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"ABSTRACTLatar Belakang: Serotonin merupakan monoamine yang berperan sebagai neurotransmitter di sistem saraf pusat dan perifer. Penelitian terbaru menyatakan bahwa serotonin juga mempengaruhi fungsi sel T dan sel B. Serotonin transporter merupakan pusat regulasi sistem serotonergic dan menyebar diekspresikan pada sel-sel di sistem imun. Polimorfisme pada promotor gen serotonin transporter (5-HTTLPR) menunjukkan aspek genetic pada terjadinya depresi. Cheilitis angularis merupakan penyakit kompleks dengan keterlibatan faktor geneti. Adanya polimorfisme ini menyebabkan inflamasi pada penyakit cheilitis angularis yang dimediasi oleh sel T dan meningkatnya prevalensi depresi pada pasien cheilitis angularis. Tujuan: Mendeteksi adanya polimorfisme gen Serotonin transporter SLC6A4 (5-HTTLPR) pada penderita cheilitis angulari. Metode: Analisis polimorfisme gen Serotonin transporter SLC6A4 (5-HTTLPR) dilakukan dengan metode PCR-VNTR. Analisis statistic dilakukan dengan uji Chi-square. Hasil: Dalam penelitian ini, pada kelompok cheilitis angularis ditemukan 24 sampel dengan genotip SS, 23 sampel dengan genotip LS, dan 3 sampel dengan genotip LL. Sedangkan pada kelompok non-cheilitis angularis, ditemukan 5 sampel dengan genotip SS, 18 sampel dengan genotip LS, dan 27 sample dengan genotip LL. Pada kelompok cheilitis angularis ditemukan 71 alel S dan 29 alel L, dan pada kelompok non-cheilitis angularis ditemukan 28 alel S dan 72  alel L. Kesimpulan: Terdapat perbedaan bermakna pada distribusi polimorfisme gen Serotonin transporter SLC6A4 (5-HTTLPR)cheilitis angularis dengan non-cheilitis angularis (p = 0.001).

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ABSTRACTSerotonin is a monoamine acting as a neuromediator in the central and peripheral nervous system. Recently, serotonin has also been shown to influence T- and B-cell function. The serotonin transporter is central in the regulation of the serotonergic system and widely expressed on cells of the immune system. A functional length polymorphism in the promoter of the serotonin transporter gene (5-HTTLPR) has been implicated in the genetic background of depression. Cheilitis angularis is a complex disease with a polygenetic inheritance. This polymorphism cause inflammation in cheilitis angularis mediated by the role of T cell and increased prevalence of depression in cheilitis angularis patients. To determine the relationship between the Serotonin transporter SLC6A4 (5-HTTLPR) gene polymorphism in cheilitis angularis patients in Indonesia. Analysis of the Serotonin transporter SLC6A4 (5-HTTLPR) gene polymorphism was observed by carrying out PCR method followed by electrophoresis for the analysis, without the usage of restriction enzyme. The chi-square test was used for statistical analysis. In this study, in the cheilitis angularis group there were 24 samples with SS genotype, 23 samples with LS genotype, and 3 samples with LL genotype. Whereas in the non-cheilitis angularis group, there were 5 samples with SS genotype, 18 samples with LS genotype, and 27 samples with LL genotype. In the cheilitis angularis group found 71 S alleles and 29 L alleles, and in the non-cheilitis angularis group 28 S alleles and 72 L alleles were found. There were significant differences in the distribution of the Serotonin transporter SLC6A4 (5-HTTLPR) gene polymorphism between cheilitis angularis and non-cheilitis angularis groups (p = 0.001). "

"ABSTRAKIndonesia merupakan salah satu negara dengan populasi terpadat di dunia, namunternyata statistik menunjukan bahwa tingkat kemandulan di Indonesia mengalamipeningkatan selama 10 tahun terakhir. Salah satu faktor yang menyebabkankemandulan adalah faktor genetik pada pria. MTHFR merupakan enzim yangdikode oleh gen MTHFR dan polimorfisme pada titik A1298C telah dibuktikanmemiliki asosiasi terhadap azoospermia di berbagai negara. Tujuan dari penelitianini adalah untuk identifikasi distribusi frekuensi genotip dan alotip daripolimorfisme gen MTHFR A1298C pada laki-laki normal dan azoospermia yangdatang ke Klinik Yasmin untuk berobat. Metode yang digunakan adalah studicross sectional dan penelitian dilakukan di Klinik Yasmin dan department biologiFakultas Kedokteran Universitas Indonesia sejak Oktober 2011 sampai Mei 2013.Sampel darah diambil dari pasien lalu diisolasi DNA dan dianalisa genotipnya.Data di analisa menggunakan perangkat lunak SPSS 21 dengan tes Chi Square.Hasil dari penelitian ini menunjukan bahwa 66,7% laki-laki normal memilikigenotip AA, 23,8% memiliki AC, dan 9,5% memiliki CC. Sedangkan pada priaazoospermia, 41,0% genotip nya adalah AA, 59,0% adalah AC, dan tidakditemukan pria bergenotip CC. Selain itu, ada asosiasi antara polimorfisme genMTHFR A1298C dengan laki-laki azoospermia (p=0,049), namun tidakditemukan asosiasi antara alotip A atau C terhadap azoospermia (p=0,340). Olehkarena itu, dapat disimpulkan bahwa ada asosiasi terhadap polimorfisme genMTHFR pada laki-laki dengan azoospermia.

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ABSTRACTIndonesia is one of the densely populated countries in the world, howeverstatistics revealed that infertility in Indonesia has been increasing over the last 10years. One of the factors causing infertility is genetic predisposition in the male.MTHFR is an enzyme coded by the MTHFR gene and its A1298C polymorphismhas been proven to cause infertility in many other countries. The purpose of thisstudy was to identify the genotype and allotype distribution of A1298C genepolymorphism in normal and azoospermia men who came to Klinik Yasmin toseek for treatment. The method used in this research is cross sectional and it tookplace at Klinik Yasmin and biology department of Faculty of MedicineUniversitas Indonesia from October 2011 until May 2013. Patients blood weredrawn and DNA was isolated in order to obtain the patient’s genotype. The datawas analyzed by SPSS 21 using Chi Square test. The result of this researchshowed that the normal men’s genotype consist of 66.7% AA, 23.8% AC, and9.5% CC. While in azoospermic patients, 41.0% AA, 59.0% AC, and CCgenotype was not found. In addition, There is association between MTHFR genepolymorphism A1298C with azoospermic men (p=0.049), however associationbetween A or C allotype with azoospermia was not found (p=0.340). To conclude,there is association between MTHFR gene polymorphism A1298C withazoospermia."

"Polimorfisme gen VDR -1056 T/C berperan dalam metabolisme tulang dan mempengaruhi fungsi imun yang memicu terjadinya resorpsi tulang pada periodontitis. Tujuan: Untuk mengetahui perbedaan pola distribusi polimorfisme gen VDR -1056 T/C pada penyakit periodontitis dengan kelompok kontrol. Metode: Polimorfisme gen -1056 VDR dianalisis menggunakan metode PCR-RFLP dengan enzim restriksi Taq I. Hasil: Terdapat polimorfisme gen VDR -1056 T/C pada kasus dengan frekuensi genotip TC 44.5 dibandingkan dengan kelompok kontrol 55.6 . Sedangkan untuk frekuensi alel C pada kasus 44.4, dan kelompok kontrol 55.6. Kesimpulan: Distribusi polimorfisme gen VDR -1056 T/C pada penyakit periodontitis sebesar 44.5 genotip TC, 50.5 genotip TT, dan 0 genotip CC. Namun tidak terdapat perbedaan yang bermakna antara distribusi polimorfisme gen VDR -1056 T/C pada penyakit periodontitis dan kelompok kontrol p=1,0.

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VDR 1056 T C gene polymorphism is involved in bone metabolism and affect the immune function that leads to bone resorption in periodontitis.

Objective: To know the difference of distribution pattern of the gene VDR 1056 T C polymorphism in periodontitis disease with control group.

Methods: The VDR 1056 T C gene polymorphism was analyzed by the PCR RFLP method with Taq I restriction enzyme digestion.

Results: There are VDR 1056 T C gene polymorphism in the case with TC genotype frequency 44.55 compared with the control group 55.6 . As for the frequency of C alleles in the case 44.4 , and control group 55.6.

Conclusion: The distribution of VDR 1056 T C gene polymorphism in periodontitis disease was 44.5 TC genotype, 50.5 TT genotype, and 0 CC genotype. But there was no significant difference between the distribution of VDR T C gene polymorphism in periodontitis and control group p 1.0."

"ABSTRACTStunting or short stature in children is a significant nutritional problem in developing and underdeveloped countries. Stunting during childhood might affect brain development and impair development cognitive function. Additionally, this condition associated with the increased risk for obesity during adulthood. Several studies have shown that the increment risk of obesity and overweight in children with a short stature was due to their metabolic efficiency. Children with stunting have lower resting energy expenditure compared to non stunting children. Additionally, stunted children has higher respiratory quotient and carbohydrate oxidation but lower fat oxidation compared to non-stunting children. These results might explain why stunted children easily become obese, which is due to lower fat oxidation and leading to tendency to store fat.This review discussed the current status on studies in the nutrigenetic aspects of the relationship between stunting in the childhood and obesity in adulthood. I hypothesized that stunted children are more likely to become obese in their later life because they have lower metabolic rate and higher tendency of fat storage. There are several candidate genes and pathway involved in obesity and I suspected that ghrelin and its receptor growth hormone secretague receptor (GHSR) were responsible."

"Patogenesis nefropati diabetik (ND) merupakan hasil interaksi faktor hemodinamik, metabolik dan lingkungan serta faktor genetik. ND biasanya tidak terdeteksi secara klinis sampai terjadi kerusakan ginjal yang bermakna dapat berupa glomerulosklerosis, tubular atrofi dan fibrosis interstitial. KIM-1 dapat digunakan sebagai penanda adanya kerusakan tubulus ginjal. Hubungan polimorfisme gen ACE dengan nefropati diabetes masih tidak konsisten. Penelitian ini merupakan studi cross sectional komparasi antara dua kelompok penyandang DMT2 dengan atau tanpa nefropati yang bertujuan untuk mengetahui adanya kerusakan tubulus, polimorfisme gen ACE dan menganalisis hubungannya dengan kadar KIM-1 terhadap terjadinya kelainan tubulus. Didapatkan adanya peningkatan ekskresi KIM-1 urin pada 19 subjek pre-nefropati dengan median 1,3 (interquartile 1,5) ng/mL, 25 subjek nefropati insipien dengan median 1,6 (interquartile 2,3) ng/mL dan 12 subjek nefropati overt dengan rerata kadar KIM-1 3,1 ± 2,4 ng/mL. Terdapat polimorfisme gen ACE pada penyandang DMT2. Proporsi genotipe DD 9,3%, ID 33,3% dan II 57,4% pada kelompok NND, pada kelompok ND proporsi genotipe DD 4,7%, ID 34,1% dan genotipe II 61,2%. Dijumpai adanya hubungan bermakna antara alel D dengan peningkatan ekskresi KIM-1 urin pada kelompok pre-nefropati (p = 0,030). Peningkatan kadar KIM-1 urin pada kelompok pre-nefropati menunjukkan adanya kerusakan tubulus yang merupakan proses awal nefropati DM. Distribusi genotipe polimorfisme gen ACE pada penelitian ini menyerupai penelitian lain di negara-negara Asia, sedangkan di negara Eropa genotipe DD lebih banyak daripada genotipe II. Hubungan bermakna alel D dengan kadar KIM-1 hanya pada kelompok prenefropati mungkin disebabkan adanya faktor lain seperti kadar glukosa, kontrol glikemik, ureum, kreatinin dan kadar trigliserida yang memengaruhi. Simpulan: Terdapat peningkatan ekskresi KIM-1 urin pada penyandang DMT2 kelompok pre-nefropati yang meningkat secara bermakna pada penyandang DMT2 dengan nefropati overt. Peningkatan ekskresi KIM-1 urin dapat dipakai sebagai penanda kerusakan tubulus. Terdapat polimofisme gen ACE pada penyandang DMT2. Genotipe II lebih banyak dibanding genotipe ID dan DD. Dijumpai adanya hubungan alel D dengan peningkatan kadar KIM-1 urin pada penyandang DMT2 pre-nefropati.

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The pathogenesis of nephropathy diabetic (ND) is the result of the interaction of haemodynamic, metabolic, environment, and genetic factors. In general, ND was clinically undetectable until kidney has been damaged significantly, in the form of glomerulosclerosis, tubular atrophy, or interstitial fibrosis. KIM-1 can be used as the initial indicator of kidney tubules damage. The relationship between ACE gene polymorphism and diabetic nephropathy was still inconsistent.

This research was a comparative cross-sectional study on two groups of DMT2 patients with and without nephropathy diabetic. The objectives of this study were to identify the tubules damage, ACE gene polymorphism, and to analyze the relationship between the degree of KIM-1 and the tubules damage. The increase of KIM-1 urine excretion was found in 19 pre-nephropathy subject (median = 1.3 with interquartile 1.5 ng/mL), in 25 incipient nephropathy subject (median = 1.6 (2.3) ng/mL), in 12 overt nephropathy subject (Mean = 3.1 ± 2,4 ng/mL). ACE polymorphism gene was found in DMT2 patients. In the NDD group, the genotype proportion of DD = 9.3%, ID = 33.3% and II = 57.4%. Whereas, in the ND group, the figures were 4.7%, 34.1% and 61.2%, respectively.

Significant relationship was found between allele D and the increase of KIM-1 urine on pre-nephropathy group (p = 0.030). The increase of KIM-1 urine on prenephropathy group shows the tubules damage which is the initial process of nephropathy diabetic. The genotype distribution of ACE gene polymorphism in this study was similar with the studies in Asian countries; however, in European countries the genotype DD is found higher than genotype II. The significant relationship between allele D and KIM-1 level in pre-nephropathy group might be the influence of other factors, such as glucose level, glycaemic control, urea, creatinine, and triglyceride level.

Conclusion: There was KIM-1 excretion increased on DMT2 pre-nephropathy group, which increase significantly in DMT2 overt nephropathy group. The increase of KIM-1 urine excretion can be used as the indicator of tubules damage. ACE gene polymorphism was found in DMT2 group, with genotype II was higher than genotype ID and DD. A significant relationship between allele D and the increase of KIM-1 urine excretion was found in pre-nephropathy group."

"ABSTRAKPatomekanisme dermatitis atopik melibatkan interaksi yang kompleks antara genetik danlingkungan. Satu gen yang secara konsisten berhubungan dengan DA adalah mutasi genFilaggrin yang dapat mengganggu agregasi sitoskeleton epidermis. Beberapa usahapencegahan telah dilakukan antara lain dengan pemberian ASI eksklusif dan suplementasiLCPUFA, tetapi studi klinis dan meta-analisis tidak menunjukkan hasil yang konsisten.Inkonsistensi ini dapat disebabkan adanya variasi aktivitas enzim desaturase yang dapatmemodulasi metabolisme PUFA, yang diatur oleh gen FADS1 dan FADS2, serta usiasaat intervensi dilakukan. Diperkirakan periode in-utero memegang peran penting untukkeberhasilan intervensi.Penelitian ini bertujuan mengetahui peran mutasi gen FLG dan polimorfisme gen FADS1dan FADS2 terhadap timbulnya DA pada usia satu tahun. Tujuan Khusus yaitumengetahui frekuensi mutasi gen FLG dan polimorfisme gen FADS1 dan FADS2,mengetahui peran polimorfisme gen FADS1 dan FADS2 terhadap substrat dan produkLCPUFA dan efeknya terhadap timbulnya DA, mengetahui pengaruh peningkatan rasioAA terhadap DHA di awal kehidupan terhadap timbulnya DA, mengetahui peranprotektif ASI eksklusif untuk pencegahan DA.Digunakan dua desain penelitian 1) potong lintang untuk mengetahui peran polimorfismegen FADS1 dan FADS2 terhadap perubahan komposisi LCPUFA saat lahir, 2) analisiskesintasan untuk melihat pengaruh mutasi gen Filaggrin dan polimorfisme gen FADS1dan FADS2 terhadap timbulnya DA, mengetahui peran peningkatan rasio AA/DHA sertamengetahui efek protektif ASI eksklusif terhadap timbulnya DA pada usia satu tahun.Insidens DA dalam penelitian ini sebesar 15,4%. Tidak ditemukan 5 mutasi gen Filaggrinsesuai dengan data NCBI. Frekuensi alel minor pada polimorfisme gen FADS1 22−27%,sedangkan untuk FADS2 berkisar 15−48%. Dalam penelitian ini terlihat pengaruhpolimorfisme gen FADS1 dan FADS2 terhadap perubahan komposisi LCPUFA,khususnya peningkatan asam arakidonat pada kelompok alel minor. Dalam penelitian initidak ditemukan hubungan antara komposisi LCPUFA dan polimorfisme gen FADSterhadap timbulnya DA. Pemberian ASI eksklusif selama 3−6 bulan tampaknya memberiefek proteksi terhadap DAPeneIitian ini diharapkan dapat menjadi landasan untuk tindakan pencegahan DA.Penelitian ini tidak berhasil menemukan common mutation yang dilaporkan NCBI.Mutasi gen Filaggrin tergantung perbedaan ras, maka untuk menemukan mutasi yangbaru lebih baik digunakan sekuensing gen secara penuh. Adanya perbedaan frekuensi alelminor antara anak Indonesia dan Eropa dan aktivitas enzim yang bekerja dengan arahyang berlawanan dengan alel minor populasi Eropa, mengakibatkan peningkatan kadarAA dan DGLA pada populasi alel minor dalam penelitian ini.

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ABSTRACTPathomechanism of atopic dermatiis is linked to the gene-environment interactions. Onegenetic locus consistently linked with AD is mutations of filaggrin gene that can inducedisruption in epidermal cytoskeleton aggregation. Some protective measures for theprevention of AD are breastfeeding and the provision of LCPUFA, but clinical studiesand meta-analysis have shown inconsistent results, which maybe due variation in theactivity of desaturating enzymes modulating PUFA metabolism, which are encoded bythe FADS1 and FADS2 gene cluster and the age at which LCPUFA interventions areprovided.The general objective is to characterize the impact of genetic variation in the FLG andFADS1, FADS2 genes cluster on LC-PUFA concentration in Indonesian infants. Specificobjectives including the characterization of the frequency of FLG and FADS1, FADS2gene single nucleotide polymorphisms (SNPs), the influence of FADS genepolymorphisms on fatty acid composition and on the occurence of AD, the impact ofincreasing ratio of arachidonic acid to docosahexaenoic acid on the progression of AD,and to see the protective effect of exclusive breastfeeding for the prevention of AD in thefirst year of life in Indonesian infants.Designs were 1) cross-sectional study to see the role of FADS1 and FADS2 genepolymorphism on the composition of LCPUFA at birth, 2) survival analysis to see therole of FLG mutation and FADS1 and FADS2 gene polymorphism on the progression ofAD, the role of increasing ratio of AA/DHA and the protective effect of exclusivelybreastfeeding on the occurence of AD in the first year of life.The incidence of AD in this study is 15.4%, No Filaggrin gene mutations based on 5reported pathogenic SNP was found. The minor allele frequency of FADS1 genepolymorphism were 22−27%, whereas for FADS2 were 15−48%. We found a strongcorrelation between FADS gene polymorphisms with the changes of LCPUFAcomposition, especially for the increment of arachidonic acid. No association was foundbetween the composition of LCPUFA and between FADS genes polymorphisms withAD. Exclusive breastfeeding until 3 months was found to be protective against AD.In this study we did not find Filaggrin mutation that reported as pathogenic from NCBI.The frequency of FADS1 polymorphism were 22−27%, whereas FADS2 polymorphismwere 15−48%. Strong correlation was seen between genetic variations of FADS geneswith the alteration of LCPUFA. Arachidonic acid as the product of LCPUFA was higherin the minor allele compared with the major allele. No association were found betweengenetic variation of FADS genes and the increased ratio of AA/DHA with the occurenceof AD. Exclusive breastfeeding for 3−6 months seems to give protective effect"

"Belakang: Polimorfisme gen MMP-9 berperan dalam degradasi kolagenase tipe IV pada matriks ekstraselular yang memicu terjadinya destruksi tulang pada periodontitis. Tujuan: Untuk membandingkan distribusi polimorfisme gen MMP-9 -1562 C/T rs3918242 pada penyakit periodontitis dengan kontrol. Metode: Polimorfisme gen MMP-9 -1562 C/T di analisis menggunakan metode PCR-RFLP dengan enzim restriksi SphI. Hasil: Mayoritas frekuensi alel T ditemukan pada sampel periodontitis 11 dibandingkan dengan sampel kontrol 2. Sedangkan untuk frekuensi genotipe CT pada sampel periodontitis 22 ditemukan lebih tinggi dibandingkan dengan sampel kontrol 4. Kesimpulan: Ditemukan gambaran polimorfisme Gen MMP-9 ndash;1562 C/T pada penyakit periodontitis dan terdapat hubungan bermakna antara distribusi polimorfisme gen tersebut pada penyakit periodontitis dan individu sehat p = 0,018.

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Background: MMP 9 gene polymorphism is involved in degradation of type IV collagenases in the extracellular matrix ECM that leads to bone destruction in periodontitis.

Objectives: To compare the distribution of the MMP 9 1562 C T rs3918242 polymorphism in Indonesian males with and without periodontitis.

Methods: The MMP 9 1562 C T polymorphism was investigated by the PCR ndash RFLP method with SphI restriction enzyme digestion.

Results: The T allele in periodontitis sample 11 are higher than the healthy controls 2 . As well as the CT genotype, was found higher in periodontitis sample 22 than the healthy controls 4.

Conclusion: MMP 9 1562 C T gene polymorphism was found in this study and significantly associated with periodontitis p 0.018. "

"Tujuan: Mengetahui hubungan antara polimorfisme gen Myosin 1H dan P561T dengan pertumbuhan dan perkembangan mandibula pada kasus maloklusi kelas I, II dan III. Metode penelitian: Subjek merupakan pasien dengan dengan kasus maloklusi skeletal kelas I, II dan III berusia 17 - 45 tahun yang sedang dan akan melakukan perawatan ortodonti di klinik ortodonti RSGM-FKGUI, yaitu 50 orang dengan maloklusi skeletal kelas I sebagai kontrol, 50 orang dengan maloklusi skeletal kelas II dan 50 orang dengan maloklusi skeletal kelas III. Penentuan maloklusi kelas I, II dan III berdasarkan analisis radiografis sefalometri awal dengan metode Stainer. Sampel DNA diekstraksi dari potongan kuku dan folikel rambut pada kasus maloklusi skeletal kelas III dan menggunakan sampel yang sudah diekstraksi dari usapan bukal dan sel darah pada pada kasus maloklusi skeletal kelas I dan II. Amplifikasi sekuens DNA dilakukan dengan menggunakan PCR (Polymerase Chain Reaction). Analisis Polimorfisme Genetik gen Myosin 1H dan P561T dengan teknik RLFP (Restriction Fragment Length Polymorphism). Pearson Chi-Square dilakukan untuk menganalisis hubungan antara polimorfisme dan pengukuran kraniofasial pada gen Myosin 1H dan Fisher Exact Test untuk menganalisis hubungan antara polimorfisme dan pengukuran kraniofasial pada gen P561T. Hasil: Terdapat hubungan polimorfisme gen Myosin 1H dengan maloklusi skeletal kelas I, II dan III. Tidak terdapat hubungan polimorfisme gen P561T dengan maloklusi skeletal kelas I, II dan III. Kesimpulan: Polimorfisme gen Myosin 1H merupakan salah satu faktor resiko dari maloklusi kelas I, kelas II dan kelas III. Ekstraksi DNA dari folikel rambut memberikan hasil yang cukup baik dalam hal kualitas DNA dan cara pengambilan sampel yang relatif lebih mudah dibandingkan purifikasi sel darah dan usapan bukal.

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Objectives: To determine the relationship between polymorphisms of Myosin 1H and P561T genes and the growth and development of the mandible in Class I, II, and III malocclusion cases. Methods: Subjects were patients aged 17-45 years old with Class I, II, and III skeletal malocclusion cases who were undergoing and/ or would undergo orthodontic treatment at the orthodontic clinic at RSGM-FKG UI, namely 50 people with Class I skeletal malocclusion, 50 people with Class II skeletal malocclusion, and 50 people with Class III skeletal malocclusion. Class I skeletal malocclusion was used as control group. Class I, II and III malocclusion were determined based on radiographic analysis of the initial cephalometry using the Stainer method. DNA samples were extracted from buccal swabs and blood cells in Class I and II malocclusion while nail clippings and hair follicles extracts were used in Class III malocclusion. DNA sequence amplification was carried out using the PCR (Polymerase Chain Reaction), while Genetic Polymorphism Analysis of Myosin 1H and P561T genes was performed with RLFP (Restriction Fragment Length Polymorphism). Pearson Chi-Square was used to analyze the relationship between polymorphism and craniofacial measurements in the Myosin 1H gene, while the Fisher Exact Test was used to analyze the relationship between polymorphism and craniofacial measurements in the P561T gene. Results: There is a relationship between Myosin 1H gene polymorphism and Class I, II, and III skeletal malocclusion. There was no correlation between P561T gene polymorphism and Class I, II, and III skeletal malocclusion. Conclusions: Myosin 1H gene polymorphism is one of the risk factors for Class I, II, and III malocclusion. Extraction of DNA from hair follicles gave good results in terms of DNA quality and was a relatively easier sampling method compared to blood cell purification and buccal swabs."