白露 張洪雷 陳鵬 李偉 江長青 張文濤

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·論著·

肱骨頭內(nèi)翻畸形導(dǎo)致肱骨近端骨折內(nèi)固定失敗的生物力學(xué)研究

白露 張洪雷 陳鵬 李偉 江長青 張文濤

目的 探討肱骨頭內(nèi)翻狀態(tài)下鎖定鋼板固定肱骨近端骨折內(nèi)固定失敗的生物力學(xué)原因。方法 采用防腐處理肱骨標(biāo)本6對(duì)，經(jīng)肱骨外科頸截骨制作肱骨近端骨折模型。根據(jù)不同臨床情況分為力線正常組和肱骨頭內(nèi)翻組。通過循環(huán)軸向壓縮試驗(yàn)(5 000次)和靜態(tài)軸向壓縮破壞試驗(yàn)對(duì)兩組骨折內(nèi)固定模型進(jìn)行生物力學(xué)測試。結(jié)果 在循環(huán)軸向壓縮試驗(yàn)早期，肱骨頭內(nèi)翻組骨折塊間隙移位與力線正常組差異無統(tǒng)計(jì)學(xué)意義(P>0.05)。在循環(huán)壓縮3 000次后，肱骨頭內(nèi)翻組骨折端移位明顯高于力線正常組。在破壞力學(xué)實(shí)驗(yàn)中，肱骨頭內(nèi)翻組內(nèi)固定失敗所需載荷明顯小于力線正常組(t=3.812,P=0.003)。內(nèi)固定失敗軸向最大移位，力線正常組明顯高于肱骨頭內(nèi)翻組(t=2.994,P=0.013)。結(jié)論 肱骨頭內(nèi)翻畸形顯著降低了肱骨近端骨折鎖定鋼板內(nèi)固定系統(tǒng)的穩(wěn)定效能。

肱骨骨折,近端；肱骨頭；內(nèi)翻畸形；鎖定鋼板

肱骨近端骨折是創(chuàng)傷骨科常見疾病，由于肱骨近端骨密度隨著年齡增長而逐漸降低，故肱骨近端骨折在中老年人群中更為常見，其發(fā)生率約為全身骨折的5%[1]。而隨著社會(huì)老齡化進(jìn)程，肱骨近端骨折的發(fā)生率有增高的趨勢[2]。近20年來，不穩(wěn)定肱骨近端骨折的手術(shù)治療方法有了較大變化。即由以往經(jīng)皮穿針固定、普通鋼板逐漸轉(zhuǎn)變?yōu)橐浴皟?nèi)固定支架”為主流的鎖定鋼板固定。由于鎖定鋼板板釘之間“一體化”，加之多個(gè)方向的鎖定螺釘可以從不同角度對(duì)肱骨頭進(jìn)行把持，故無論在臨床實(shí)踐還是生物力學(xué)研究中，其相對(duì)于普通鋼板的優(yōu)勢均得到了很好的體現(xiàn)[3-4]。

隨著鎖定鋼板大規(guī)模應(yīng)用于治療肱骨近端骨折，一些中長期的臨床隨訪資料表明，在內(nèi)側(cè)皮質(zhì)缺損的2部分或3部分肱骨近端骨折病例中出現(xiàn)了骨折復(fù)位丟失、肱骨頭內(nèi)翻畸形和繼發(fā)內(nèi)固定失敗[5-7]等現(xiàn)象。臨床隊(duì)列研究發(fā)現(xiàn)，該類并發(fā)癥多表現(xiàn)為內(nèi)側(cè)皮質(zhì)缺損伴有肱骨頭內(nèi)翻畸形相關(guān)，并隨著時(shí)間的推移繼而出現(xiàn)肱骨頭內(nèi)翻脫出，螺釘斷裂或鋼板斷裂[8-11]。從生物力學(xué)角度講，肱骨近端缺少內(nèi)側(cè)皮質(zhì)的力學(xué)支撐是潛在的不穩(wěn)定因素。但并非所有伴內(nèi)側(cè)皮質(zhì)缺損者都出現(xiàn)內(nèi)固定失敗，并且內(nèi)固定失敗的類型也各不相同。那么，肱骨頭內(nèi)翻是否為內(nèi)固定失敗的又一危險(xiǎn)因素？我們從生物力學(xué)的角度研究肱骨頭內(nèi)翻畸形與鎖定鋼板治療肱骨近端骨折后內(nèi)固定失敗的相互關(guān)系。

材 料 與 方 法

一、標(biāo)本處理與骨折模型的建立

取6對(duì)防腐處理的成人肱骨標(biāo)本(標(biāo)本來自深圳大學(xué)醫(yī)學(xué)院解剖學(xué)系)，拍片檢查排除骨病、陳舊骨折等病理情況。在力學(xué)實(shí)驗(yàn)前于-20 ℃冷藏，待進(jìn)行力學(xué)實(shí)驗(yàn)時(shí)于室溫(18 ℃)下解凍8 h。解凍過程中噴灑生理鹽水以免標(biāo)本干燥。

將每對(duì)標(biāo)本隨機(jī)取左右側(cè)，入組肱骨頭內(nèi)翻組和力線正常組并制作骨折模型。骨折模型在X-Y工作臺(tái)上完成。首先統(tǒng)一對(duì)肱骨標(biāo)本自近端截取20 cm。使用擺鋸在肱骨干骺端與肱骨頭移行的外科頸處平行于肱骨頭頂點(diǎn)切線位截骨。截骨時(shí)保留肱骨近端外側(cè)大結(jié)節(jié)部周徑皮質(zhì)的1/3，以便PHILOS鋼板打入。截骨面之間骨折間隙為10 mm。肱骨頭內(nèi)翻畸形的制備按照Voigt等[12]的方法：在X-Y工作臺(tái)上通過角度測量尺將肱骨頭內(nèi)翻20°。所有骨折均采用Synthesis PHILOS五孔鎖定鋼板進(jìn)行固定。按照AO組織推薦方法：將鋼板放置于大結(jié)節(jié)上，距離結(jié)節(jié)間溝5～8 mm，距離大結(jié)節(jié)頂部8～10 mm處，均固定PHILOS鋼板近端A、B、C、D、E孔。遠(yuǎn)端使用3枚鎖定螺釘固定。所有螺釘均采用3.5 mm鎖定螺釘。

二、力學(xué)實(shí)驗(yàn)流程

1.標(biāo)本的固定與測試方法：力學(xué)實(shí)驗(yàn)在Instron 8874(2 kN，±1%)力學(xué)試驗(yàn)機(jī)上進(jìn)行(圖1)。骨折模型固定于試驗(yàn)機(jī)工作臺(tái)，肱骨干軸線與力學(xué)試驗(yàn)機(jī)壓頭垂直。軸向壓縮的力學(xué)壓頭內(nèi)使用骨水泥預(yù)塑形，使之與肱骨頭外形相適配，避免加壓過程中部分區(qū)域應(yīng)力集中導(dǎo)致肱骨頭表面破壞。循環(huán)軸向壓縮實(shí)驗(yàn)條件：最小壓力50 N，最大壓力300 N，允許的最大移位5 mm，測試循環(huán)數(shù)5 000次。實(shí)驗(yàn)得到的生物力學(xué)曲線以移位-載荷曲線表示。

2.內(nèi)固定失敗的判定：在循環(huán)軸向加壓實(shí)驗(yàn)中，如每一例實(shí)驗(yàn)標(biāo)本數(shù)據(jù)曲線的變化均在彈性變量的曲線范圍以內(nèi)，認(rèn)定其為內(nèi)固定失敗。在破壞力學(xué)實(shí)驗(yàn)中，實(shí)時(shí)觀測力學(xué)試驗(yàn)機(jī)移位-載荷曲線。在破壞力學(xué)實(shí)驗(yàn)中，以移位-載荷曲線出現(xiàn)趨于移位零點(diǎn)的“拐點(diǎn)”為內(nèi)固定失敗。內(nèi)固定失敗后不再進(jìn)行力學(xué)測量，取下標(biāo)本觀察內(nèi)固定失敗類型并記錄。

圖1 Instron力學(xué)實(shí)驗(yàn)機(jī)及實(shí)驗(yàn)圖片

循環(huán)次數(shù)最小移位肱骨頭內(nèi)翻力線正常P值最大移位肱骨頭內(nèi)翻力線正常P值10.00(0.00-0.01)0.00(0.00-0.00)0.9220.29(0.02-0.36)0.22(0.01-0.29)0.44100.11(0.03-0.29)0.07(0.03-0.18)0.5760.51(0.18-0.66)0.36(0.12-0.51)0.3572000.19(0.12-0.53)0.09(0.02-0.36)0.1451.08(0.31-1.77)0.78(0.26-1.31)0.2625000.35(0.18-0.71)0.21(0.12-0.57)0.0871.65(0.53-2.08)0.92(0.24-1.35)0.18910000.56(0.20-0.72)0.33(0.16-0.63)0.2271.99(0.72-2.23)1.08(0.39-1.56)0.08720000.67(0.22-0.82)0.34(0.20-0.66)0.0782.19(0.89-2.56)1.37(0.72-1.86)0.05630000.72(0.29-0.89)0.38(0.22-0.71)0.0622.37(1.01-2.78)1.73(0.91-2.08)0.044*40000.83(0.39-1.00)0.43(0.31-0.81)0.039*2.78(1.32-3.17)1.97(1.32-2.21)0.037*50000.91(0.39-1.23)0.56(0.37-0.86)0.026*3.08(1.78-3.67)2.32(1.58-2.94)0.019*

注：測量值平均數(shù) *P<0.05

三、統(tǒng)計(jì)學(xué)分析

結(jié) 果

一、循環(huán)力學(xué)結(jié)果

在軸向載荷5 000次中，6對(duì)標(biāo)本均未出現(xiàn)內(nèi)固定失敗。在軸向循環(huán)壓力檢測中，肱骨頭內(nèi)翻組在2 000次以內(nèi)的軸向壓縮中，最小移位和最大移位均較力線正常組大，但差異無統(tǒng)計(jì)學(xué)意義(P>0.05)。在循環(huán)軸向加壓3 000次肱骨頭內(nèi)翻組平均最大移位為2.37 mm (1.01～2.78)，較力線正常組1.73 mm(0.91～2.08)差異有統(tǒng)計(jì)學(xué)意義(P=0.044)。在循環(huán)軸向加壓4 000次后，肱骨頭內(nèi)翻組最小移位(P=0.039)與最大移位(P=0.037)均明顯高于力線正常組。在循環(huán)軸向加壓5 000次時(shí)。肱骨頭內(nèi)翻組平均最小移位為0.91 mm (0.39～1.23)，平均最大移位為3.08 mm (1.78～3.67)。力線正常組則分別為0.56 mm(0.37～0.86)和2.32 mm(1.58～2.94)，其平均最小移位(P=0.026)和平均最大移位(P=0.019)均明顯小于肱骨頭內(nèi)翻組。見表1。

二、破壞力學(xué)實(shí)驗(yàn)結(jié)果

在標(biāo)本完成循環(huán)載荷實(shí)驗(yàn)后，即刻進(jìn)行破壞力學(xué)實(shí)驗(yàn)。力線正常組平均破壞載荷(870±104) N，內(nèi)翻畸形組為(632±111) N。組間比較差異有統(tǒng)計(jì)學(xué)意義(t=3.812,P=0.003)。內(nèi)固定失敗時(shí)力線正常組平均骨折間隙移位為(6.72±0.71) mm，肱骨頭內(nèi)翻組為(5.67±0.53) mm組間比較差異有統(tǒng)計(jì)學(xué)意義(t=2.994,P=0.013)，見表2和圖2。

討 論

近10年來，肱骨近端骨折在治療理念上完成了由過去的“T型鋼板+松質(zhì)骨螺釘內(nèi)固定”向“角度穩(wěn)定的鎖定鋼板內(nèi)固定”的轉(zhuǎn)變。在鎖定鋼板將穩(wěn)定固定的問題推上了新高度的同時(shí)，復(fù)位丟失和內(nèi)翻畸形成為了臨床關(guān)注的另一焦點(diǎn)。在以往使用普通鋼板固定骨折時(shí)，由于肱骨頭內(nèi)骨量不足，肱骨近端生物力學(xué)的不穩(wěn)定往往導(dǎo)致螺釘松動(dòng)脫出，或者螺釘難以把持肱骨頭，與肱骨頭之間不斷出現(xiàn)相對(duì)活動(dòng)，最終造成螺釘松動(dòng)，內(nèi)固定失敗。當(dāng)鎖定鋼板固定雖然改善了固定物對(duì)骨質(zhì)疏松骨的把持力，但同時(shí)也出現(xiàn)了不同于以往的內(nèi)固定失敗的類型：肱骨頭內(nèi)翻，內(nèi)固定螺釘不能把持肱骨頭；或內(nèi)固定鋼板或螺釘自肱骨大結(jié)節(jié)外側(cè)壁處斷裂，而有的病例即使使用了肱骨距螺釘也依然出現(xiàn)內(nèi)固定失敗[13-15]。肩關(guān)節(jié)雖為非負(fù)重關(guān)節(jié)，但由于肩胛帶周圍肌肉的張力作用，肱骨頭仍對(duì)關(guān)節(jié)盂有一定的應(yīng)力。在體生物力學(xué)研究表明：肩關(guān)節(jié)在靜息狀態(tài)下盂肱關(guān)節(jié)面的受力方向?yàn)榕c肱骨頭軸線在冠狀面成角大約22.5°～23°，在矢狀面成角40°左右。且該致畸力量達(dá)到整個(gè)體重的1/3～1/2。在術(shù)后7個(gè)月，肩關(guān)節(jié)正常狀態(tài)下外展時(shí)肱骨頭受力約為整個(gè)體重的1.1倍；肩關(guān)節(jié)上舉時(shí)受力約為整個(gè)體重的1.3倍[16]。正因如此，肱骨近端骨折內(nèi)固定系統(tǒng)處于上述應(yīng)力中，如存在其他不穩(wěn)定因素如復(fù)位不良、骨缺損等，則有可能內(nèi)固定系統(tǒng)出現(xiàn)應(yīng)力集中或局部松動(dòng)，從而出現(xiàn)內(nèi)固定失敗。

表2 各組標(biāo)本破壞力學(xué)實(shí)驗(yàn)數(shù)據(jù)

注：藍(lán)色曲線代表內(nèi)翻畸形標(biāo)本，紅色曲線代表正常對(duì)照標(biāo)本，在相同軸向載荷加載過程中，骨折間隙的移位隨著載荷增加而增大，在標(biāo)本內(nèi)固定系統(tǒng)失敗時(shí)達(dá)到曲線拐點(diǎn)圖2 6對(duì)標(biāo)本的移位-載荷曲線

在肱骨近端骨折內(nèi)固定生物力學(xué)研究中，內(nèi)側(cè)皮質(zhì)缺損與復(fù)位丟失的相互關(guān)系及病理生理變化均已經(jīng)得到闡明[15,17-19]。但內(nèi)翻畸形與內(nèi)固定失敗的關(guān)系尚不完全明了。Lescheid等[20]對(duì)缺少內(nèi)側(cè)皮質(zhì)支撐的肱骨近端骨折進(jìn)行的破壞生物力學(xué)測試。結(jié)果顯示：無內(nèi)側(cè)皮質(zhì)支撐的肱骨近端骨折更加容易移位，具有冠狀面(旋轉(zhuǎn))和矢狀面(內(nèi)翻)的不穩(wěn)定。雖然內(nèi)側(cè)皮質(zhì)缺損已被證實(shí)是導(dǎo)致肱骨近端骨折術(shù)后復(fù)位丟失的重要原因，但在內(nèi)側(cè)支撐不穩(wěn)定的力學(xué)條件下，肱骨頭出現(xiàn)了怎樣的致畸移位，而該過程是否能繼發(fā)內(nèi)固定失敗也未得到完全闡明。Voigt等[12]證明，內(nèi)翻狀態(tài)下的肱骨近端骨折在力學(xué)構(gòu)型上更加不穩(wěn)定，但并未對(duì)內(nèi)翻是如何影響肱骨近端內(nèi)固定的動(dòng)態(tài)穩(wěn)定進(jìn)行研究。在本研究中，肱骨頭固定于內(nèi)翻畸形狀態(tài)較力線正常組在軸向壓力下更容易出現(xiàn)骨折間隙的移位[(6.72±0.71) mm VS (5.67±0.53) mm，t=2.994,P=0.013]。而就內(nèi)固定系統(tǒng)的穩(wěn)定性而言，內(nèi)翻畸形內(nèi)固定破壞強(qiáng)度顯著低于力線正常組[(870±104) N VS (632±111) N，t=3.812,P=0.003]。由于肱骨頭位于肱骨近端所受應(yīng)力的偏心位，而內(nèi)翻則可能增加致畸作用的力臂，從而使得肱骨頭處于不穩(wěn)定的力學(xué)狀態(tài)。

臨床報(bào)道的肱骨近端骨折鎖定鋼板術(shù)后內(nèi)固定失敗者大致可分為兩種：(1)肱骨頭內(nèi)翻畸形，骨折端不愈合或畸形愈合。此時(shí)，由于肱骨頭的內(nèi)翻，鎖定螺釘相對(duì)于肱骨頭位置發(fā)生變化，出現(xiàn)螺釘穿出關(guān)節(jié)面。(2)內(nèi)側(cè)皮質(zhì)缺損較大，肱骨頭內(nèi)側(cè)缺乏有效的力學(xué)支撐，肱骨頭內(nèi)翻的致畸力作用于鎖定鋼板，導(dǎo)致內(nèi)固定疲勞，鋼板斷裂或鋼板螺釘鎖定部位斷裂[12,14,21-22]。在本研究的動(dòng)態(tài)力學(xué)實(shí)驗(yàn)中，隨著循環(huán)載荷的增加，內(nèi)翻畸形組骨折端移位明顯高于力線正常組。這有可能解釋上述臨床情況：內(nèi)翻帶來的內(nèi)固定系統(tǒng)的不穩(wěn)定，而不穩(wěn)定的骨折端又成為內(nèi)固定系統(tǒng)的骨-螺釘界面的薄弱環(huán)節(jié)。使得骨折端不能得到穩(wěn)定的力學(xué)環(huán)境而影響愈合。由于鎖定鋼板固定是一種整體穩(wěn)定，即肱骨頭內(nèi)打入的鎖定螺釘與鋼板為一整體，所以在肱骨頭漸進(jìn)性內(nèi)翻畸形的過程中，位于肱骨近端外側(cè)壁的鋼板受的是偏心作用力，應(yīng)力集中于肱骨-鎖定鋼板的外側(cè)，從而可能導(dǎo)致鋼板或鋼板螺釘鎖定部位在反復(fù)多次的集中應(yīng)力作用下出現(xiàn)斷裂。如鋼板未發(fā)生斷裂，肱骨頭畸形移位，螺釘釘?shù)罃U(kuò)大，出現(xiàn)繼發(fā)性螺釘穿出。

就本研究而言，由于內(nèi)翻成角，肱骨近端的主要承力結(jié)構(gòu)(內(nèi)側(cè)皮質(zhì))并非處于解剖復(fù)位狀態(tài)，而由于內(nèi)側(cè)支撐的缺失，肱骨頭在應(yīng)力作用下更容易出現(xiàn)內(nèi)翻的傾向。作為偏心固定的鎖定鋼板，壓力側(cè)的支撐缺損必然會(huì)引起張力側(cè)的應(yīng)力集中。故臨床多見肱骨頭內(nèi)翻畸形后繼發(fā)鎖定鋼板在外科頸骨折線水平斷裂。

肩關(guān)節(jié)雖為非負(fù)重關(guān)節(jié)，但從本實(shí)驗(yàn)來看，肱骨近端骨折術(shù)后內(nèi)固定失敗也難以用經(jīng)典的“負(fù)重→內(nèi)固定失效或骨折局部應(yīng)力集中→骨折端過度活動(dòng)→復(fù)位丟失→內(nèi)固定失效”理論來解釋。但本研究尚有不足：(1)未能測量各組標(biāo)本的骨密度，沒有將骨密度作為另一個(gè)考證參數(shù)印證其與內(nèi)固定失敗的關(guān)系。(2)本研究僅測量了肱骨近端在致畸作用力下軸向移位，而未能對(duì)旋轉(zhuǎn)穩(wěn)定進(jìn)行研究。也就是說，內(nèi)翻的肱骨頭在三維平面內(nèi)的致畸移位與肱骨近端內(nèi)固定失敗的關(guān)系仍需進(jìn)一步的實(shí)驗(yàn)探索。

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(本文編輯：李靜)

白露，張洪雷，陳鵬，等.肱骨頭內(nèi)翻畸形導(dǎo)致肱骨近端骨折內(nèi)固定失敗的生物力學(xué)研究[J/CD].中華肩肘外科電子雜志,2015,3(2):74-80.

Biomechanical study of failed internal fixation for proximal humerus fractures caused by varus deformity of humeral head

BaiLu,ZhangHonglei,ChenPeng,LiWei,JiangChangqing,ZhangWentao.

DepartmentofSportsMedicine,PekingUniversityShenzhenHospital,Shenzhen518000,China

ZhangWentao,Email:zhangwt2007@sina.cn

Background Proximal humerus fracture (PHF) is a common disease in the traumatic orthopedics due to decreased density of bone in the proximal humerus with age.It occurs more often in the medium-and old-age people,accounting for 5% of fractures.With the process of aging population,the incidence of PHF tends to increase.In recent 20 years,the surgery methods of unstable PHF change greatly from the percutaneous fixation and common plate for fractures to locking plate fixation with "internal fixator" as mainstay.As the locking plate is widely used for PHF,some medium-and long-term clinical follow-up data indicated loss of reduction of fracture,varus deformity of humeral head,and secondary internal fixation failure were found in PHF cases with two or three sites of defective medial cortex.These complications are characterized by defective medial cortex and varus deformity of humeral head.Over time,it causes varus and prolapsed of humeral head,breakage of screws or plate.From biomechanics,the loss of support for proximal humerus by the medial cortex is an unstable factor.But not all cases with defective medial cortex develop internal fixation failure.The types of internal fixation failure vary in patients.Is the varus deformity of humerus head another risk factor for internal fixation failure? This study investigated the relationship between the varus deformity of humeral head and the internal fixation failures after locking plate treatment for PHF from the biomechanics.Methods Sample treatment and establishment of fracture model:6 pairs of adult humeral samples with antiseptic treatment were obtained from the anatomy department of the Shenzhen University-affiliated Medical School.The pathological symptoms such as bone disease and chronic fracture were excluded by radiograph.The samples were stored at -20 ℃ before biomechanical study and thawed at room temperature (18 ℃) for 8 h when the biomechanical study was about to start.During thawing,samples were sprayed with normal saline to prevent drying.Either right or left side of the samples was randomly assigned to the varus deformity group and normal alignment group to establish the fracture model.The fracture model was established on the X-Y workbench.First,20 cm was removed from the proximal ends of all samples.The osteotomy was performed in parallel with the vertex tangent of the humeral head at the surgical neck on the junction between humeral metaphysis and the humeral head using oscillating saw.The cortex of the lateral greater tuberosity in proximal humerus was reserved at an amount accounting for 1/3 of the perimeter,which helped to insert the PHILOS plate.The fracture gap between the osteotomy surfaces was 10 mm.The varus deformity of humeral head was prepared using the method described by Voigt et al.The varus of humeral head by 20° was measured using gauge on the X-Y workbench.All fractures were fixed using 5-hole Synthesis PHILOS locking plate.According to recommendation by the AO Organization,the plate was placed on the greater tuberosity 5-8 mm away from the intertubercular sulcus,8-10 mm away from the greater tuberosity tip.The PHILOS plate was fixed in holes A,B,C,D and E.Three locking screws were used to fix the distal end.All screws were 3.5 mm locking screws.Procedures of mechanical study:Fixation and testing of samples:The mechanics study was performed on the Instron 8874 (2 kN,±1%) mechanical tester.The fracture model was fixed at the workbench of the tester.The axis of the humeral shaft was vertical to the pressure head of the mechanical tester.The pre-moulding for mechanical pressure head in the axial compression was prepared using bone cement,which was matched for the shape of humeral head to avoid damage of the surface of humeral head at the area with concentrating stress during compression.The circular axial compression experiment was performed under the following conditions:minimum pressure of 50 N,maximum pressure of 300 N,permitted maximum displacement of 5 mm,cycle number of 5,000.The biomechanical curve was expressed by displacement-load curve.Determination of internal fixation failure:In the axial compression experiment,the sample was regarded as internal fixation failure if the variation of the data curve of each sample was within the range of the curve for flexible variables.In the damage mechanical experiment,real-time displacement of mechanical tester-load curve was observed.In the damage mechanical experiment,the presence of inflection point on the displacement-load curve when the displacement curve tended to be zero indicated failure of internal fixation.The mechanical measurement was stopped after failure of internal fixation.The samples were removed for observation.The types of internal fixation were recorded.Statistical analysis:The statistical analysis was performed using PASW18.0 (SPSSInc IBM Chicago,USA).The measurement data was expressed as±s.The difference of maximum load to damage internal fixation in different groups was compared using student t test.The differences in the maximum and minimum displacement of circular mechanics between the varus group and alignment normal group were compared using Mann Whitney-Wilcoxon.The independent-sample test was performed for comparison of differences in maximum damage load and maximum displacement of the samples with internal fixation failure between groups.P<0.05 indicated statistical significance.Results (1)Results of circular mechanics:In 5,000 axial compressions,6 pairs of samples did not show internal fixation failure.In measurement of the pressure during axial cycles,the varus group had greater minimum and maximum displacements than the normal alignment group within 2,000 cycles of axial compression,although no significant difference was found (P>0.05).The mean maximum displacement in the varus group was 2.37 mm (1.01-2.78) at 3,000 cycles of axial compression,significantly different from 1.73 mm (0.91-2.08) in the normal alignment group (P=0.044).After 4,000 cycles of axial compression,the varus group had significantly higher minimum displacement (P=0.039) and maximum displacement (P=0.037) than the normal alignment group.After 5,000 cycles of axial compression,the varus group had a mean minimum displacement of 0.91 mm (0.39-1.23) and a mean maximum displacement of 3.08 mm (1.78-3.67).The normal alignment group had a mean minimum displacement of 0.56 mm (0.37-0.86) and a mean maximum displacement of 2.32 mm (1.58-2.94).The normal alignment group had significantly lower mean minimum displacement (P=0.026) and mean maximum displacement (P=0.019) than the normal alignment group.(2) Results of damage mechanics:The damage mechanical experiment was performed immediately after the circular load experiment.The mean damage loads were 870±104 N for the normal alignment group and 632±111 N for the varus deformity group.There was significant difference between two groups (t=3.812,P=0.003).In cases with internal fixation failure,the mean fracture gap displacements were 6.72±0.71 mm for the normal alignment group and 5.67±0.53 mm for the varus group.There was significant difference between the two groups (t=2.994,P=0.013).Conclusion The varus deformity of the humeral head significantly lowered the stabilization performance of the locking plate internal fixation system for the PHF.

Humral fracture,proximal；Humral head；Inversion deformity；Locking plate

10.3877/cma.j.issn.2095-5790.2015.02.002

深圳市衛(wèi)生計(jì)生系統(tǒng)科研項(xiàng)目(201402027)

518000北京大學(xué)深圳醫(yī)院運(yùn)動(dòng)醫(yī)學(xué)科

張文濤,Email:zhangwt2007@sina.cn

2015-03-16)