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- 1. TAI BI N M C RĂNGẾ ỌTAI BI N M C RĂNGẾ Ọ BS Lê Hà Thuỳ Nhung
- 2. Quá trình m c răng có hai th i kỳ:ọ ờ * Th i kỳ m c răng s a:ờ ọ ữ t 6 - 26 tháng, v iừ ớ 20 R. * Th i kỳ m c răng vĩnh vi nờ ọ ễ : chia làm 4 giai đo n:ạ - Kho ng 6 tu i m c 4 R6.ả ổ ọ - Kho ng 6 - 12 tu i, R s a r ng và thay b ngả ổ ữ ụ ằ 20 RVV. - Kho ng 12 tu i, R7 m c k R6.ả ổ ọ ế - Kho ng 18-25 tu i, b t đ u m c 4 R8.ả ổ ắ ầ ọ
- 3. TRÌNH T PHÁT TRI N VÀ M C RĂNGỰ Ể Ọ
- 4. B RĂNG S A (2 THÁNG – 26 THÁNG)Ộ Ữ Lúc mới sinh, niêm mạc miệng phủ trên xor dày lên để hình thành nướu hàm trên + dưới. Hàm trên và dưới hiếm khi ăn khớp: khoảng hở tăng lên ở vùng R trước; nướu hàm trên phủ hàm dưới phía môi má. Xương hàm dưới ptriển ra trước, xuống dưới để ăn khớp với hàm trên. Năm đầu, nướu pt nhanh (sang bên) để cung cấp khoảng hở cho R đang phát triển. XOR hàm trên và dưới ko pt tốt sau sinh. R sơ sinh
- 5. B RĂNG S A T 6 THÁNG - 2Ộ Ữ Ừ TU IỔ
- 6. B RĂNG S A LÚC 3 TU IỘ Ữ Ổ R cửa trục thẳng đứng -Độ cắn phủ lớn -Khe hở R cửa, phía gần Rnanh trên, phía xa R nanh dưới
- 10. B RĂNG H N H P (6 TU I – 11Ộ Ỗ Ợ Ổ TU I)Ổ
- 14. B RĂNG VĨNH VI NỘ Ễ (12 TU I – 25 TU I)Ổ Ổ
- 17. 1. Bất thường trong lúc mọc răng 1.1.Răng mọc sớm 1 1.1. Răng sữa mọc sớm * Răng mọc sớm thật sự Hình dáng đầy đủ, R cứng mọc trên nướu lành mạnh, tồn tại đến lúc rụng. Nguyên nhân: - Mầm R có sớm và nảy nở bình thường. - Mầm R có đúng ngày nhưng nảy nở nhanh bất thường. - Mầm R ở vị trí gần màng nhầy.
- 18. * Răng m c s m gi t oọ ớ ả ạ - Nguyên nhân: ch n th ng khiấ ươ sinh, V.mi ng tr s sinh,viêmệ ở ẻ ơ nang R. - Lâm sàng: R có khi m i sinh /r tớ ấ s m, dính c ng vào hàm và b lungớ ứ ị lay khi tr bú. Hình dáng R b tẻ ấ th ng ho c không có chân.ườ ặ Th ng g p R c a d i/ R c a trênườ ặ ử ướ ử (KH môi vòm mi ngệ - Ch n đoán phân bi t:ẩ ệ . R m c th t s .ọ ậ ự . R m c gi t o m c r t nhanh , Rọ ả ạ ọ ấ lung lay, n u xung quanh viêmướ - Đi u tr : nh .ề ị ổ
- 19. 1.1.2. Răng vĩnh vi n m c s mễ ọ ớ - Ch có m t R m c lên s m.ỉ ộ ọ ớ - Khó có k t lu n b nh lý v RVV s m.ế ậ ệ ề ớ - YTNC: + Tr em g y y uẻ ầ ế + Răng s a m t s m (sâu răng / b nh thi uữ ấ ớ ệ ế phosphatase làm cho cement c u t o ch a đ y đ )ấ ạ ư ầ ủ + R i lo n n i ti t (c ng tuy n yên / tuy n giáp)ố ạ ộ ế ườ ế ế
- 20. 1.2. Răng m c trọ ễ 1.2.1. Răng s a m c trữ ọ ễ X y ra trên nh ng đ a tr có th l c y u.ả ữ ứ ẻ ể ự ế Ch n đoánẩ : Tr 10 tháng tu i mà răngẻ ổ c a d i ch a m c ho c sau 3 năm hàmử ướ ư ọ ặ răng s a ch a đ .ữ ư ủ Nguyên nhân: do nh ng RL chung khóữ xác đ nh nh b nh giang mai, còi x ng,ị ư ệ ươ thi u D.D, thi u sinh t , RL tiêu hoá.ế ế ố
- 21. 1.2.2 Răng vĩnh vi n m c trễ ọ ễ * NN: (1)NN toàn thân: - B nh r i lo n quá trình tăng tr ng x ngệ ố ạ ưở ươ hàm và quá trình m c răng (lo n s n x ng,ọ ạ ả ươ Giang mai, SDD) x.hàm kém pt - Trong quá trình m c răng, s t caoọ ố sai l chệ tu i m c răngổ ọ - KS Tetracycline ah hình thành m m Rầ (2) T i ch :ạ ỗ - R s a t n t i lâu / m t s mữ ồ ạ ấ ớ - Do thi u ch (R5, R8) (x ng hàm không cònế ỗ ươ tăng tr ng + đ c ng cao/ m t R s mưở ộ ứ ấ ớ không nhai 1 bên x.hàm kém pt) - Do nh ng ch ng ng i ngăn ch n s m c răngữ ướ ạ ặ ự ọ (niêm m c + mô m m ph trên x ng dày) .ạ ề ủ ươ
- 22. * Th ng g p :ườ ặ ở - R c a hàm trên: R d / u răng / n uử ư ướ x hoáơ - R8 hàm d i / trên: R l ch / ng mướ ệ ầ - R3 hàm trên: Thi u ch / R s a t nế ỗ ữ ồ t i lâu / R vv m c sai chạ ọ ỗ - R c i l n: R s a b c ng kh p / R bố ớ ữ ị ứ ớ ị vùi l i trong x ng (ch n th ng / viêmạ ươ ấ ươ nhi m)ễ
- 23. Khi m khuy t di truy n (b t th ng m c răngế ế ề ấ ườ ọ nguyên phát) T l : 50%ỷ ệ nh h ng ch y u R sau vvẢ ưở ủ ế Không th t m c lên và không đáp ng v i Ch nh hình.ể ự ọ ứ ớ ỉ
- 24. a. Răng c a m c tr :ử ọ ễ * NN: - R s a m t s mữ ấ ớ s ng hoá b m t n uừ ề ặ ướ - R dư * ĐT: - R c a n m nôngử ằ r ch mô m m b c l Rạ ề ộ ộ - R n m sâu h n: b c l thân răngằ ơ ộ ộ - Tr : PT b c l thân răng + Ch nh hìnhễ ộ ộ ỉ
- 25. RĂNG NANH NG MẦ
- 26. b. Răng c i l n th nh t hàm trênố ớ ứ ấ m c trọ ễ (1) R6 m c sai v trí (XHT nh , lùi sau + Rọ ị ỏ c i vv có kích th c l n, m c nghiêng):ố ướ ớ ọ LS: không đau; phát hi n nh X quangệ ờ BC: m t R c i s aấ ố ữ m t kho ngấ ả Rvv m c nghiêng g n.ọ ầ ĐT: - Tiêu R c i s a nh : R t đi u ch nh.ố ữ ẹ ự ề ỉ - Rvv k t, không m c đ c (6 tháng) /ẹ ọ ượ R c i s a ti p t c tiêu: di chuy n Rvv =ố ữ ế ụ ể ch nh hìnhỉ
- 27. (2) R s a c ng kh p / R s a vùi l i trong xor:ữ ứ ớ ữ ạ BC: Rvv m c tr ho c m c l ch l cọ ễ ặ ọ ệ ạ ĐT: nh R s a + đ t b ph n gi kho ng sauổ ữ ặ ộ ậ ữ ả khi đã đi u ch nh kh p c n + d ng l i Rvvề ỉ ớ ắ ự ạ nghiêng. (3) R s a t n t i lâu trên cung hàm:ữ ồ ạ LS: R s a t n t i khi chân răng vv t ng ngữ ồ ạ ươ ứ đã thành l p > ¾ chi u dài.ậ ề BC: gây l ch l c ho c c n chéo Rvvệ ạ ặ ắ ĐT: nh R s a + b ph n gi kho ng+ Rvv tổ ữ ộ ậ ữ ả ự m c đúng v trí (v trí / h ng m c thích h p) /ọ ị ị ướ ọ ợ t đi u ch nh b ng cân b ng môi má l i (l chự ề ỉ ằ ằ ưỡ ệ ngoài / trong nh ) / PT b c l R và kéo vàoẹ ộ ộ cung hàm = CH
- 28. RĂNG VÙI L I TRONGẠ X NGƯƠ
- 29. c. Răng c i l n th baố ớ ứ *NN: - Xu hướng mất cân đối kích thước giữa răng và xương hàm Rvv mọc sau có nguy cơ kẹt và ngầm do thiếu chỗ. - Các R khôn mọc khoảng từ 18-25 tuổi, R mọc sau cùng trên cung hàm / xương hàm không còn tăng trưởng và xương trưởng thành có độ cứng cao - Hiện diện R dư phía xa R8 (hàm trên)
- 31. 2. Tai bi n m c răng s 8ế ọ ố Hay g p R8 d i v i t l 20/1 c a tai bi n m c R8.ặ ướ ớ ỷ ệ ủ ế ọ
- 32. * Phôi h c:ọ - R đ c sinh ra sau khi đã có m m R7.ượ ầ - M m R6,7,8 hàm d i có cùng th ng liên bào;ầ ướ ừ R6,7 m c tr c kéo thân R8 nghiêng v phíaọ ướ ề R7, trong khi chân R d nghiêng v phía gócễ ề hàm do tác đ ng c a c ch tăng tr ng x ngộ ủ ơ ế ưở ươ hàm. - R8 nghiêng b i đ nghiêng kh i thu c a lá Rở ộ ở ỷ ủ + nghiêng thêm do s n y n ra phía sau c aự ả ở ủ góc hàm → R8 m c nghiêng t d i lên trênọ ừ ướ và t sau ra tr c.ừ ướ - Đ đi u ki n, R s m c bình th ng. Ng c l iủ ề ệ ẽ ọ ườ ượ ạ n u đ nghiêng kh i thu quá l n và không đế ộ ở ỷ ớ ủ ch , R s đ ng vào m t xa c a R7.ỗ ẽ ụ ặ ủ
- 33. * Gi i ph uả ẫ : X ng hàm g m có 2 ph n, ph n x ngươ ồ ầ ầ ươ th t s và ph n XOR.ậ ự ầ - Trong th i gian R8 thành hình và vôi hoá, x ngờ ươ hàm d i đ ng th i tăng tr ng = tiêu x ng m tướ ồ ờ ưở ươ ặ trong và đ p x ng m t ngoàiắ ươ ặ góc hàm d i đ cướ ượ n y n và hàm d i phát tri n xu ng d i và raả ở ướ ể ố ướ tr c.ướ - Khi phát tri n ra phía sau, hàm kéo theo m m R8ể ầ đang hình thành, làm thân hay l ch phía g n vàệ ầ chân R l ch phía xa,ệ - XOR ch n y n khi có R, XOR thay đ i th tích,ỉ ả ở ổ ể kích th c nhi u trong lúc R không thay đ i. Kho ngướ ề ổ ả 1000 năm g n đây x ng hàm con ng i ngày càngầ ươ ườ nh trong lúc đó R v n gi nguyên kích th c gâyỏ ẫ ữ ướ nên s m t cân đ i gi a x ng hàm và R. R8 m c sauự ấ ố ữ ươ ọ cùng không đ ch , R8 trên m c l ch ra phía ngoài,ủ ỗ ọ ệ R8 d i khó ki m đ ch và th ng gây tai bi n.ướ ế ủ ỗ ườ ế
- 34. Cách b trí màng nh y xung quanh túi quanhố ầ răng: Màng nh y khi R m c có th 1 trong 2 v trí sau:ầ ọ ể ở ị - Kho ng gi a R7 và nhánh lên XHD r ng thì R8ả ữ ộ đ ch m củ ỗ ọ : khi m c lên m t nhai b che b i 1ọ ặ ị ở ph n c a túi quanh răng và m t l p m ng màngầ ủ ộ ớ ỏ nh y.ầ - Kho ng gi a R7 và nhánh lên XHD h p, không đả ữ ẹ ủ ch m cỗ ọ , R8 n m 1 ph n trong nhánh lên c aằ ầ ủ XHD. Khi đó m t nhai b che b i m t l p dàyặ ị ở ộ ớ màng nh y c a c t tr c màng h uầ ủ ộ ướ ầ → t n t iồ ạ m tộ ph n túi quanh Rầ → nhi m trùng.ễ
- 35. 2.1. Biến chứng 2.1.1. Bệnh nha chu - Trong khi mọc, R8 có thể chạm vào mặt xa của R7, túi quanh R8 có thể ăn thông với vùng dây chằng của R7. Nếu vùng này bị nhiễm độc do sâu R hoặc bệnh nha chu thì túi quanh R8 sẽ bị nhiễm độc và gây tai biến. - R7 cũng có thể thông với túi quanh R8 và với bên ngoài cho nên dễ bị nhiễm trùng.
- 36. - R8 d i l ch:ướ ệ R8 làm gi m l ng x ng phía xa R7 k c nả ượ ươ ế ậ + khó gi VS m t xa R7ữ ở ặ VK gây viêm n u xâm nh p vào m t chân Rướ ậ ặ VNC - R8 trên: Túi nha chu m r ng v phía chópở ộ ề BNC ti n tri n nhanh và tr m tr ng (Vùng chế ể ầ ọ ẽ R7 trên) ĐT BNC t i ch xung quanhạ ỗ R7 trên khó vì liên quan vùng ch phía xaẽ - Nh s m R8ổ ớ ngăn ng a BNC, x ng l pừ ươ ắ kín vùng thân R l ch chi m ch tr c đó.ệ ế ỗ ướ
- 37. Ng.nhân chính cuả tai biến mọc R8 là sự tập trung của VK gây nhiễm trùng, những ng. nhân khác như R nghiêng, hàm hẹp chỉ là phụ.
- 38. 2.1.2. Sâu răng - R l ch t a vào răng k bênệ ự ế nh i nhétồ th c ăn + khó làm s chứ ạ VK sâu răng xâm nh p vào m t R k c nậ ặ ế ậ sâu răng l ch + R k bên.ệ ế - Th ng g p R8 d i l ch phía g nườ ặ ở ướ ệ ầ
- 39. 2.1.3. Tiêu chân răng R l ch và ng m gây áp l c lên chân răng k c nệ ầ ự ế ậ đ gây tiêu chân răng.ủ Quá trình tiêu chân răng ch a xác đ nh rõ, = quáư ị trình tiêu chân răng s a khi có Rvv thay thữ ế 2.1.4. Gãy x ng hàmươ R8 ng m trong XHD chi m m t ph n x ng hàmầ ế ấ ầ ươ bình th ng do x ng l p đ yườ ươ ấ ầ XHD y u và dế ễ b t n th ng.ị ổ ươ 2.1.5. Răng chen chúc hàm d iở ướ Nh R8 ch a m c tr c khi ch nh hìnhổ ư ọ ướ ỉ gi mả nguy c chen chúc răng BN C’Hình và khôngơ ở C’hình’ Không nên PT l y m m R8 lúc 7-9 tu iấ ầ ổ
- 40. 2.1.6. U và nang - R ng m trong x ng hàm, bao R t n t i v iầ ươ ồ ạ ớ kích th c ban đ u / thoái hoá thành nangướ ầ thân răng ho c nang s ng.ặ ừ N u kho ng bao m m răng quanh thân R >ế ả ầ 3mm ch n đoán là nang răngẩ - U răng phát sinh t bi u mô trong bao răng.ừ ể Th ng g p là u menườ ặ
- 41. U nguyên bào men: U gây bi n d ng m tế ạ ặ Răng đ i di n c n cham gây in d u trên uố ệ ắ ấ
- 42. 2.1.7. Viêm quanh thân răng (Viêm l i trùm)ợ - Là nhi m trùng c a mô m m xung quanh thânễ ủ ề răng c a R ng m 1 ph n và do VK th ng trúủ ầ ầ ườ trong mi ng gây ra.ệ - NN: Th phát do ch n th ng t R8 trên: mô m mứ ấ ươ ừ ề bao ph m t nhai R8 d i ch n th ng + s ng.ủ ặ ướ ấ ươ ư Do nh i nhét th c ăn bên d i mô m m baoồ ứ ướ ề ph m t nhai + khó làm s chủ ặ ạ VK xâm nh pậ
- 43. * Viêm quanh thân răng c p /ấ Viêm xu t huy tấ ế : - ∆+: v t l i ph thân răng và t ch c lân c n, tri uạ ợ ủ ổ ứ ậ ệ ch ng h ch lân c n, nhi m trùng toàn thânứ ạ ậ ễ - Tri u ch ng ch quan:ệ ứ ủ đau t i ch phía xa răngạ ỗ ở 7, lan lên tai, sàn mi ng, thành h ng,đau tăng khiệ ọ nhai - T/c kquan: N u vùng R8 s ng đ đôi khi có d u c aướ ư ỏ ấ ủ R trên ch m, có th nhìn th y múi răng lú ra, đè vàoạ ể ấ n u có d ch vàng ho c máu r ra. Ngoài m t: s ngướ ị ặ ỉ ặ ư góc hàm. - Toàn thân: có th s t, m t m i, tăng b ch c u.ể ố ệ ỏ ạ ầ - Bi n ch ng:ệ ứ Áp xe quanh thân răng khôn/ Viêm mô t bào vùng m t ngoài x ng hàm d i, viêm h uế ặ ươ ướ ầ h ng / Viêm Amidan / Viêm t y lan t aọ ấ ỏ *
- 44. * Viêm m quanh thân răng:ủ - T/c ch quan:ủ Đau liên t c, đau lan lên tai m tụ ắ thái d ngươ →m t ng ; C ng khít hàm, nhi mấ ủ ứ ễ trùng lan đ n amydan, vùng tr c c a màng h uế ướ ủ ầ → nhai nu t đ u đau .ố ề - T/c kquan: S b x ng hàm d i ngoài vàờ ờ ươ ướ ở trong v n bình th ng; Đè lên n u có m ch y;ẫ ườ ướ ủ ả Viêm h ch.ạ - Toàn thân: s t, v m t nhi m trùng.ố ẻ ặ ễ - ĐT: t i ch + thu c KS-GĐ; c t l i trùm/ nh Rạ ỗ ố ắ ợ ổ l ch/ ĐT tu R7.ệ ỷ - Tình tr ng chung b nh h ng trong vài ngày,ạ ị ả ưở có th tái phát, ch h t h n khi m t nhai R8 đãể ỉ ế ẳ ặ đ c lo i b mô m mượ ạ ỏ ề
- 45. * Viêm quanh thân răng m n tínhạ : Do m ch y không h tủ ả ế → viêm m n tínhạ v i nh ng đ t k ch phát.ớ ữ ợ ị Đau nh h n viêm m , BN ê răng khóẹ ơ ủ ch u t i ch , há mi ng khó nh ng khôngị ạ ỗ ệ ư đau.
- 46. 2.2. Bi n ch ng c a viêm quanh thân răngế ứ ủ 2.2.1. Bi n ch ng màng nh yế ứ ầ +Viêm loét m c mi ng kèm s ng h ch góc hàm,ạ ệ ư ạ d i c m và nh ng d u hi u toàn thân.ướ ằ ữ ấ ệ + C n ch n đoán phân bi t:ầ ẩ ệ - Viêm loét m c mi ng do m c R:ạ ệ ọ l loét màngở nh y, có m t l p tr ng ph lên răng nguyênầ ộ ớ ắ ủ nhân, b t d n răng c a và ch m d t răng sớ ầ ở ử ấ ứ ở ố 3 đ i di n. Má và l i đ i di n răng nguyênố ệ ưỡ ố ệ nhân có th b loét.ể ị - V. do nhi m đ c, nhi m trùngễ ộ ễ lan tràn toàn mi ng.ệ
- 47. 2.2.2. Bi n ch ng v u, nangế ứ ề VQTR m n tính làm tăng s n nh ng môạ ả ữ c a túi răng còn sót l i, t o u h t / u nangủ ạ ạ ạ bên R.
- 48. 2.2.3. Bi n ch ng t bàoế ứ ế - Gây m t áp xe nh gi a thân răng và màng nh y,ộ ỏ ữ ầ - Viêm t y khu trú/ lan to vùng Amidan/ bên y t h uấ ả ế ầ - M lan ra sau lên trên, vào trong, ra ngoài ta có:ủ Áp xe thái d ngươ : Khi m lan ra sau lên trên.ủ Áp xe vùng c nhaiơ : Khi m lan ra sau và ra tr c, áp xe có đ c đi m c ngủ ướ ặ ể ứ khít hàm n ng và m t ngoài nhánh lên XHD s ng l n.ặ ặ ư ớ Viêm t y sàn mi ng:ấ ệ M lan vào trong và xu ng sàn mi ngủ ố ệ →viêm t y lanấ to r ng b nh nhân có th ch t.ả ộ ệ ể ế Áp xe má hàm: M lan ra tr c và phía ngoàiủ ướ áp xe di chuy n, v iể ớ d u hi u áp xe đ m m đ i di n v i vùng RCN, áp xe cóấ ệ ỏ ề ố ệ ớ th dò ra vùng màng nh y ngách hành lang ho c ngoàiể ầ ặ da
- 50. 2.2.4. Bi n ch ng x ngế ứ ươ - Ít . - Th ng x y ra khi tu răng ch t và nhi mườ ả ỷ ế ễ trùng. - Tr ng h p R8 m c l ch ch m vào m t xa R7,ườ ợ ọ ệ ạ ặ gây tiêu x ng . Tiêu x ng + R7ch t tuươ ổ ươ ế ỷ → R lung lay, BN không đau R8 mà đau R7.ở ở - Viêm quanh thân răng có m lan r ng vàoủ ộ x ngươ → viêm màng x ng. Ti n tri n ch m, ítươ ế ể ậ có d u hi u đ c bi t và tan ch m sau khi nhấ ệ ặ ệ ậ ổ răng nguyên nhân. M có th vào tu x ng gâyủ ể ỷ ươ viêm tu x ng.ỷ ươ
- 51. 2.2.6. Bi n ch ng liên quan đ n tĩnh m chế ứ ế ạ Viêm tĩnh m ch huy t kh i xoang hangạ ế ố 2.2.7. Bi n ch ng th n kinhế ứ ầ - Khi R8 m c có đau t i ch r i lan to ra chungọ ạ ỗ ồ ả quanh - Có th có hi n t ng đ ng th ng, co khít hàmể ệ ượ ồ ố nh / n ngẹ ặ 2.2.8. Bi n ch ng liên quan đ n t ng tr ngế ứ ế ổ ạ chung S t nh / cao tùy nhi m trùng nh / n ng, s cố ẹ ễ ẹ ặ ứ kho suy y u.ẻ ế 2.2.5. Bi n ch ng viêm h chế ứ ạ Viêm h ch góc hàm /d i hàmạ ướ
- 52. 2.3. Tai bi n v c năngế ề ơ - S c ép c a R8 vào c R7 (sâu ngà, viêmứ ủ ổ tu ).ỷ - S c ép c a R8 tác đ ng xa gây nên sâuứ ủ ộ ở răng nh ng răng phía tr c nh t làở ữ ướ ấ ở m t xa và g n c a RCN.ặ ầ ủ - R8 n m nghiêng khi m c có th làm xêằ ọ ể d ch t R nanh đ n R c a, R nanh th ngị ừ ế ử ườ m c l ch ngoài, R c a xoay gây nh ng r iọ ệ ử ữ ố lo n v kh p c n và viêm n u.ạ ề ớ ắ ướ
- 53. 2.4. Điều trị * Viêm quanh thân răng chưa có mủ - Rửa sạch vùng bị viêm bằng nước Hypochloride sodium - Súc miệng thường xuyên bằng nước muối loãng và ấm. - Điều trị kháng sinh, kháng viêm và giảm đau - Múi răng nhú lên chấm axit tricloroacetic (AT) đậm đặc. - Múi răng chưa nhú lên dùng dao mổ cắt quanh mặt răng.
- 54. * Viêm quanh thân răng có mủ - Đi u tr t i ch nh trênề ị ạ ỗ ư - Đi u tr kháng sinh, kháng viêm và gi mề ị ả đau - N u m không h t c t l i trùm.ế ủ ế ắ ợ - Tr ng h p múi răng nhú lên còn ít màngườ ợ niêm ch m AT.ấ - Răng m c l ch nh răng.ọ ệ ổ - Răng s 7 viêm tu do R8: đ t thu c di t tuố ỷ ặ ố ệ ỷ răng s 7, nh R8 sau đó đi u tr tu răng số ổ ề ị ỷ ố 7.
- 55. 3. Tai biến mọc răng sữa 3.1. Tại chỗ * Nhẹ. - Nướu quanh thân răng viêm đỏ. - Trẻ thường cho tay vào miệng ngay nơi răng mọc. - Bỏ ăn, bỏ bú, nước miếng chảy nhiều và khó chịu. * Nặng - Viêm quanh thân răng có mủ, trẻ mất ngủ, nướu sưng đỏ, đè vào nướu có nước vàng chảy hoặc có mủ. 3.2. Tai biến chung - Nước miếng nhiều, mặt đỏ bên răng mọc. - Sốt 38- 40 ºc có thể có co giật, rối loạn tiêu hoá, rối loạn hô hấp Điều trị: tại chỗ hoặc cho uống thuốc ho
Hinweis der Redaktion
- Mọc răng là một hiện tượng sinh lý. Có sự tham gia của mô xương và màng nhầy. + R có thể mọc sớm / muộn, tai biến mọc răng lệ thuộc nhiều vào môi trường. + Tai biến tại chỗ xảy ra bất cứ lúc nào. + Tai biến toàn thân ít dần khi trẻ lớn và thường xảy ra ở TK mọc răng sữa, ít thấy ở TK mọc răng vĩnh viễn.
- The human dentitions are usually categorized as being primary, mixed (transitional), and permanent dentitions. The transition from the primary/deciduous dentition to the permanent dentition is of particular interest because of changes that may herald the onset of malocclusion and provide for its interception and correction. Thus of impor- tance for the practitioner are the interactions between the morphogenesis of the teeth, development of the dentition, and growth of the craniofacial complex.
- At birth, the oral mucosa over the developing alveoli is greatly thick- ened to form the maxillary and mandibular gum pads. They show a series of elevations, each of which corresponds to an underlying deciduous tooth. The elevations associated with the second deciduous molars do not, however, become prominent until the age of about 6 months (Fig. 26.43). The maxillary and mandibular gum pads rarely come into occlusion, the space left between them being increased in the anterior region and being occupied by the tongue. The maxillary gum pad overlaps the mandibular gum pad both buccally and labially, the overjet usually being considerableThis reflects the small mandible. With normal growth, the anteroposterior position of the mandible will move forwards (and downwards) to match that of the maxilla during the mid-teenage years. Beneath the gum pads, there is generally considerable crowding of the developing teeth, espe- cially the incisors. During the first year of life, however, the gum pads grow rapidly, especially in lateral directions, thus providing space for the developing teeth. The maxillary and mandibular alveolar processes are not well developed at birth. Occasionally, a ‘natal tooth’ is present. This tooth is usually a supernumerary tooth (see page 311), formed by an aberration in the
- The deciduous teeth start to erupt at the age of 6 months and the deciduous dentition is complete by the age of 3 years. -6-8 tháng: R cửa trên + dưới -12-16 tháng: R cối thứ nhất trên + dưới -16-20 tháng: R nanh trên + dưới -21-30 tháng: R cối thứ hai trên + dưới EMERGENCE OF THE PRIMARY TEETH At about 8 (6 to 10) months of age, the mandibular central incisors emerge through the alveolar gingiva, followed by the other anterior teeth, so that by about 13 to 16 months, Chapter 2 Development and Eruption of the Teeth 27 Oral epithelium Alveolar cryptbone United epithelium CEJ Hertwig’s epithelial sheath Permanent tooth Figure 2-7 Section of mandible in a 9-month-old infant cut through an unerupted primary canine and its permanent successor, which lies lingually and apically to it. The enamel of the primary canine crown is completed and lost because of decalcification. Root formation has begun. CEJ, Cementoenamel junction. (Modified from Schour I, Noyes HJ: Oral histology and embryology, ed 8, Philadelphia, 1960, Lea & Febiger.) all eight primary incisors have erupted (see Table 2-1). Then the first primary molars emerge by about 16 months of age and make contact with opposing teeth several months later, before the canines have fully erupted. Passage through the alveolar crest (Figure 2-7) occurs when approximately two thirds of the root is formed,17 followed by emergences through the alveolar gingiva into the oral cavity when about three fourths of the root is completed.18 The emergence data are consistent with those of Smith.14 The primary first molars emerge with the maxillary molar tending most often to erupt earlier than the mandibular first molar.19 Some evidence shows a difference by gender for the first primary molars, but no answer is available for why the first molar has a different pattern of sexual dimorphism.7 The primary maxillary canines erupt at about 19 (16 to 22) months (Figure 2-8), and the mandibular canines erupt at 20 (17 to 23) months. The primary second mandibular molar erupts at a mean age of 27 (23 to 31, boys) (24 to 30, girls) months, and the primary maxillary second molar follows at a mean age of 29 (25 to 33 ± 1SD) months. In Figures 2-8, A and B, the first molars are in occlusion.
- At this time, the occlusion of the deciduous dentition differs from that of the permanent dentition in the following respects (Fig. 26.33c): The incisors are more vertically positioned within the alveolus and are often spaced. The overbite is usually greater. There may be significant spacings distal to the mandibular canines and mesial to the maxillary canines (the anthropoid or primitive spaces). Although the anteroposterior relationships of the deciduous arches have not been adequately assessed, it appears that the distal edges of the maxillary and mandibular deciduous molars are flush and the mesiobuccal cusps of the maxillary first and second deciduous molars occlude in the buccal grooves of the mandibular first and second deciduous molars respectively.
- The primary/deciduous dentition is considered to be com- pleted by about 30 months or when the second primary molars are in occlusion (Figure 2-9). The dentition period includes the time when no apparent changes occur intraorally (i.e., from about 30 months to about 6 years of age). The form of the dental arch remains relatively constant without significant changes in depth or width. A slightincrease in the intercanine width occurs about the time the primary incisors are lost, and an increase in size in both jaws in a sagittal direction is consistent with the space needed to accommodate the succedaneous teeth. An increase in the vertical dimension of the facial skeleton occurs as a result of alveolar bone deposition, condyle growth, and deposition of bone at the synchondrosis of the basal part of the occipital bone and sphenoid bones, and at the maxillary suture complex.20 The splanchnocranium remains small in com- parison with the neurocranium. The part of the jaws that contain the primary teeth has almost reached adult width. At the first part of the transition period, which occurs at about age 8, the width of the mandible approximates the width of the neurocranium. The dental arches are complete, and the occlusion of the primary dentition is functional. During this period, attrition is sufficient in many children and is quite observable. The primary occlusion is considered in Chapter 16.
- PRIMARY TEETH Enamel organs (Figure 2-5) do not all develop at the same rate; some teeth are completed before others are formed, which results in different times of eruption for differentgroups of teeth. Some of the primary/deciduous teeth are undergoing resorption while the roots of others are still forming. Not all the primary teeth are lost at the same time; some (e.g., central incisors) are lost 6 years before the primary canines. Groups of teeth develop at specific rates so that the sequence of eruption and emergence of the primary/ deciduous teeth is well defined with few deviations. Even so, for the individual child, considerable variation in the times of emergence of the primary dentition may occur. Theprimary dentition is completely formed by about age 3 and functions for a relatively short period of time before it is lost completely at about age 11. Permanent dentition is com- pleted by about age 25 if the third molars are included (see Figures 2-3 and 2-4).9 Calcification of the primary teeth begins in utero from 13 to 16 weeks postfertilization. By 18 to 20 weeks, all the primary teeth have begun to calcify. Primary tooth crown formation takes only some 2 to 3 years from initial calcifica- tion to root completion. However, mineralization of the permanent dentition is entirely postnatal, and the formation of each tooth takes about 8 to 12 years. The variability in tooth development is similar to that for eruption, sexual maturity, and other similar growth indicators.10 Crown formation of the primary teeth continues after birth for about 3 months for the central incisor, about 4 months for the lateral incisor, about 7 months for the primary first molar, about 8.5 months for the canine, andabout 10.5 months for the second primary molar. During these periods before and after birth, disorders in shape, pigmentation, mineralization, and structure sometimes occur (fluorosis is considered later in this chapter). Crown and Root Development Dental development can be considered to have two compo- nents: (1) the formation of crowns and roots and (2) the eruption of the teeth. Of these two, the former seems to be much more resistant to environmental influences; the latter can be affected by caries and tooth loss.11,12 After the crown of the tooth is formed, development of the root portion begins. At the cervical border of the enamel (the cervix of the crown), cementum starts to form as a root covering of the dentin. The cementum is similar in some ways to bone tissue and covers the root of the tooth in a thin layer. In the absence of a succeeding permanent tooth, the root of the primary tooth may only partially resorb. When root resorption does not follow the usual pattern, the per- manent tooth cannot emerge or is otherwise kept out of its normal place. In addition, the failure of the root to resorb may bring about prolonged retention of the primary tooth. Although mandibular teeth do not begin to move occlusally until crown formation is complete, their eruption rate does not closely correlate with root elongation. After the crown and part of the root are formed, the tooth penetrates the alveolar gingiva and makes its entry (emergence) into the mouth. Further formation of the root is considered to be an active factor in moving the crown toward its final position in the mouth. The process of eruption of the tooth is com- pleted when most of the crown is in evidence and when it has made contact with its antagonist or antagonists in the opposing jaw. The root formation is not finished when the tooth emerges; however, the formation of root dentin and cementum continues after the tooth is in use. Ultimately, the root is completed with a complete covering of cemen- tum. Additional formation of cementum may occur in response to tooth movement or further eruption of the teeth. Also, cementum may be added (repaired) and/or resorbed in response to periodontal trauma from occlusion. The covering of cementum of the permanent teeth is much thicker than that of the primary teeth.
- -6-7 tuổi: R cối lớn thứ nhất trên + dưới; R cửa giữa hàm dưới -7-8 tuổi: R cửa bên dưới + R cửa giữa trên -8-9 tuổi: R cửa bên trên Transitional (Mixed) Dentition Period The first transition dentition begins with the emergence and eruption of the mandibular first permanent molars and ends with the loss of the last primary tooth, which usually occurs at about age 11 to 12. The initial phase of the transition period lasts about 2 years, during which time the permanentfirst molars erupt (Figures 2-10 and 2-11), the primary inci- sors are shed, and the permanent incisors emerge and erupt into position (Figure 2-12). The permanent teeth do not begin eruptive movements until after the crown is com- pleted. During eruption, the permanent mandibular first molar is guided by the distal surface of the second primary molar. If a distal step in the terminal plane is evident, maloc- clusion occurs (see Figure 16-5). Loss of Primary Teeth The premature loss of primary teeth because of caries has an effect on the development of the permanent dentition21 and not only may reflect an unfortunate lack of knowledge as to the course of the disease but also establishes a negative attitude about preventing dental caries in the adult denti- tion. Loss of primary teeth may lead to lack of space for the permanent dentition. It is sometimes assumed by laypersons that the loss of primary teeth, which are sometimes referred to as baby teeth or milk teeth, is of little consequence because they are only temporary. However, the primary dentition may be in use from age 2 to 7 or older, or about 5 or more years in all. Some of the teeth are in use from 6 months until 12 years of age, or 11.5 years in all. Thus these primary teeth are in use and contributing to the health and well-being of the individual during the first years of greatest development, physically and mentally.
- Premature loss of primary teeth, retention of primary teeth, congenital absence of teeth, dental anomalies, and insufficient space are considered important factors in the initiation and development of an abnormal occlusion. Pre- mature loss of primary teeth from dental neglect is likely to cause a loss of arch length with a consequent tendency for crowding of the permanent dentition. Arch length is con- sidered in more detail in Chapter 16.
- -9-10 tuổi: R nanh hàm dưới -11-12 tuổi: R nanh hàm trên Hàm trên: R61245378 Hàm dưới: R61234578
- -10-11 tuổi: R4 trên -10-12 tuổi: R4 dưới, R5 trên -11-12 tuổi: R5 dưới
- -12-13 tuổi: R cối lớn thứ hai trên + dưới -17-21 tuổi: R cối lớn thứ ba trên + dưới Permanent Dentition The permanent dentition consisting of 32 teeth is com- pleted from 18 to 25 years of age if the third molar is included. Apparently there are four or more centers of formation (developmental lobes) for each tooth. The formation of each center proceeds until a coalescence of all of them takes place. During this period of odontogenesis, injury to the developing tooth can lead to anomalous morphological fea- tures (e.g., peg-shaped lateral incisor). Although no lines of demarcation are found in the dentin to show this develop- ment, signs are found on the surfaces of the crowns and roots; these are called developmental grooves (see Figure 4-12, B). Fractures of the teeth occur most commonly along these grooves (see Figure 13-26 ). The follicles of the developing incisors and canines are in a position lingual to the deciduous roots (see Figures 2-7 and 2-11; see also Figure 3-4). The developing premolars, which eventually take the place of deciduous molars, are within the bifurcation of primary molar roots (Figure 2-13, A and B). The permanent incisors, canines, and premolars are called succedaneous teeth because they take the place of their primary predecessors. The central incisor is the second permanent tooth to emerge into the oral cavity. Eruption time is quite close to that of the first molar (i.e., tooth emergence occurs between 6 and 7 years) (Table 2-2). As with the first molar, at 6 years 50% of individuals have reached the stage considered to be the age of attainment of the stage or, more specifically, the age of emergence for the central incisor. The mandibular permanent teeth tend to erupt before maxillary teeth. The mandibular central incisor usually erupts before the maxil- lary central incisor (see Figure 2-12) and may erupt simul- taneously with or even before the mandibular first molar. The mandibular lateral incisor may erupt along with the central incisor. Before the permanent central incisor can come into posi- tion, the primary central incisor must be exfoliated. This is brought about by the resorption of the deciduous roots. The permanent tooth in its follicle attempts to move into the position held by its predecessor. Its influence on the primary root evidently causes resorption of the root, which continues until the primary crown has lost its anchorage, becomes loose, and is finally exfoliated. In the meantime, the perma- nent tooth has moved occlusally so that when the primary tooth is lost, the permanent one is at the point of eruption and in proper position to succeed its predecessor. Mandibular lateral incisors erupt very soon after the central incisors, often simultaneously. The maxillary central incisors erupt next in chronological order, and maxillary lateral inci- sors make their appearance about 1 year later (see Table 2-2 and Figures 2-3 and 2-4). The first premolars follow the maxillary laterals in sequence when the child is about 10 years old; the mandibular canines (cuspids) often appear at the same time. The second premolars follow during the next year, and then the maxillary canines follow. Usually, the second molars come in when the individual is about 12 years of age;
- One or more teeth may be present at birth and are referred to as natal teeth. They are common in the mandibular incisor region (Fig. 26.48). If they appear during the first month of birth they are called neonatal teeth. Natal teeth may be found in the anterior region of the maxilla in association with cleft lip/palate. They have only a small amount of root formed and are mobile. For this reason (together with difficulty associated with breastfeeding), they are often extracted Có thể gây tai biến như sốt, gầy yếu, có những cơn đau dạ dày, ruột gây nguy hại cho tính mạng của trẻ. - Chẩn đoán phân biệt: Khác với răng mọc thật sự, răng mọc giả tạo mọc lên rất nhanh, trong một thời gian ngắn răng có thể nhú lên từ 2-3mm, răng lung lay và nướu xung quanh đỏ tấy.
- Permanent teeth may erupt early when their deciduous predecessors have been extracted prematurely because of dental caries. Early eruption of the whole dentition may be associated with a general hormonal disturbance such as hyperpituitarism or hyperthyroidism.
- The most common eruptive disorders are delayed eruption (or non- eruption) of one (or more) permanent anterior maxillary teeth or the mandibular third molar(s). In the case of mandibular third molars, the reason is lack of space so that the tooth is impacted against the second permanent molar immediately in front If the crown of the impacted third molar is partially erupted, food debris may accumulate in the stagnation area between the overlying gum flap and the crown and may lead to an inflammatory reaction in the gingiva (pericoronitis). This may eventually spread to involve surrounding tissue spaces (see pages 76–80). If the tooth is malaligned, it may remain unerupted.
- There are many human syndromic conditions that can disrupt eruption and these are shown in Table 26.2. Approximately 50% of these conditioncan now be attributed to a genetic defect. Note that ‘primary failure of eruption’ affects mainly permanent posterior teeth and refers to a localized failure with no other systemic involvement. It has been suggested that this condition is a defect of the eruption mechanism itself. However, the precise cause of the lack of eruption is presently unknown. As an example of a syndromic condition, Figure 26.55 represents an orthopantomogram of a patient with cleidocranial dysplasia (dysostosis). This syndrome is caused by a mutation in the Cbfa1 gene (see page 212). The majority of teeth are unerupted and a number of supernumerary teeth may be encountered.
- Delayed eruption of maxillary permanent first incisors is most commonly due to obstruction by a supernumerary tooth (Fig. 26.50) or an odontome (see Fig. 21.42). Removal of the obstruction will allow for eruption with or without the aid of orthodontic appliances. In some cases, no obstruction is present and the occlusal margins of the anterior teeth can be seen just beneath the oral mucosa and yet the teeth refuse to erupt. In such cases, surgical exposure will usually be sufficient to allow eruption. Delayed eruption may also be associated with teeth where the enamel organ has undergone a cystic change to form a dentigerous (eruption) cyst above its tooth, hence pre- venting its eruption (Fig. 26.51). Fig. 26.50 Orthopantomogram of a 14-year-old patient with two supernumerary teeth (small arrows) preventing the eruption of the two maxillary first permanent incisors (large arrows). Note the associated retention of the two maxillary first deciduous incisors.
- Because of its high developmental position within the maxilla, its mal- alignment and the presence of crowding within the dental arch, the maxil- lary permanent canine may be prevented from erupting into the dental arch and this is reflected in the retention of its deciduous predecessor (Fig. 26.52). Assuming such impacted teeth are favourably positioned, they may be drawn into the dental arch by suitably designed orthodontic appliances. Fig. 26.52 (a) Orthopantomogram of a 15-year-old patient with an unerupted maxillary permanent canine (arrow), above which is a retained deciduous maxillary canine. (b) Maxillary occlusal radiograph showing the unerupted maxillary permanent canine (large arrow) and the retained maxillary deciduous canine (small arrow).
- If the periodontal ligament is damaged, the root of a tooth may become fixed (ankylosed) to the adjacent alveolar bone. The deciduous tooth is then unable to move. Its position within the jaw remains constant so that, as height of the alveolar bone increases, the tooth appears to sink gradually below the level of the adjacent teeth. Such ankylosed teeth are referred to as ‘submerged’ teeth (Figs 26.53, 26.54). The submergence may continue to such an extent that the teeth become completely buried within bone. The cause of this condition is not always apparent, although there may be an association with trauma/inflammation. It may also affect permanent molars. 4. ANKYLOSIS Ankylosis [ang ki LO sis] may be initiated by an infec- tion or trauma to the periodontal ligament, resulting in the loss of its periodontal ligament space so the tooth root is truly fused to the alveolar process or bone. These teetherupt into the oral cavity but after ankylosis, fail to reach occlusion with the opposing arch and appear shorter than adjacent teeth in its arch. Many times, ankylosis of a primary tooth occurs when the permanent successor is missing. Primary mandibular second molars most oftenfail to continue erupting as the jaw grows. Consequently, the ankylosed tooth will be 2 to 4 mm short of occluding with an opposing tooth.
- Fig. 26.53 Patient with a submerging mandibular right deciduous second molar (arrow). Courtesy of Dr P. Smith. ig. 26.54 Orthopantomogram of patient with a submerging mandibular second deciduous molar (arrow) that will prevent the eruption of the second premolar beneath it. Courtesy of Dr P. Smith.
- The presence of supernumerary teeth distal to the third molars is more common in the maxillary arch but does occur in the mandible. These supernumer- ary teeth are often called distomolars, paramolars, or fourth molars. These extra teeth rarely erupt into the oral cavity and, thus, are usually discovered through radiographs 1. UNERUPTED (IMPACTED) TEETH Unerupted teeth are embedded teeth that fail to erupt into the oral cavity because of a lack of erup- tive force. Impacted teeth, on the other hand, fail to erupt due to mechanical obstruction, often related to the evolutionary decreasing size of modern man’s jaw. The most common teeth to be impacted are maxillary and mandibular third molars (Fig. 11-35) and maxil- lary canines.2,4,34 (At least 10% of the population have impacted teeth.) 2. MISPLACED TEETH (TRANSPOSITION) Occasionally, the cells that form a tooth (tooth buds) seem to get out of place, causing teeth to emerge in unusual locations. The most common tooth involved is the maxillary canine seen in Figure 11-36 (20 of 25 cases reported),35 followed by the mandibular canine (Fig. 11-37). Maxillary canines can even be transposed to the central incisor region.36,37 3. TOOTHROTATION Rotation is a rare anomaly, most common for the maxillary second premolar (Fig. 11-38), sometimes the maxillary incisor, first premolar, or mandibular second premolar.38 A tooth may be rotated on its axis by as much as 180°.
- Paramolars, distomolars, or fourth (supernu- merary) molars. A. Radiograph showing a maxillary (fourth) distomolar. B. Mandibular (fourth) distomolar just distal to the permanent third molar. Supernumerary teeth in mandibular premolar region. A. View of extra mandibular first premolar (on the left side of the mouth) fully erupted but crowded. (Courtesy of Dr. L. Claman.) B. Extra mandibular first premolars on each side of the mandibular arch are positioned lingually.
- Periodontal disease As a result of the unsatisfactory relationship between the second and third molars, the area is prone to periodontal disease, which may compromise the second molar. This can be improved by the removal of the third molar.
- Untreatable caries, pulpal or periapical pathology Another common indication for removal of wisdom teeth is the development of caries either in the wisdom tooth itself or in the adjacent second molar. This occurs because the patient is unable to clean the distal aspect of the second molar or the area around the wisdom tooth, which is often partially erupted. This leads to the accumulation of food debris and plaque and then caries of the adjacent tooth surfaces. This may lead to untreatable pulpal or periapical pathology.
- Atrophic mandible It has been argued that an unerupted third molar in an already atrophic mandible might be a potential site for fracture and consideration should be given to removing it in a controlled manner before a fracture occurs.
- Cystic change When third molars are unerupted they may be the source of a dentigerous cyst, which can enlarge considerably before giving rise to symptoms. The risk of developingthese cysts is low but is also unpredictable and gives rise to a clinical dilemma of how often radiographic assess- ment of unerupted third molars is necessary to diagnose a cyst before its size makes the management more complicated. External or internal resorption A less common reason for removal of third molars is external resorption of the second molar due to pressure from the unerupted third molar. As with the formation of the dentigerous cyst, this resorption can be extensive before the patient experiences symptoms. Internal resorption within the wisdom tooth is also an indication for removal.
- Giai đoạn đầu là sự nhiễm trùng của túi quanh răng (VQTR) Pericoronitis This condition is characterised by inflammation around the crown of a tooth and only occurs when there is com- munication between the tooth and the oral cavity. The tooth is normally partially erupted, and hence visible, but occasionally there may be little evidence of communi- cation between it and the oral cavity and careful probing of the gingiva immediately distal to the second molar may be necessary to demonstrate some communication, however small. The patient's main complaint will be pain, which initially may be of low intensity. As the condition develops the pain increases in intensity. Swelling over the affected site may develop and this will cause further discomfort when the patient occludes with the opposing teeth. As the swelling increases, the pain on occluding becomes more severe and the patient will be discouraged from bringing the teeth together. The 'lid' of gum over the involved tooth is known as the operculum and this may show evidence of trauma from the cusps of the opposing maxillary teeth. There may be pus formation and a bad taste. There will be marked inflammation in the tissue adjacent to the affected tooth and this can lead to trismus and difficulty in swallowing. The patient may be generally unwell, with lymphadenitis and pyrexia. There will often be marked halitosis.
- Spread of infection from pericoronitis On occasion, pus associated with an impacted lower wisdom tooth will track buccally forwards above the buccinator attachment forming a sinus in the region of the first permanent molar. This may lead to some c o n - fusion as to the source of the infection and can lead to unnecessary removal of the first permanent molar. This condition is referred to as a migratory abscess. Pericoronitis can also be associated with acute ulcerative gingivitis causing marked halitosis and gingival sloughing and ulceration. Spread of infection can occur in various directions (Table 27.4), including laterally into cheek, or distobuccally under the masseter muscle to give rise to a submasseteric abscess characterised by profound trismus. It can also spread to the sublingual or sub- mandibular region and also into the area around the tonsils and parapharyngeal space (see Ch. 33). Less commonly, it can ascend through the anterior pillar of fauces into soft palate causing marked dysphagia. Early and competent management of acute pericoronitis will hopefully limit this spread.
- Treatment of pericoronitis The management of pericoronitis is similar to the man- agement of any acute oral infection. It is essential to provide drainage for any pus. Once drainage is adequate it is important to clean the area beneath the operculum. This can be carried out mechanically by irrigation with warm chlorhexidine or saline solution. This should remove any accumulated food debris and plaque. Application of antiseptic or mildly caustic solutions underneath the operculum may be beneficial. Examples include Talbot's iodine and trichloracetic acid. These agents are astringents and will cause soft tissue damage, and must therefore be used with caution. If the maxillary third molar has overerupted and is causing trauma to the operculum, the single most effective treatment is its removal. This can be carried out easily, even in the presence of some degree of trismus, and often leads to resolution. The patient's general condition needs to be assessed and a decision made regarding the prescription of an antibiotic (see Ch. 33). The patient should be encouraged to use regular hot saline mouthwashes and discouraged from applying heat to the cheek area extra- orally. Arrangements should be made for early review of the patient's condition (within 2-3 days), when some resolution should have occurred.