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Periodontitis

MedGen UID:
42217
Concept ID:
C0017563
Disease or Syndrome
Synonyms: Gum disease; Periodontal disease; Pyorrhea
SNOMED CT: Gingival disease (18718003); Gingival disorder (18718003); Gum disease (18718003)
 
HPO: HP:0000704

Definition

If you have gum disease, you're not alone. Many U.S. adults currently have some form of the disease. It ranges from simple gum inflammation, called gingivitis, to serious damage to the tissue and bone supporting the teeth. In the worst cases, you can lose teeth. In gingivitis, the gums become red and swollen. They can bleed easily. Gingivitis is a mild form of gum disease. You can usually reverse it with daily brushing and flossing and regular cleanings by a dentist or dental hygienist. Untreated gingivitis can lead to periodontitis. If you have periodontitis, the gums pull away from the teeth and form pockets that become infected. If not treated, the bones, gums and connective tissue that support the teeth are destroyed. NIH: National Institute of Dental and Craniofacial Research.  [from MedlinePlus]

Conditions with this feature

Periodontitis, chronic
MedGen UID:
120593
Concept ID:
C0266929
Disease or Syndrome
Chronic periodontitis, formerly called adult periodontitis, is the most frequently occurring form of periodontitis and is characterized by slowly progressing alveolar bone destruction and attachment loss. Although chronic periodontitis is most prevalent in adults and has a slow progression, it can occur in children and adolescents and may have periods of rapid progression (Armitage, 1999).
Ehlers-Danlos syndrome, type 4
MedGen UID:
82790
Concept ID:
C0268338
Disease or Syndrome
Vascular Ehlers-Danlos Syndrome (vEDS) is characterized by thin, translucent skin; easy bruising; characteristic facial appearance (in some individuals); and arterial, intestinal, and/or uterine fragility. Vascular dissection or rupture, gastrointestinal perforation, or organ rupture are the presenting signs in the majority of adults identified to have vEDS. Arterial rupture may be preceded by aneurysm, arteriovenous fistulae, or dissection but also may occur spontaneously. Neonates may present with clubfoot and/or congenital dislocation of the hips. In childhood, inguinal hernia, pneumothorax, recurrent joint subluxation or dislocation, and bruising can occur. Pregnancy for women with vEDS has an estimated 5.3% risk for death from peripartum arterial rupture or uterine rupture. One fourth of individuals with vEDS, confirmed by laboratory testing, experienced a major complication by age 20 years and more than 80% by age 40 years. The median age of death in this reviewed population was 50 years.
Ehlers-Danlos syndrome, type 8
MedGen UID:
82791
Concept ID:
C0268347
Congenital Abnormality
Ehlers-Danlos syndrome (EDS) is a clinically and genetically heterogeneous group of connective tissue disorders defined by joint laxity and skin alterations that include hyperextensibility, atrophic scarring, and bruising. Periodontal EDS (EDSPD; previously designated 'EDS VIII') is a specific subtype of EDS with autosomal dominant inheritance, in which the defining feature is an EDS phenotype combined with severe periodontal inflammation. In childhood, periodontal inflammation in EDSPD is characterized by extensive gingivitis in response to mild plaque accumulation. In the teens, early-onset periodontitis leads to inflammatory destruction of dental attachment and premature loss of teeth. Other clinical features include pretibial hyperpigmentation, acrogeria, skin and gum fragility, scarring, generalized and/or distal joint hypermobility, and bruising out of proportion to trauma. There are also reports of life-threatening complications such as arterial or gastrointestinal ruptures (summary by Kapferer-Seebacher et al., 2016). Genetic Heterogeneity of Ehlers-Danlos Syndrome, Periodontal Type Ehlers-Danlos syndrome periodontal type 2 (EDSPD2; 617174) is caused by mutation in the C1S gene (120580) on chromosome 12p13. Reviews Kapferer-Seebacher et al. (2016) tabulated the clinical features of 93 EDSPD patients with mutations in the C1R or C1S genes (77 and 16 patients, respectively) and observed that the most prevalent features included early-onset periodontitis, gingival recessions, and thin gingiva and/or absence of attached gingiva. Easy bruising was present in most patients, as were pretibial hyperpigmentation, skin fragility, and mildly elastic skin. About half of patients exhibited atrophic scars or wide scarring and/or prominent vasculature. Joint hypermobility was not a consistent finding, and if present was mild and often limited to small joints. Other variable features included recurrent infections, joint pain, flat feet, marfanoid facial features, scoliosis, osteoarthritis, and hernias. A minority of patients had joint dislocations; aneurysms occurred in 4 families, and autoimmune disorders occurred in 1 family. Cancer appeared to be more prevalent in patients with C1S mutations.
Kindler syndrome
MedGen UID:
96060
Concept ID:
C0406557
Congenital Abnormality
Kindler syndrome (KS), a rare subtype of inherited epidermolysis bullosa, is characterized by skin fragility and acral blister formation beginning at birth, diffuse cutaneous atrophy, photosensitivity (which is most prominent during childhood and usually decreases after adolescence), poikiloderma, diffuse palmoplantar hyperkeratosis, and pseudosyndactyly. Mucosal manifestations are also common and include hemorrhagic mucositis and gingivitis, periodontal disease, premature loss of teeth, and labial leukokeratosis. Other mucosal findings can include ectropion, esophageal strictures/stenosis, anal stenosis, colitis, urethral stenosis/strictures, and severe phimosis. Severe long-term complications of KS include periodontitis, mucosal strictures, and aggressive squamous cell carcinomas. Manifestations can range from mild to severe.
Geroderma osteodysplastica
MedGen UID:
98149
Concept ID:
C0432255
Disease or Syndrome
Congenital disorder of glycosylation type 2C
MedGen UID:
162913
Concept ID:
C0796132
Disease or Syndrome
Congenital disorder of glycosylation type IIc (CDG2C) is an autosomal recessive disorder characterized by moderate to severe psychomotor retardation, mild dysmorphism, and impaired neutrophil motility. It is a member of a group of disorders with a defect in the processing of protein-bound glycans. For a general overview of congenital disorders of glycosylation (CDGs), see CDG1A (212065) and CDG2A (212066). The neutrophil defect in CDG2C has been referred to as 'leukocyte adhesion deficiency type II' (LAD2), which is a manifestation of the disorder; there are no cases of 'primary' LAD II (Frydman, 1996). Etzioni and Harlan (1999) provided a comprehensive review of both LAD1 (116920) and LAD2. While the functional neutrophil studies are similar in the 2 LADs, the clinical course is milder in LAD2. Furthermore, patients with LAD2 present other abnormal features, such as growth and mental retardation, which are related to the primary defect in fucose metabolism. Delayed separation of the umbilical cord occurs in LAD1.
Hermansky Pudlak syndrome 2
MedGen UID:
374912
Concept ID:
C1842362
Disease or Syndrome
Hermansky-Pudlak syndrome (HPS) is a multisystem disorder characterized by: tyrosinase-positive oculocutaneous albinism; a bleeding diathesis resulting from a platelet storage pool deficiency; and, in some cases, pulmonary fibrosis, granulomatous colitis, or immunodeficiency. The albinism is characterized by: hypopigmentation of the skin and hair; and ocular findings of reduced iris pigment with iris transillumination, reduced retinal pigment, foveal hypoplasia with significant reduction in visual acuity (usually in the range of 20/50 to 20/400), nystagmus, and increased crossing of the optic nerve fibers. Hair color ranges from white to brown; skin color ranges from white to olive and is usually a shade lighter than that of other family members. The bleeding diathesis can result in easy bruising, frequent epistaxis, gingival bleeding, postpartum hemorrhage, colonic bleeding, and prolonged bleeding with menses or after tooth extraction, circumcision, and other surgeries. Pulmonary fibrosis, a restrictive lung disease, typically causes symptoms in the early thirties and can progress to death within a decade. Granulomatous colitis is severe in about 15% of affected individuals. Neutropenia and/or immune defects are associated primarily with HPS-2.
Leukocyte adhesion deficiency type 1
MedGen UID:
348448
Concept ID:
C1861766
Disease or Syndrome
Leukocyte adhesion deficiency (LAD) is an autosomal recessive disorder of neutrophil function resulting from a deficiency of the beta-2 integrin subunit of the leukocyte cell adhesion molecule. The leukocyte cell adhesion molecule is present on the surface of peripheral blood mononuclear leukocytes and granulocytes and mediates cell-cell and cell-extracellular matrix adhesion. LAD is characterized by recurrent bacterial infections; impaired pus formation and wound healing; abnormalities of a wide variety of adhesion-dependent functions of granulocytes, monocytes, and lymphocytes; and a lack of beta-2/alpha-L, beta-2/alpha-M, and beta-2/alpha-X expression.
Alopecia, epilepsy, pyorrhea, mental subnormality
MedGen UID:
350833
Concept ID:
C1863090
Disease or Syndrome
Plasminogen deficiency, type I
MedGen UID:
369859
Concept ID:
C1968804
Disease or Syndrome
Congenital plasminogen deficiency is a rare autosomal recessive disorder characterized clinically by chronic mucosal pseudomembranous lesions consisting of subepithelial fibrin deposition and inflammation. The most common clinical manifestation is ligneous ('wood-like') conjunctivitis, a redness and subsequent formation of pseudomembranes mostly on the palpebral surfaces of the eye that progress to white, yellow-white, or red thick masses with a wood-like consistency that replace the normal mucosa. The lesions may be triggered by local injury and/or infection and often recur after local excision. Pseudomembranous lesions of other mucous membranes often occur in the mouth, nasopharynx, trachea, and female genital tract. Some affected children also have congenital occlusive hydrocephalus. A slightly increased female:male ratio has been observed (1.4:1 to 2:1) (Schuster and Seregard, 2003; Tefs et al., 2006). Type I plasminogen deficiency is characterized by decreased serum plasminogen activity, decreased plasminogen antigen levels, and clinical symptoms, whereas type II plasminogen deficiency, also known as 'dysplasminogenemia,' is characterized by decreased plasminogen activity with normal or slightly reduced antigen levels. Patients with type II deficiency are usually asymptomatic. Ligneous conjunctivitis and pseudomembranous formation has only been associated with type I plasminogen deficiency. Presumably, normal amounts of plasminogen antigen with decreased activity, as seen in type II, is sufficient for normal wound healing (Schuster and Seregard, 2003).
Chronic familial neutropenia
MedGen UID:
384521
Concept ID:
C2267231
Disease or Syndrome

Recent clinical studies

Etiology

Wang HF, He FQ, Xu CJ, Li DM, Sun XJ, Chi YT, Guo W
Genet Mol Res 2017 Feb 23;16(1) doi: 10.4238/gmr16019315. PMID: 28252166
Sun JY, Li DL, Dong Y, Zhu CH, Liu J, Li JD, Zhou T, Gou JZ, Li A, Zang WJ
Int Immunopharmacol 2016 Jul;36:86-93. Epub 2016 Apr 22 doi: 10.1016/j.intimp.2016.04.012. PMID: 27107801
Redman RS, Kerr GS, Payne JB, Mikuls TR, Huang J, Sayles HR, Becker KL, Nylén ES
Biotech Histochem 2016;91(2):77-85. doi: 10.3109/10520295.2015.1082625. PMID: 26800284Free PMC Article
Shin HS, Shin MS, Ahn YB, Choi BY, Nam JH, Kim HD
J Am Geriatr Soc 2016 Jan;64(1):162-7. doi: 10.1111/jgs.13781. PMID: 26782867
Adegboye AR, Boucher BJ, Kongstad J, Fiehn NE, Christensen LB, Heitmann BL
Public Health Nutr 2016 Feb;19(3):503-10. Epub 2015 May 4 doi: 10.1017/S1368980015001202. PMID: 25936381

Diagnosis

Redman RS, Kerr GS, Payne JB, Mikuls TR, Huang J, Sayles HR, Becker KL, Nylén ES
Biotech Histochem 2016;91(2):77-85. doi: 10.3109/10520295.2015.1082625. PMID: 26800284Free PMC Article
Shin HS, Shin MS, Ahn YB, Choi BY, Nam JH, Kim HD
J Am Geriatr Soc 2016 Jan;64(1):162-7. doi: 10.1111/jgs.13781. PMID: 26782867
Al Habashneh R, Azar W, Shaweesh A, Khader Y
Obes Res Clin Pract 2016 Jan-Feb;10(1):15-23. Epub 2015 Apr 15 doi: 10.1016/j.orcp.2015.03.010. PMID: 25890852
Salminen A, Kopra KA, Hyvärinen K, Paju S, Mäntylä P, Buhlin K, Nieminen MS, Sinisalo J, Pussinen PJ
Front Cell Infect Microbiol 2015;5:69. Epub 2015 Oct 1 doi: 10.3389/fcimb.2015.00069. PMID: 26484315Free PMC Article
Ji S, Choi Y
Front Cell Infect Microbiol 2015;5:65. Epub 2015 Sep 3 doi: 10.3389/fcimb.2015.00065. PMID: 26389079Free PMC Article

Therapy

Sun JY, Li DL, Dong Y, Zhu CH, Liu J, Li JD, Zhou T, Gou JZ, Li A, Zang WJ
Int Immunopharmacol 2016 Jul;36:86-93. Epub 2016 Apr 22 doi: 10.1016/j.intimp.2016.04.012. PMID: 27107801
Ide M, Harris M, Stevens A, Sussams R, Hopkins V, Culliford D, Fuller J, Ibbett P, Raybould R, Thomas R, Puenter U, Teeling J, Perry VH, Holmes C
PLoS One 2016;11(3):e0151081. Epub 2016 Mar 10 doi: 10.1371/journal.pone.0151081. PMID: 26963387Free PMC Article
Adegboye AR, Boucher BJ, Kongstad J, Fiehn NE, Christensen LB, Heitmann BL
Public Health Nutr 2016 Feb;19(3):503-10. Epub 2015 May 4 doi: 10.1017/S1368980015001202. PMID: 25936381
Akinkugbe AA, Saraiya VM, Preisser JS, Offenbacher S, Beck JD
J Clin Periodontol 2015 Jul;42(7):609-21. Epub 2015 Jul 14 doi: 10.1111/jcpe.12425. PMID: 26076661Free PMC Article
Hach M, Holm-Pedersen P, Adegboye AR, Avlund K
Int J Dent Hyg 2015 Nov;13(4):261-7. Epub 2015 Feb 12 doi: 10.1111/idh.12121. PMID: 25684316

Prognosis

Ide M, Harris M, Stevens A, Sussams R, Hopkins V, Culliford D, Fuller J, Ibbett P, Raybould R, Thomas R, Puenter U, Teeling J, Perry VH, Holmes C
PLoS One 2016;11(3):e0151081. Epub 2016 Mar 10 doi: 10.1371/journal.pone.0151081. PMID: 26963387Free PMC Article
Eke PI, Zhang X, Lu H, Wei L, Thornton-Evans G, Greenlund KJ, Holt JB, Croft JB
J Dent Res 2016 May;95(5):515-22. Epub 2016 Feb 4 doi: 10.1177/0022034516629112. PMID: 26848071
Zhao B, Jin C, Li L, Wang Y
Oral Health Prev Dent 2016;14(1):71-5. doi: 10.3290/j.ohpd.a35006. PMID: 26525131
Hsu CC, Hsu YC, Chen HJ, Lin CC, Chang KH, Lee CY, Chong LW, Kao CH
Medicine (Baltimore) 2015 Dec;94(51):e2347. doi: 10.1097/MD.0000000000002347. PMID: 26705230Free PMC Article
Boillot A, Bouchard P, Moss K, Offenbacher S, Czernichow S
J Clin Periodontol 2015 Apr;42(4):342-9. Epub 2015 Apr 7 doi: 10.1111/jcpe.12388. PMID: 25728988

Clinical prediction guides

Kurtulus Waschulewski I, Gökbuget AY, Christiansen NM, Ziegler M, Schuster V, Wahl G, Götz W
Arch Oral Biol 2016 Dec;72:75-86. Epub 2016 Aug 2 doi: 10.1016/j.archoralbio.2016.07.013. PMID: 27552374
Hong JW, Noh JH, Kim DJ
Medicine (Baltimore) 2016 Apr;95(14):e3226. doi: 10.1097/MD.0000000000003226. PMID: 27057854Free PMC Article
Eke PI, Zhang X, Lu H, Wei L, Thornton-Evans G, Greenlund KJ, Holt JB, Croft JB
J Dent Res 2016 May;95(5):515-22. Epub 2016 Feb 4 doi: 10.1177/0022034516629112. PMID: 26848071
Lages EJ, Costa FO, Cortelli SC, Cortelli JR, Cota LO, Cyrino RM, Lages EM, Nobre-Franco GC, Brito JA, Gomez RS
J Periodontol 2015 Sep;86(9):1058-68. Epub 2015 Jun 11 doi: 10.1902/jop.2015.150087. PMID: 26062839
Knight ET, Leichter JW, Tawse-Smith A, Thomson WM
J Periodontol 2015 Aug;86(8):945-54. Epub 2015 Apr 23 doi: 10.1902/jop.2015.150048. PMID: 25903984

Recent systematic reviews

Wang HF, He FQ, Xu CJ, Li DM, Sun XJ, Chi YT, Guo W
Genet Mol Res 2017 Feb 23;16(1) doi: 10.4238/gmr16019315. PMID: 28252166
Weng H, Yan Y, Jin YH, Meng XY, Mo YY, Zeng XT
Sci Rep 2016 Apr 20;6:24812. doi: 10.1038/srep24812. PMID: 27095260Free PMC Article
Yin WT, Pan YP, Lin L
Genet Mol Res 2016 Feb 5;15(1) doi: 10.4238/gmr.15017325. PMID: 26909953
Shungin D, Cornelis MC, Divaris K, Holtfreter B, Shaffer JR, Yu YH, Barros SP, Beck JD, Biffar R, Boerwinkle EA, Crout RJ, Ganna A, Hallmans G, Hindy G, Hu FB, Kraft P, McNeil DW, Melander O, Moss KL, North KE, Orho-Melander M, Pedersen NL, Ridker PM, Rimm EB, Rose LM, Rukh G, Teumer A, Weyant RJ, Chasman DI, Joshipura K, Kocher T, Magnusson PK, Marazita ML, Nilsson P, Offenbacher S, Davey Smith G, Lundberg P, Palmer TM, Timpson NJ, Johansson I, Franks PW
Int J Epidemiol 2015 Apr;44(2):638-50. Epub 2015 Jun 6 doi: 10.1093/ije/dyv075. PMID: 26050256Free PMC Article
Nascimento GG, Leite FR, Do LG, Peres KG, Correa MB, Demarco FF, Peres MA
J Clin Periodontol 2015 Jun;42(6):495-505. Epub 2015 Jun 2 doi: 10.1111/jcpe.12417. PMID: 25952821

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