
Title: Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline
Source: J. Clin. Periodontol 10:465-486, 1983
Type: Clinical study
Rating: Good
Keywords: Actinobacillus actinomycetemcomitans, localized juvenile periodontitis, periodontal therapy
Purpose: To determine the effectiveness of subgingival debridement, topical betadine solution, and systemic tetracycline in suppressing A.a. & other microorganisms in localized juvenile periodontitis (LJP) patients.
Methods: 6 LJP pts with 20 deep periodontal pockets & 10 normal periodontal pockets were included in this study. Each patient was treated in 3 stages over 22 weeks:
1st stage – plaque control, SRP (each pt got at least 6 hrs of debridement);
2nd stage - Betadine-saturated gauze inserted into pockets 10 min;
3rd stage - systemic tetracycline (1g/day) for 14 days; culturing done at various stages for A.a. & Capnocytophaga. Direct microscopic exam was also done. Changes in AL, PD, radiographic bone mass were measured.
Results: SRP reduced total subgingival bacterial counts, but did not totally eliminate A.a. from any pocket; Betadine had little effect on subgingival bacteria. Systemic tetracycline reduced A.a., Capnocytophaga, & spirochetes in all pockets to undetectable levels. A.a. reappeared in 9 of the deep pockets after systemic administration of tetracycline. A.a. responded slower to tetracycline treatment than Capnocytophaga.
Conclusion: 14 days of tetracycline therapy lowered subgingival counts of A.a, Capnocytophaga and spirochetes to below detectable levels in most periodontal pockets, and that these organisms remained markedly suppressed for at least 8 months following the tetracycline therapy. The authors suggest tetracycline therapy should be continued for 3 weeks; No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes, or motile rods. Four deep pockets continued periodontal destruction and still had high levels of A.a. post-tetracycline therapy. 6 pockets demonstrated a gain in attachment with no cultivable A.a. A.a. is an important etiologic agent in LJP; its subgingival eradication cannot be resolved by root surface debridement alone (bacteria may be attached to pocket epithelium), but can be resolved with SRP in conjunction w/systemic tetracycline therapy.
Topic: Antibiotics
Authors: Van Winkelhoff AJ, et al ARTICLE
Title: Metronidazole plus amoxicillin in the treatment of Actinobacillus actinomycetemcomitans associated periodontitis
Source: J Clin Periodontol 16:128-131, 1989
Type: Clinical study
Rating: Good
Keywords:
Purpose: To investigate the use of Metronidazole + Amoxicillin for the subgingival elimination of A.a in periodontitis patients.
Material and methods:
22 patients, 11 with LJP (localized juvenile periodontitis) and 11 with rapidly progressing periodontitis. Of the 22 patients, 14 had received initial treatment in the past, 7 with an adjunctive use of Minocycline, Tetracycline or Doxycycline therapy. Microbiological data before treatment with the combination showed that all 22 patients were sub-gingivally infected with
A.a. Antibiotic regimen of 250mg metronidazole and 375mg amoxicillin t.i.d. for 7 days in combination with sub-gingival debridement was performed in order to eradicate A.a
The rational for using these two antibiotics is that metronidazole is very effective against anaerobic microorganisms and is known to act synergistically with penicillin. Both drugs are bactericidal that helps eliminate sub-g microorganisms and also the combination covers a very broad spectrum of the microflora.
4 sites selected on the basis of BOP and/or suppuration on probing, PDs of at least 5mm, and radiographic evidence of bone loss. Sub-g samples were taken. Clinical and microbiological evaluation was performed at 2-4 and 9-11 months after therapy.
Results: A.a. suppressed below detection level in all patients. (also for P.g.). Clinical improvements, decrease of PD from 7.4 to 5.5mm in patients with no history of periodontal treatment and from 7.2 to 5.3mm in patients who had received periodontal treatment in the past. The number of pockets showing BOP decreased from 98% to 48%. At 9-11 months, microbiological re-examination of 16 patients showed that Aa was still undetectable. P.gingivalis could not be isolated after therapy (with the exception og 1 patient) and P. Intermedia was recovered from 6 patients after therapy.
BL: Combination of Metronidazole + Amoxicillin is a valuable adjunct to mechanical treatment in Aa associated periodontal infections.
Topic: Aggressive periodontitis
Authors Mandell RL, Socransky SS NO ARTICLE
Title: Microbiological and clinical effects of surgery plus doxycycline on juvenile periodontitis.
Source: J. Periodontol. 59:373-379, 1988.
Type: Clinical study
Rating: Good
Keywords: Aggressive periodontitis, juvenile periodontitis, treatment
Purpose: To document clinical outcome of surgery plus doxycycline and levels of Aa present w/in a JP population for 1 year.
Method: 8 patients (168 sites/pt) (13-22 y/o) with active disease (loss of > 2mm connective tissue attachment within a 37 day period) were monitored for progression. PD, AL, BOP and gingival redness documented. FTF surgery with no osseous, no previous SRP. Patients were given 100 mg doxy q 12h for day 1 and then 100mg/day for 14 days. OHI. Recall visits at 3 and 12 months for microbiological and clinical measurements. Mean PD before treatment was avg 7.6mm (3-10mm). Supragingival plaque was removed, subgingival samples taken with sterile curettes.
Results:
7/8 pts showed a mean AL-gain on a site basis.
SSD in BOP reduction (from 95% to 75%) and gingival redness at 3 and 12-month recall appts.
3 months after surgery: Aa eliminated from 17/22 sites and in 4/8 pts.
Conclusion: Surgery and doxycycline effectively eliminated Aa from JP pockets that persisted over 12 months and lead to gain of attachment at 3 and 12 months. 3 months following surgery+ doxycycline may be the ideal time for follow up by clinical and microbiological monitoring.
Discuss the success of non-surgical, surgical and regenerative periodontal therapy in AgP patients.
Topic: localized juvenile periodontitis
Authors: Lindhe J, Liljenberg B ARTICLE
Title: Treatment of localized juvenile periodontitis: results after 5 years.
Source: J. Clin. Periodontol. 11:399-410, 1984.
Type: Clinical study
Rating: Good
Keywords: localized juvenile periodontitis, localized aggressive periodontitis
Purpose: To describe the 5-year follow-up result on LJP, of a treatment that included tetracycline, surgical correction, SRP and plaque control.
Methods: 16 pts (14-18 y/o) in the juvenile group & 12 (39-48 yr ) in the adult group. Lesions in 1st molars and incisors of the patients with adult perio disease were treated in an identical manner and served as controls. Angular bony defects and clinical conditions (hygiene status, gingival conditions, PD and AL) were documented in all pts. Treatment consisted of tetracycline 250 mg qid x 2 weeks, Surgery was MWF (2 days after start of ttc regimen), CHX 0.2% x 2 min bid x 2 weeks and professional cleanings every 3 months for 5 years. Patients were reevaluated at 6, 12, 24, and 60 months.
Results: After active treatment, in both groups there was a general reduction of plaque scores of 15- 20%. BOP declined to 5–13%. The average initial PD in LJP was 8 mm w/ AL of 7 mm. In the adult cases, PD of 6 mm w/ AL of 5.8 mm. Following treatment, PD varied between 3 and 4 mm in both groups. In LJP, the average ALgain was 2-5 mm, and in adult patients 2-3 mm. In adult pts, PD reduction and AL gain observed at 6 months after active treatment remained unchanged through the 5-year follow-up examination. No adult patients showed signs of recurrence, while 4 LJP pts showed recurrent lesions during the first 12 months. These 6 sites were retreated in an identical manner and did not show subsequent recurrence. “The soft tissue of the bony defects was excised because it contains an inflammatory cell infiltrate with large numbers of plasma cells and blast cells which might interfere with bone regeneration”
Conclusion: Combined approach resulted in resolution of gingival inflammation, gain of clinical attachment, and refill of bone in angular defects. The healing of the lesions of this patient sample was similar to healing observed in patients with adult periodontitis.
Cr: They show some before and after x-rays in the discussion, but do not mention them in the M&M or Results section.
Topic: Aggressive Periodontitis
Authors: Kornman KS, Robertson PB ARTICLE
Title: Clinical and microbiological evaluation of therapy for juvenile periodontitis.
Source: J. Periodontol. 56:443-446, 1985.
Type: Clinical
Rating: Good
Keywords: tetracycline, juvenile periodontitis
Purpose: To assess the clinical and microbiological characteristics of affected sites in juvenile periodontitis patients treated by scaling and root planing alone, by SRP concurrent with systemic administration of TTC and by periodontal surgery concurrent with systemic administration of TTC.
Material and methods: 8 patients (6 female, 2 male) age 12-23 years old with severe molar-incisor bone loss and pocket formation participated in the study. At initial examination, all patients received clinical (PI, GI, PD, BOP, suppuration) and microbiological assessment. Sub-g plaque samples were collected from the affected sites on sterile paper points placed to the depth of the pocket for 10s and analyzed for percentage of total cultivable microflora composed of black- pigmented Bacteroides species (BPB), surface translocating bacteria (STB) and A.a.
STAGE 1: All patients received SRP, 1-2 months after srp the patients were evaluated clinically and samples for microbiological studies were again obtained. Patients who responded to treatment were placed on 3-month recall. Patients with no PD reduction, BOP or suppuration were placed in STAGE 2 therapy.
STAGE 2: Patients were prescribed oral TTC 1gm/day for 28 days. During this period, srp was repeated. 2 months after the last day of TTC therapy, patients underwent clinical and microbiological assessment patients were either placed on recall or received STAGE 3 therapy.
STAGE 3: Surgical access to clinically unresponsive sites by MWF plus a second 28-day course of TTC.
Results: At the initial evaluation PDs averaged 8.0 1.1mm, 7/8 sites were positive for suppuration and all sites presented BOP. STB were detected in 1/8 site, BPB in 4/8 sites, and all sites had Aa (40% of total flora). SRP alone had no effect on clinical or microbiological findings, and all patients progressed to STAGE 2. 2 months after the completion of STAGE 2, 2/8 patients showed PD reduction and absence of suppuration and were placed on recall. 1/8 patient withdrew from the study and remaining 5/8 patients received STAGE 3 therapy. 3 months after surgical treatment PDs were reduced in all sites to approximately 4mm. Both BPB and Aa were reduced to undetectable levels. SRP with systemic TTC was clinically & microbiologically more effective at sites where Aa was more predominant. Surgery was required in all sites containing high levels of both BPB & Aa.
Conclusion: SRP alone had no effect clinically or microbiologically. SRP and systemic TTC more effective where Aa was predominant. Surgery with systemic TTC was required in all sites containing high levels of Black Pigmented Bacteria and Aa.
Topic: juvenile periodontitis
Author: Wennstrom A, et al NO ARTICLE
Title: Healing following surgical and non-surgical treatment of juvenile periodontitis (JP). A 5-year longitudinal study.
Source: J. Clin. Periodontol. 13:869-882, 1986
Type: Case series/discussion article
Rating: Good
Keywords: juvenile periodontitis, non-surgical therapy, aggressive periodontitis
Purpose: To assess the effect of SRP alone or combined with granulation tissue excision in the treatment of juvenile periodontitis lesions in patients not receiving adjunctive antibiotic therapy.
Materials and methods:
16 young patients referred for treatment of localized periodontitis. Inclusion criteria: 1.localized sites had PD of at least 5mm; 2. Loss of probing attachment of 2mm or more; 3.angular bony defects could be identified radiographically.
Patients divided into 2 groups: JP group (11pts, 14-19 years old, lesions only on perm 1st molars and incisors) and post-JP group (5 pts, 23-29 years old, lesions on perm 1st molars, incisors, and other areas).
Used split mouth design. One side of the jaw was treated by SRP + MWF, and the contralateral side with SRP alone.
Professional cleanings were given every 4 weeks for 6 months and then every 3 months until 2 years post treatment. Exam was done for PI, BOP, PD, probing attach level (PAL), recession, and alveolar bone level at baseline, 6, 24 and 60 months after treatment.
No antibiotics during the 5-year observation period. Microbiological tests were done at 5 years.
Results:
At the initial examination about 75% of the diseased sites harbored supra-gingival plaque and 100% BOP.
Following treatment (6 months) the plaque scores decreased in both groups to 5-10% and BOP decreased to 10-20%.
Mean PD at initial examination was 7mm, following treatment PD decreased to 3–4 mm in both groups.
CAL gain was 2-3 mm at 6 months and 1-2 mm after 5 years in all groups.
There was NSSD between the surgical and non-surgical groups. At 5 year microbial sample, 3/30 of the JP patients- showed A.a. and 1/30 showed P. gingivalis. In the post-JP patients- 1/12 had A.a. and 1/12 showed P. gingivalis.
BL: SRP yielded comparable improvement in PI, BOP, PD reduction and CAL gain to treatment with SRP+MWF in JP and post-JP patients. Antibiotic therapy is not necessary. JP patients respond to both surgical and non-surgical therapy in a manner similar to post-JP patients.
Topic: Aggressive Periodontitis
Authors: Christersson LA, Slots J, Rosling BG, Genco RJ. ARTICLE
Title: Microbiological and clinical aspects of surgical treatment of localized juvenile periodontitis.
Source: J. Clin. Periodontol. 12:465-476, 1984.
Type: Clinical study
Rating: Good
Keywords: Localized juvenile periodontitis, AA, periodontal therapy
P: To examine whether soft tissue curettage and MWF were capable of suppressing subgingival Aa in LJP.
M&M: 7 Pts ages 10-20 with LJP. All pts healthy except one pt had diabetes and another sickle cell. All pts received supragingival scaling and OHI. Baseline measurements were recorded and thorough SRP performed on all pts (average time of 4 hours per pt). 8 lesions in 3 pts did not receive any additional treatment, 8 lesions in 4 pts received soft tissue curettage, 9 lesions in 4 pts received MWF. Outcomes were assessed by PPD, PI, GI, PAL with a stent and subtraction radiography. Subgingival Aa measurements were also recorded. CAL was considered SS when there was a change of 2mm or more.
R: All lesions had high Aa counts prior to SRP. SRP alone: PPD and PAL–no improvement, CAL 67% decreased and none gained at 8 and 16 weeks, no sig Aa suppression. Curettage: PPD SSD decreased at 8 wks(p= 0.002) and 16 wks(p=.001) , PAL NSSD at 8 wks, but was SSD (p=.005) at 16wks. 25% gained PAL and none lost at 16wks. Aa suppression below detectable levels in 75% of lesions 1wk after tx, and 4/8 lesions still had Aa below detectable levels at 16wks. MWF: PPD SSD decreased at 8 wks (p= 0.003) and 16 wks (p=.001) , PAL not SSD at 8 wks SSD (p=.001) gain in PAL at 16wks, CAL no SSD at 8 wks, but 33% gained and none lost at 16wks. Aa suppression at 89% of sites at 1wk after tx and 56% at 16. Digital subtraction radiography correlated well with clinical findings. There was NSSD in PAL between the sx tx groups, however, these groups did have a SS difference in comparison to the SRP group. There was a positive correlation between Aa 16wks post-tx and PALoss. All sites with PALoss had Aa. Of sites showing no change in PAL, 57% had Aa. Only 22% of lesions that had PALgain harbored Aa.
D: The results of this study are lower than in other studies when TTC is utilized systemically. When periodontal sx was used, Aa was eradicated in about half of the studies but when 14 days of systematic TTC was used in combination of SRP, the surface free from AA increased.
BL: There is a close relationship between post-tx Aa levels and clinical response to therapy. Substantial suppression of Aa cannot be achieved through SRP alone, but can be accomplished through surgery.
Topic: aggressive perio
Authors: Evans GH, Yukna RA, Sepe WW, ARTICLE
Title: Effect of various graft materials with tetracycline in localized juvenile periodontitis
Source: J Periodontol 60:491-497,1989. DOI: 10.1902/jop.1989.60.9.491
Type: clinical
Rating: good
Keywords: antibiotic treatment, bone graft, aggressive periodontitis treatment
Purpose: To compare Synthograft, Periograft (b-TCP, HA) and FDBA combined with local and systemic tetracycline therapy in the treatment of osseous defects associated with LJP.
Methods: Ten young (16-28), systemically healthy patients with a diagnosis of LJP, bilateral osseous defects more than 2mm in depth usually limited to first molars. Total of 51 defects. Pregnant females and children less than 14 yrs. were excluded due to possible toxic effects of tetracycline. Documentation (intraoral photos, charting and radiographs) was accomplished prior to the surgery, at 6 months post-surgically and at the re-entry surgery performed.
Initial therapy was consisted of oral hygiene instructions, coronal polishing of the whole dentition, occlusal adjustment and splinting if indicated. The standard surgical procedure was performed in two half-mouth sessions. Defects were grafted with the materials under study according to a randomized code utilizing a split mouth design. Defects on the same side of the mouth were treated with one material and the other half randomly received one of the remaining two. TTC powder was added to each graft material at a 4:1 graft to TTC powder ratio. Beginning the day of surgery all patients received 100mg of doxycycline daily for 10 days. Ten days after surgery periodontal dressing and sutures were removed. Patients were then placed on a strict maintenance schedule following surgery. Surgical re-entry was performed on average 9 months after grafting.
Results: No apparent clinical problems related to the use of any of the graft materials in combination with local and systemic tetracycline.
In general, there were no significant differences regarding hard and soft tissue changes among three graft materials except for a significantly lower percentage defect fill with b-TCP compared to HA.
b-TCP had the lowest frequency of positive (≥50% defect fill) responses. HA and FDBA resulted in substantial furcation fill, while b-TCP was mostly ineffective in this regard.
Conclusion: The use of bone grafts combined with systemic and local TTC is more beneficial in achieving repair and fill of the bony deformities, based on the findings of this study and comparison with other reports. The grafting materials are equally safe, beneficial, and effective.
What are the inheritance patterns of AgP? Discuss the role of genetics in AgP?
Topic: Juvenile periodontitis
Author: Saxen L. ARTICLE
Title: Heredity of juvenile periodontitis
Source: J. Clin. Periodontol. 7:276-,1980
Type: Family study
Rating: Good
Keywords: Heredity, juvenile periodontitis, genetics
Purpose: To collect a larger series of families, which would give information about a possible familial occurrence of juvenile periodontitis not only in the siblings but also in the parents.
Materials and methods
-31 families, six of them were non-informative in the genetic ratio analysis. In 2 of the families, there was only one affected child, and in four of the families the siblings were too young to have the disease.
-60 parents were examined, 64 siblings 13 years of age or over, 3 children under 13 years of age
-Radiographic analysis (Pano) was the main diagnostic tool
-Sex distribution, health and effected individual, age of onset, occurrence, severity, and progress of the different sign, similarity and dissimilarity of different feature and lack of effected person among parents and children
Results
-In 8 families juvenile periodontitis was diagnosed in one or more of the siblings and the total number of affected siblings was 11.
-The mean age of onset was 20.3 years old.
-Clinical Signs: the occurrence of the two types of the disease, and primarily the generalized form become more frequent with age.
-The theoretical total number of children for each of the families would always be four and the genetic ratio of affected/total would be 0.25.
-The results of this study suggest that juvenile periodontitis should be considered a disease entity.
BL: The genetic analysis suggesting an autosomal recessive mode of inheritance further supports the postulate that juvenile periodontitis is a clinical and etiological disease entity.
Topic: Aggressive periodontitis
Authors: Marazita ML ARTICLE
Title: Evidence for autosomal dominant inheritance and race-specific heterogeneity in early-onset periodontitis
Source: J Periodontol. 1994 Jun;65(6):623-30
Type:
Rating: Good
Keywords: periodontitis, early-onset/etiology, periodontitis, juvenile/etiology
Purpose: To test most of transmission of early onset periodontitis (EOP) using mixed model segregation analysis in a large sample of families, and to test for race specific heterogeneity in the segregation patterns of EOP, given the pronounced racial differences in prevalence.
Methods: EOP probands were identified by the Clinical Research Center for Periodontal Disease at the Medical College of Virginia. Periodontal records were obtained for probands, as well as complete periodontal records on all available first degree relatives. Probands and family members were classified into the following categories:
-LJP- severe periodontal destruction with ≥4mm AL, at least 1 permanent first molar and at least one other first molar or incisor, plus no more than 2 affected teeth that are not first molars or incisors, and aged 13-35 years.
-GJP-severe destruction with ≥5mm AL, 8 or more affected teeth, and least 1 permanent first molar plus three or more other affected teeth that are not first molars or incisors, aged 13-35 years.
Note: Probands were confined to the LJP and GJP diagnosis groups.
-AP (adult periodontitis)-chronic periodontitis
-ED (edentulous)
-NP- periodontally healthy
Note: Family members of probands, the above LJP and GJP criteria were applied with reduced attachment loss acceptable (2 and 3 mm, respectively).
104 probands identified 100 families. Periodontal status, race and sex were taken into account and analyzed.
Results: Among probands, significantly more were female (74%). Based on the total dataset, a major locus alone is sufficient to explain the familial patters of EOP and appears to have a dominant inheritance pattern for both black and non-black families.
Conclusion: It appears there are genetic and environment factors that contribute to the phenotype of EOP. The Black EOP allele frequency was 0.016 compared to 0.001 in non-blacks. About two-thirds of EOP probands are female, however there was no significant difference in the ratio of males to females in family members. The statistical analysis of this study also suggests an autosomal dominant pattern of recession.
Topic: Juvenile periodontitis
Authors: Melvin WL, Sandifer JB, Gray JL ARTICLE
Title: The prevalence and sex ratio of juvenile periodontitis in a young racially mixed population.
Source: J Periodontol. 1991 May;62(5):330-4.
Type: Clinical study
Reviewer:
Rating: Good
Keywords: prevalence, sex ratio, juvenile/periodontitis, ethnic groups
P: To determine the prevalence and sex ratio of juvenile periodontitis in a large group of young recruits and to compare these values between different racial populations.
M&M: 5013 naval recruits received a clinical exam, panoramic radiograph and bitewings during basic training. 139 patients were selected for further clinical exam and full mouth series based on suggested bone loss on original radiographs (bone loss in the molar and/or incisor region. Cases demonstrating greater CAL loss and bone loss on the 1st molars and/or incisors than on the other teeth were classified as having Juvenile Periodontitis. Epidemiologic data for each patient with Juvenile Periodontitis including age, sex and race were recorded
R: From 139 recruits selected for further evaluations, 38 cases of LJP were diagnosed. Mean age was 20.4 years (55% 17-19 years).
Recruit population: Caucasian 69%, African American 21%, Other 10%
Diagnosed with JP: 81.5% African American, 8% Caucasian, 10.5% other (Hispanic, Asian)
Overall 0.76% prevalence. African Americans had a much higher JP prevalence (2.1%) than Caucasians (0.09%)
Prevalence rate for females was 0.81% slightly higher than that of males 0.73% (ratio 1.1:1). The difference was not SS.
When data from race and sex were combined:
Prevalence of JP in African American males was 3.81%, Caucasian males 0.042%. (91 times greater-SS difference)
Prevalence of JP in African American females was 1.99% and Caucasian females 0.18% (11 times greater- SS difference)
|
Ethnic groups |
% overall screened |
% Dx with JP |
% Prevalence |
F/M ratio |
|
African American |
21 |
81.5 |
2.9 |
0.52:1 |
|
Caucasian |
69 |
8 |
0.09 |
4.3:1 |
|
Other (Hisp, Asian) |
10 |
10.5 |
0.8 |
3.0:1 |
BL: As there are such large variances between races and sexes of different ethnic populations, epidemiological data should look at individual prevalence rates.
Topic: Aggressive periodontitis
Authors: Meng ARTICLE
Title: Review article about host susceptibility in aggressive periodontitis
Source: Periodontol 2000. 2007;43:133-59
Type: Review
Rating: Good
Keywords: Aggressive periodontitis, juvenile periodontitis, regeneration, inheritance
Purpose: Review article about host susceptibility in aggressive periodontitis
Definition: Mode of inheritance: No single mode has been proven; autosomal dominant, autosomal recessive, and x-linked transmission have all been reported. The largest study in kindreds indicated that the most likely mode of inheritance is autosomal dominant with 70% penetrance in African-American and 73% penetrance in Caucasians. (Marazita 1994)
IL-1 polymorphisms: Conflicting data, not applicable to African Americans (IL-1B +3954 allele 1 was found to be carried by >99% of the control group and by 100% of the juvenile patients with localized periodontitis +3954 polymorphisms would provide little diagnostic or predictive information for localized juvenile periodontitis
IL-4 polymorphisms: Conflicting data
IL-10 polymorphisms: No positive association data reported in all three studies
TNF-a polymorphisms: No association with aggressive (only with chronic)
Fc gamma/alpha receptors gene polymorphisms: although results varied, it seems that there is a relation to increased susceptibility to aggressive periodontitis, Fc gamma receptor IIB NA1/NA1 genotype in aggressive periodontitis were significantly higher than controls. Different populations studied had different polymorphisms associated with aggressive disease.
Human Leukocyte antigen polymorphisms: This has also been associated, different polymorphisms associated with different populations
Vitamin D-receptor polymorphisms: This has been associated with localized but not generalized, although some researchers reported no association.
N-Formyl peptide receptor polymorphisms: Multiple studies have shown significant association with multiple gene polymorphisms implicated in aggressive periodontitis.
Lactoferrin polymorphisms: Have been reported to be significantly different in patients with aggressive disease and in controls
Other mutations like MMP-1 and -3, estrogen receptors, Toll-like receptors and Calprotectin have also been studied with no association, whereas PG-D and IL-6 have been shown to be associated with aggressive patients
Neutrophil defects: these include
Adherence: lymphocyte function-associated antigen -1, complement 3 receptor, and a-X receptor all appear to be abnormal in generalized prepubertal periodontitis but normal in localized, and rapidly progressive patients
Chemotaxis: is the most studied dysfunction, in LAgP there are decreased numbers of several receptors for chemotactic factors, including N-formylpeptide, IL-8, and C5a
A surface glycoprotein dubbed GP110 seems to be decreased by about 50% in LAgP patients, the function of which is unknown
86% of patients with juvenile periodontitis show modest leukotactic defects, most of which were intrinsic cell abnormalities, 48% of rapidly progressive periodontitis patients show detectable leukotactic defects and 66% of patients with early onset periodontitis manifest chemotactic abnormalities. Defects were also shown to be present in the diacylglycerol kinase-a signaling of neutrophils in LAgP patients. Chemotaxis defects are not reversible by treatment. (Suzuki)
Although chemotaxis abnormalities appear generalized, some researchers in Northern-European and Chinese populations reported no chemotaxis dysfunctions.
Phagocytosis: has been shown to be defective and abnormal in neutrophils in aggressive periodontitis patients. Intracellular killing of A.a. and P. g. also appears impaired
Antibody response: IgA and IgM are not different between aggressive patients and control, however, LAgP show significantly higher IgG titer to P. g. than in GAgP, this lead to the notion that decreased antibody response might lead to the more severe and more spread disease, but in both LAgP and GAgP IgG titers to P. g. are higher than chronic periodontitis. The study of such response is more complicated than previously thought, since factors like race, smoking, stress and age affect antibody response. Smoking for example significantly lower IgG production.
Smoking and stress: Significantly related to future attachment loss and response to therapy
Root abnormality: Significantly associated with amount of bone loss in AgP patients
Herpes infections: recent evidence has implicated herpes virus with AgP, in one study it was reported that P. g. and cytomegalovirus are independently and strongly associated with LAgP. Herpes and CMV have been proven to be strong indicators of the presence of P. g. and CMV and EBV have been strongly associated with chronic periodontitis.
Conclusion: AgP is a multifactorial, genetically complex disease. Genetic polymorphisms may influence the generalized type of the disease in a complex way, acting with genetic variants and environmental factors. An increased host susceptibility of AgP patients may be caused by the combined effect of multiple genes,
interacting with environmental factors and local contributing factors. Also, herpesviruses may serve as a putative susceptibility and severity factor of aggressive periodontitis.
Is AgP associated with any defects in any immune cells or immunoglobulins?
Topic: Neutrophil locomotion in juvenile periodontitis
Authors: Van Dyke TE, Horoszewiez HU, Genco RJ ARTICLE
Title: The polymorphonuclear leukocyte (PMNL) locomotor defect in juvenile periodontitis. Study of random migration, chemokinesis, and chemotaxis.
Source: J. Periodontol. 53:682 - , 1982.
Type: Multi-center clinical study
Rating: Good
Keywords: PMN, neutrophil, juvenile periodontitis, aggressive periodontitis
Purpose: To observe the PMN locomotor defect in JP.
Methods: Evaluated pts w/LJP (60 pts), post-LJP (15 pts over 30 y.o.), and GJP (17 pts under 30y.o. affecting most of the teeth); used regression line analysis to eval cell migration, chemokinesis, & chemotaxis.
Results: Neutrophil locomotion is reduced in LJP, post-LJP, & GJP pts; this decrease in response is due to a decrease in rate of migration in presence of a chemotactic gradient rather than being due to a population of poorly responsive neutrophils; random migration and chemokinesis were normal in these pts; therefore, PMN locomotion disturbances in JP pts are cell associated and not due to humoral factors. There are a reduced number of chemotactic factor receptors present on the cell surface.
Conclusion: Random migration & chemokinesis are normal & chemotaxis is reduced in pts with JP.
Topic: Aggressive Periodontitis
Authors: Mason JD, Thompson JJ, Yukna RA. ARTICLE
Title: Local immunoglobulin synthesis in juvenile periodontitis: Initial findings.
Source: J Dent Res 63:1211-1213, 1984
Type: Clinical
Rating: Good
Keywords: juvenile, periodontitis
Background: Previous studies have shown juvenile periodontitis to be an inflammatory disease, with increased Ig levels in the gingival tissues. As albumin is a reference protein for serum levels, a variation in the ratio of serum Ig to albumin in the blood would result from local production of Ig, as opposed to systemic.
Purpose: To determine simultaneously IgG and albumin concentrations in gingival tissue and serum obtained from patients diagnosed with JP to ascertain whether gingival tissue Ig was produced systemically or locally.
Materials and methods: Samples were obtained from 11 patients diagnosed with LJP and were scheduled for surgical correction of the periodontal defects. 7 patients were finally included in the study (6F/1M), 15-24 years. Local anesthesia was administered, FTFs were reflected, tissue samples and serum samples were obtained during the surgery. Assays of samples were taken to obtain concentrations of IgG & albumin.
Results: Gingival homogenate IgG/albumin ratios in the interval 0.5-0.7 were not SD from the patient serum ratios. However, gingival homogenate ratios 0.7 were highly SD from patient serum ratios. 72% of IgG found in diseased gingival tissue of JP patients was of local origin.
Conclusion: A definite local IgG accumulation was observed in juvenile periodontitis lesions, probably by local synthesis.
Topic: Aggressive Periodontitis
Authors: Spindler SJ, Thompson JJ, Yukna RA, Costales AD. NO ARTICLE
Title: Juvenile periodontitis. I. Demonstration of local immunoglobulin synthesis.
Source: J Periodontol. 1986 May;57(5):300-4.
Type: Clinical
Rating: Good
Keywords: juvenile Periodontitis
Purpose: To determine the presence and quantity of immunoglobulin G (IgG) and albumin (ALB) in specified periodontal tissues and serum from patients diagnosed as having juvenile periodontitis (JP), using an immunoelectrophoresis technique and to determine which portion of the lesion generated the greatest local immunoglobulin production.
Method: Serum and tissue samples were obtained from 19 patients (ages 13-21 years) who were diagnosed as having JP; 18 were female; 16 were black. Normal, diseased, and granulomatous gingival/periodontal tissues were collected during full thickness flap surgery, then minced, homogenized, and centrifuged. Supernatants containing the gingival/periodontal protein and the serum were electrophoresed against rabbit antihuman IgG and ALB. The relative IgG/ALB ratios in each specimen were plotted against known concentrations of IgG using a least squares analysis to provide evidence for local synthesis.
Results/Conclusion: In comparing mean IgG/ALB ratios for all tissue types, it was noted that normal gingiva did not differ significantly from serum. Diseased and granulomatous tissues, taken together or separately, had significantly higher IgG/ALB ratios than normal gingiva or serum, demonstrating that 73.6% of the IgG present was due to local synthesis. However, the greatest amounts of locally produced IgG were found in the granulomatous tissue from the deepest areas of the defects.
Topic: juvenile periodontitis
Author: Van Dyke T, et al ARTICLE
Title: Neutrophil function in localized juvenile periodontitis-Phagocytosis, superoxide production and specific granule release.
Source: J. Periodontol. 57:703, 1986
Type: Case series/discussion article
Rating: Good
Keywords: juvenile periodontitis, non-surgical therapy, aggressive periodontitis
Purpose: To evaluate a specific granule (lactoferrin) release and superoxide anion production from neutrophils from LJP patients who exhibited defective chemotaxis and phagocytosis.
Materials and methods:
· 23 LJP patients less than 30 years old, exhibiting alveolar bone loss localized to molars and incisors and not more than two additional teeth.
· The control group was comprised of healthy individuals who had no radiographic evidence of bone loss or evidence of periodontal disease other than mild gingivitis.
· Patients and controls were age and sex matched for most experiments.
· Neutrophil chemotaxis, phagocytosis, Lactoferrin release stimulated by chemotactic receptor- N-formyl-L-leucyl-L-phenylalanine (FMLP) and superoxide production stimulated by phagocytosis receptor C3b were evaluated.
Results:
· 23/23 patients exhibited chemotaxis depression to FMLP and endotoxin-activated serum (EAS).
· 14/14 patients tested showed defective phagocytosis.
· Both granule release and superoxide production were found to be NSSD in chemotactically defective LJP pts.
BL: Since both granule release and superoxide production were found to be normal in chemotactically defective LJP patients, LJP neutrophil defect may be related to cell maturity rather than specific defect in receptor production. Neutrophil phagocytosis and chemotaxis are depressed in LJP patients.
Topic: Aggressive Periodontitis
Authors: Gronert K, Kantarci A ARTICLE
Title: A molecular defect in intracellular lipid signaling in human neutrophils in localized aggressive periodontal tissue damage.
Source: J Immunol. 2004 Feb 1;172(3):1856-61.
Type: Clinical study
Rating: Good
Keywords: Localized juvenile periodontitis, AA, periodontal therapy
BG: The importance of DAGK to leukocyte function is emphasized by DAGKα’s integral role in attenuating receptor signaling in PMNs. Defective DAGK expression provides a potential molecular basis that may explain different functional responses in PMNs from pts with LAP, especially agonist-specific reduced motility and enhanced production of superoxide anions and related reactive oxygen species.
P: To examine and compare PMNs from pts with LAP to those of other diseases and from non-diseased subjects.
M&M: Pts with LAP (11), family members without LAP (4) and pts with chronic periodontitis (6) included in the study. Smokers were not included. Neutrophils (PMN) were isolated from fresh heparinized venous blood and preparations were >98.6% PMN with > 96% viability. Superoxide anion generation, trans-endothelial migration, and diacylglycerol kinase (DAGK) activity were also determined.
R: PMNs from LAP patients showed decreased transmigration across vascular endothelial monolayers (by 82%) and increased superoxide anion generation. Pts with LAP had about 10x less DAGK expression when directly compared to asymptomatic individuals. DAG kinase activity was also significantly decreased (73 ±2%,) and correlated with increased accumulation of 1,2-diacyl-sn-3-glycerol substrates in pts with LAP.
BL: These results implicate defects in both PMN trans-endothelial migration and PMN DAG kinase α signaling as disordered functions in LAP.
Is AgP associated with altered caries levels and altered root surfaces?
Topic: aggressive perio
Authors: Fine DH, Goldberg D, Karoi R. ARTICLE
Title: Caries levels in patients with juvenile periodontitis.
Source: J. Periodontol. 55:242-246, 1984. DOI: 10.1902/jop.1984.55.4.242
Type: clinical
Rating: good
Keywords: smooth surface caries, juvenile periodontitis, periodontal disease,
Purpose: To determine the extent of smooth-surface caries among patients with juvenile periodontitis compared with that of an age- and sex- matched control population.
Methods: 23 Patients with JP under 25 years old under treatment. Subjects should not have any missing tooth (except from the 3rd molars), at least 30% bone loss around more than one first molar or incisor, PD at least 6mm around the involved teeth, little or no inflammation and minimal amount of plaque. 13 patients with LJP and 10 with GJP.
23 patients matched by age and sex with the experimental subjects was selected by computer to serve as control group. These patients had no peridontla disease, no systemic disease and fewer than two missing teeth (excl. 3rd molars).
Decayed (evaluated by standard clinical and radiographic criteria), missing and filled surfaces were recorded in both groups.
Results: Caries in the LJP and GJP groups are reasonably similar.
Not statistically significant differences between the JP group and the control group in terms of filled teeth. The JP group had significantly less proximal decay than the control group.
Conclusion: Average age of GJP patients was slightly higher than LJP. Inverse relationship between proximal caries and JP, which may be related to an undefined microbiological or immunological event.
Dietary habits, oral hygiene (answered by questionnaires) and fluoride intake (assumed it was the same because all subjects were from New York area) should be studied in a systematic manner.
Topic: Earl-onset periodontitis
Author: Waldrop TC, Hallmon WW, Mealey BL. ARTICLE
Title: Observations of root surfaces from patients with early-onset periodontitis and leukocyte adhesion deficiency
Source: J Clin Periodontol 22:168-178, 1995.
Type: Clinical study
Rating: Good
Keywords: cementum; aplasia; SEM; early-onset periodontitis; leukocyte adhesion deficiency
Purpose: To report observations of the root surfaces of teeth from 2 siblings with leukocyte adhesion deficiency (LAD) and Generalized pre-pubertal periodontitis (G-PP).
Methods:
-The family case history for these patients had been previously reported.
- Teeth examined were from the patient in question “CF” (age 18) and the brother “DF” (age 14), who were diagnosed with G-PP and LAD
-At age 3, CF had all primary teeth extracted. By age 10, all erupted permanent maxillary and mandibular teeth were affected. All teeth in pt CF were extracted by age 18.
-Pt DF presented at 3 years old with acute generalized inflammation. By age 7, permanent teeth were affected by advanced periodontal disease. By age 14, bone loss scores of 70% to 100% were noted for all permanent teeth.
-16 teeth from CF and 22 from DF were used for the study. In addition, 8 healthy bicuspids from 2 patients age 13-14 served as control
-The teeth were prepared for Scanning electron microscopy (SEM) and Light microscopy (LM).
Results:
-LM observations on healthy teeth revealed cementum with normal structural appearance, which exhibited a mosaic or mogul-like pattern with SEM.
In LAD specimens, cementum apical to the dentogingival junction exhibited resorption lacunae and areas of poor structural definition characterized by aplasia and hypoplasia (hypomineralization)
Discussion: Alteration in cementum formation and maturation may play a role in the etiology of early onset periodontitis (EOP). The three primary functions of cementum are:
1) to attach fibers of PDL to root surface; 2) to maintain width of PDL space; 3) to repair the root surface when damage occurs. Alterations of cementum could potentiate periodontal disease; however, no association b/t LAD and the presence of cemental atypia in these patients can be established.
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