Microogranisms+associated+with+periodontal+disease

Microorganisms Associated with Periodontal Disease and the Different Categories of Periodontal Disease

Plaque Made primarily of gram-postive bacteria cocci and rodsSome bacteria are more prevalent than others, those prevalent bacteria include: P.//gingivitis//, T. //forsynthis//, P. //intermedia//, F. //nucleantum//During the later stages of plaque formation, the mass of plaque will be made up of mostly gram-negative bacteria.**Primary Colonizers**: streptococci and actinomycetes**Secondary Colonizers**: //P. intermedia//, //P. loescheii//, //Capnocytophaga// spp., //F. nucleatum//, //Porphyromonas gingivalis// The shift in bacterial plaque goes as follows.
 * Gram positive to gram negative
 * From cocci to rods to spirochetes
 * Non motile to motile
 * Facultative anaerobes to obligated anaerobes.
 * Fermenting to proteolytic



Chronic Periodontitis This form of periodontal disease is the most common and may have clinical features such as swelling, bleeding, loss of stippling of attached gingiva, increased pocket depths, bone loss, attachment loss, and possible suppuration. It progresses slowly and is more commonly seen in adults however it can occur in children. Clinically, bone loss can occur at any age. Chronic periodontitis has a slow to moderate rate of progression with periods of rapid destruction. The progression of the disease is not in equal rate throughout the mouth. It has been stated that the progression of the disease is more rapid interproximally than buccally or lingually. This could be due to increase in plaque accumulation in areas where the removal and control of plaque is decreased due to not flossing everyday or not having the proper technique of removing plaque. The rate of chronic periodontitis is dependent on local, systemic, or environmental factors. It can be modified by systemic diseases such as diabetes mellitus or HIV or by environmental factors such as tobacco use or stress. It may be generalized which involves more than 30% of the mouth, or localized which involves less than 30% of the mouth, and may be slight/mild (no more than 1 to 2mm of clinical attachment loss), moderate (3 to 4mm of clinical attachment loss) or severe (5mm or more clinical attachment). Clinical attachment loss is the most reliable sign/method to follow and confirm chronic periodontitis.

__**//P. gingivalis//**__ A gram negative anaerobic pleomorphic rod that has fimbriae for adhesion, and a capsule to protect itself. It has the ability to invade soft tissues and inhibit the migration of neutrophils. It can produce collagenase, proteases, and hemolysin, and can affect the degradation of cytokines (Carranza 161). //P. gingivalis// is most commonly found in chronic periodontitis.
 * Etiologic Agents:**

__**//T.// //forsythia (formerly forsythus)//**__ A gram negative, non-motile, anaerobic pleomorphic rod. It produces proteolytic enzymes that destroy immunoglobulins and induces apoptotic cell death (Carranza 161). It also states in Carranza that it takes 14 days to grow meaning that the bacterial plaque has to be present this amount of time.

__**//P. intermedia//**__ A gram negative, non-motile anaerobic rod. This bacteria has the ability to break down proteins, but is less proteolytic than //P. gingivalis// (Carranza 162)//.//

__**//C. rectus//**__ A gram negative, motile, anaerobic rod. This bacterium produces leukotoxins (Carranza 162).

__**//E. corrodens//**__ A gram negative non-motile, facultative anaerobe. Often a bacillus, but sometimes can appear coccobacillary. This bacterium has the capacity to adhere to acidic glycoproteins on the tooth surface, and it produces endotoxins.

__**//F. nucleatum//**__ A gram-negative, non-motile, anaerobic rod. This bacterium can cause apoptotic cell death, and may cause the release of elastase, cytokines, and free radicals from leukocytes (Carranza 162).

__**//A. actinomycetemcomitans//**__ A gram negative nonmotile coccobacillus (short, rounded rod).This bacterium can produce a leukotoxin, collagenase, a protease that can break down the immunoglobulin IgG, and a lipopolysacharride endotoxin (Carranza 161). This bacterium can be associated with aggressive perodontitis and treament of this condition involves mechanical debridement and adjunctive therapy with tetracycline. If the bacteria is resistant to tetracycline is Haffajee er al. recommends a combination of antibiotic amxocillin and metronidazole.

__**//P. micros//**__ A gram-positive anaerobic coccus.

__**//Treponema//**__ These are gram-negative anaerobic motile spirochetes, and are able to penetrate the soft tissues of the periodontium due to their ability to travel. There are several species, including: //Treponema denticola, T. vincentii, T. socranskii,// and //T. pallidum,// and their pathogenic features can include the ability to break down collagen, dentin, or immunoglobulins (Carranza 163).

__**//Eubacterium//**__ Gram-positive, anaerobic, pleomorphic rod.

These represent a diverse group of spiral, motile organism. The are helical rods and have three to right irregular spirals. Their wall is gram negative, but they strain poorly. Forms of spirpchetes include //T. denticola, T. vincentii, T. socranskii// (often associated with periodontitis), //T. pallidum// ( associated with secondary syphilis. The special pathogenic characteristics are that they have the ability to travel through viscous environments allows them to migrate within the crevicular fluid and penetrate through the epithelium and connective tissue. Some can even degrade collagen and even dentin.
 * Spirochetes**

Necrotizing Ulcerative Periodontits Necrotizing Ulcerative Periodontitis is a consistent loss of clinical attachment and alveolar bone. It begins as a localized ulceration and progresses to necrosis of gingival tissues with rapid distruction of the alveolar bone. Patients with NUP experience spontaneous bleeding and pain (Carranza 107). The cause of NUP is associated with the presence of fusiform-spirochete bacterial flora; in addition, there are numerous predisposing factors such as poor oral hygiene, preexisting periodontal disease, smoking, viral infections, immunocompromised status, psychosocial stress, and malnutrition (Carranza 502).

__**//Fusobacterium//**__

Aggressive Periodontitis Previously known as juvenile periodontitis or early-onset periodontitis, aggressive periodontitis can be characterized as rapid disease progression without a large amount of plaque or calculus in an otherwise healthy person. This type of periodontal disease is usually seen in people around the range of puberty and those in their second or third decade of life. A young patient with severe and sudden bone loss, with little to no visible contributing factors such as calculus, aggressive periodontitis would be at the top of the differential diagnosis (TL). Aggressive Periodontitis can be further classified into localized with involves the first molar or incisor and must include proximal attachment loss on at least two permanent teeth, one of which is a first molar; or generalized which requires proximal attachment loss affecting at least three teeth other than the first molars and incisors (Carranza 106). Localized Aggresive Periodontitis (LAP)It is usually seen at puberty where the it involves the category stated above. With the amount of bone loss and inflammation it would be suspected that a heavy build up of plaqueand calculus would be present. With LAP there is very little plaque and calculus to cause the amount of destruction seen. the bacteria that is seen in indiviudal is //A. Actinomycetemcomintans// and //Porphyromonas gingivalis// in some individuals. According to Carranza the disease show a prevalence in decreasing order to black males, black females, white females, and white males. Studies have shown that the immune response is not working properly. Particularly in the polymorphonuclear leukocytes (PMSs), and monocytes. PMSs are hindered in their ability to migrate to the infection site or phagocytose of the offending bacteria. Monocytes show an increase in the release of PGE2 to the lipopolysaccharide (LPS) produced by the gram negative bacteria. It is believed that it LAP may be an inhereted disease but further studies on a broader population is needed to determine the gene responsible.Treatment for aggressive periodontitis could be nonsurgical, surgical, placement of an antimicrobial tetracycline-based on specific site, or a combination prescription of amoxicillin and metronidazole taken orally. This bacterium is the primary pathogen associated with aggressive periodontitis (Carranza, 129). //A.a// is a gram negative anaerobe that produces lipopolysacharides (LPS), leukotoxins that kill the host's neutrophils, collagenase, and protease.. http://www.institut-iai.ch/AA.html
 * __//A. actinomycetemcomitans//__**

__**//E. corrodens//**__
 * __//P. gingivalis//__**

**//Refractory Periodontitis//** Periodontitis that is recurrent and does not respond to periodontal therapy that is executed The main bacteria that are present include P.//gingivitis//, T. //forsynthis//, F. //nucleatum//, P. //micros//, E. //corrodens//, Streptoccoccus //intermedius//

//Periimplantitis// //This is the inflammatory process that affects the tissue that surrounds an implant causing bone loss// //Microorganisms include- A.actinomycetemocmitans, P. gingivalis, T.Forsynthia, P. micros, C. rectus, Fusobacterium and Capnpcytophaga.//


 * //Sources//**


 * //Haffajee A.D., Uzel N.G., Arguello E.I., et al: Clinical and microsbiological changes associated with the use of combined antimicrobial therapies to treat " refractory " periodontitis,. J Clin Periodontology 31:869,2004.//**


 * //Carranza F. A., Klokkevold P. R., Newman M. G., Takei H. H. (2006). Carranza's clinical periodontology. 10th ed.//**

**Gram+/-, Shape, Aerobic/Anaerobic** || **Classification of periodontal disease associated with microorganism** || **Specific Pathogenic Characteristic** || Aggregatibacter actinomycetemcomitans || Bacilli Gram - Facultative anaerobe || Chronic periodontitis Localized aggressive periodontitis || It has a number of virulence factors, including lipopolysaccharide an endotoxin, a leukotoxin which forms pores in neutrophil granulocytes, monocytes, and some lymphocytes, which consequently die because of osmotic pressure, collagenase which destroys connective tissue, and a protease that is able to cleave IgG || Gram - anaerobe || Chronic periodontitis Localized aggressive periodontitis || It’s fimbriae mediate adhesion, and its capsule defends against phagocytosis. It produces proteases, a hemolysin, and a collagenase. It also inhibits migration of PMNs across the epithelial barrier and affects the production or degradation of cytokines by mammalian, it has the capacity to invade soft tissue || Gram – anaerobe || Chronic periodontitis || It produces several proteolytic enzymes that are able to destroy immunoglubulins and factors of the complement system, it also induces apoptotic cell death || Gram – anaerobe || Gingivitis Chronic periodontitis || Surface components, such as the flagellum, surface layer (S-layer), and cytotoxin, have been reported as possible virulence factors of the microorganism. Campylobacter rectus is a putative periodontopathogen which expresses a proteinaceous surface layer (S-layer) external to the outer membrane. S- layers are considered to play a protective role for the microorganism in hostile environments. || Gram - Facultative anaerobe || Chronic periodontitis Localized aggressive periodontitis || //E.// corrodens infections are typically indolent (the infection does not become clinically evident until a week or more after the injury). They also mimic anaerobic infection in being extremely foul-smelling. || Gram + anaerobe || Chronic periodontitis Localized aggressive periodontitis || Able to adhere to inanimate objects such as calculas and then colonize on the foreign body || Nucleutum || Bacilli Gram – anaerobe || Periodontal health Gingivitis Chronic periodontitis Localized aggressive periodontitis || Normal flora in the mouth, and in necrotic tissue probably as secondary invaders. Produces of tissue irritants, its synergism with other bacteria in mixed infections, and its ability to form aggregates with other suspected pathogens in periodontal disease and thus act as a bridge between early and late colonizers on the tooth surface. || Gram – anaerobe || Periodontal health Gingivitis (pregnancy) Chronic periodontitis Necrotizing periodontal diseases || P. intermedia can substitute progesterone or estradiol for vitamin K as a growth factor. Steroid hormone concentrations in crevicular fluid may parallel serum concentrations, which dramatically change during pregnancy, puberty, and menstruation and after menopause. || Gram + anaerobe || Gingivitis Chronic periodontitis || Peptostreptococcus species are commensal organisms in humans, living predominantly in the mouth, skin gastrointestinal and urinary tracts, and compose a portion of the bacterial gut flora. Under immunosuppressed or traumatic conditions these organisms can become pathogenic, as well as septicemic, harming their host || Gram – anaerobe || Periodontal health Gingivitis Locatized aggressive periodontitis || The humoral response to subgingival bacteria can be nonspecifically altered by bacterial production of IgG, IgA, IgM, C3, and C5 proteases. Enzymes to some or all of the humoral components are elaborated by capnocytophaga. Capnocytophaga splits the immunoglobulin into Fab and Fc fragments, this protease activity may inhibit the local host response and allow penetration and spread of bacteria within the tissue. || Gram – obligate anaerobe || Chronic periodontitis Localized aggressive periodontitis Necrotizing periodontal diseases || The ability of these species to travel through viscous environments enables them to migrate within the gingival crevicular fluid and to penetrate both the epithelium and the connective tissue. T. denticola produces proteolytic enzymes that can destroy immunoglubulins IgA, IgM, and IgG or complement factors. || Gram + Facultative anaerobe || Periodontal health Gingivitis || Among the normal flora in the oral cavity S. intermedius produces hyaluronidase, an enzyme that breaks down hyaluronan (HA), a major component of the extracellular matrix of connective tissue || Gram + anaerobe || Periodontal health Gingivitis || Is prominent among normal flora of the oral cavity, these microorganisms are not virulent so the require a break in the integrity of the mucous membranes and the presence of devitalized tissue to invade deeper structures to cause damage. || Gram - anaerobe || Periodontal health Gingivitis Chronic periodontitis || This organism can induce apoptotic cell death in mononuclear and polynorphonuclear cells and can trigger the release of cytokines, elastase, and oxygen, radicals from leukocytes. ||
 * **Microorganism** || **Nomenclature**
 * Actinobacillus actinomycetemcomitans
 * Porphyromonas gingivitis || Bacilli
 * Tannerella forsythensis (Bacteroides forsythus) || Bacilli
 * Campylobacter rectus || Bacilli and spirochete
 * Eikenella corrodens || Bacilli
 * Eubacterium nodatum || Bacilli
 * Fusobacterium
 * Prevotella intermedia || Bacilli
 * Peptostreptococcus micros || cocci
 * Capnocytophaga species || Bacilli
 * Treponema denticola || spirochete
 * Streptococcus intermedia-complex || Spherical chains
 * Actinomyces species || Filamentous bacilli
 * Fusobacterium species || Filamentous bacilli